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Bernardo Baldisserotto - One of the best experts on this subject based on the ideXlab platform.
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protective role of rutin dietary supplementation mediated by purinergic signaling in spleen of silver catfish rhamdia quelen exposed to organophosphate pesticide Trichlorfon
Comparative Biochemistry and Physiology C-toxicology & Pharmacology, 2021Co-Authors: Matheus D Baldissera, Carine F Souza, Aleksandro S Da Silva, Altevir Rossato Viana, Bernardo BaldisserottoAbstract:Abstract Evidence suggests the involvement of purinergic signaling, a mechanism mediated by extracellular nucleotides and nucleosides, with the impairment of immune and inflammatory responses in silver catfish (Rhamdia quelen) exposed to Trichlorfon. Plant-derived substances have been considered potent anti-inflammatory agents due to effects on the purinergic system, such as the use of the flavonoid rutin. The aim of this study was to determine whether a diet containing rutin is able to prevent or reduce Trichlorfon-induced impairment of immune responses through alteration of the purinergic pathway. Spleen adenosine triphosphate (ATP) levels were significantly higher in silver catfish exposed to 11 mg/L Trichlorfon for 48 h compared to the control group, while adenosine (Ado) levels were significantly lower. Spleen ectonucleoside triphosphate diphosphohydrolase (NTPDase) activity was significantly lower in silver catfish exposed to Trichlorfon compared to control group, while adenosine deaminase activity was significantly higher. Spleen metabolites of nitric oxide, interleukin-1, and IL-6 were significantly higher in silver catfish exposed to Trichlorfon compared to control group. Diet with 3 mg rutin/kg diet was able to prevent all the alterations elicited by Trichlorfon, except restoring spleen ATP levels. The purinergic exposure signaling is involved in impairment of immune and inflammatory responses in fish exposed to Trichlorfon due to reduction in ATP hydrolyses and by an increase in Ado deamination, leading to release of pro-inflammatory mediators. Use of rutin-added diet exerted an essential role in protecting the silver catfish spleen from Trichlorfon-induced impairment on immune and inflammatory responses, preventing all alterations on splenic purinergic signaling.
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behavioral impairment and neurotoxic responses of silver catfish rhamdia quelen exposed to organophosphate pesticide Trichlorfon protective effects of diet containing rutin
Comparative Biochemistry and Physiology C-toxicology & Pharmacology, 2021Co-Authors: Matheus D Baldissera, Carine F Souza, Renato Zanella, Osmar D Prestes, Aleksandro S Da Silva, Adriana Dillenburg Meinhart, Bernardo BaldisserottoAbstract:Abstract Trichlorfon is an organophosphate pesticide used extensively for controlling ectoparasites in aquaculture. Studies have found that Trichlorfon caused environmental pollution and severe neurotoxic effects in several freshwater species. Feed additives such as flavonoids may reduce or prevent pesticide-induced toxicity in fish. The aim of the present study was to determine whether acute exposure to Trichlorfon impairs behavior and causes oxidative damage in brains of silver catfish (Rhamdia quelen). We also sought to determine whether rutin would be capable of preventing or reducing these effects. Silver catfish were divided into four groups: groups A and C received basal feed, while groups B and D received feed containing 3 mg rutin/kg diet for 21 days. After 21 days, groups C and D were exposed for 48 h to a nominal concentration of 11 mg Trichlorfon/L water. Fish exposed to Trichlorfon showed significantly longer distances travelled and swimming performances than did unexposed fish. Cerebral levels of reactive oxygen species and lipid peroxidation were significantly higher in fish exposed to Trichlorfon than in unexposed fish, while cerebral superoxide dismutase, catalase, glutathione peroxidase, and acetylcholinesterase (AChE) activities were significantly lower. Taken together, our findings suggest that dietary supplementation rutin completely prevented all alterations elicited by Trichlorfon, except for cerebral AChE activity; the latter remained significantly lower compared to the unexposed group. In summary, rutin prevents Trichlorfon-induced neurotoxicity in silver catfish.
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organophosphate pesticide Trichlorfon induced neurotoxic effects in freshwater silver catfish rhamdia quelen via disruption of blood brain barrier implications on oxidative status cell viability and brain neurotransmitters
Comparative Biochemistry and Physiology C-toxicology & Pharmacology, 2019Co-Authors: Matheus D Baldissera, Carine F Souza, Sharine N Descovi, Renato Zanella, Osmar D Prestes, Aleksandro S Da Silva, Bernardo BaldisserottoAbstract:Abstract The aim of this study was to evaluate whether rupture on blood-brain barrier (BBB) can be a pathway for Trichlorfon-induced neurotoxic effects, and to investigate its implications on oxidative status, cell viability and brain neurotransmitters in silver catfish (Rhamdia quelen). The BBB permeability was increased in fish exposed for 24 h to 22 mg/L of Trichlorfon compared to the control group, as well as in those exposed to 11 and 22 mg/L of Trichlorfon for 48 h. Compared to the control group, brain reactive oxygen species and lipid peroxide levels were higher when exposed to 22 mg/L of Trichlorfon and 11 and 22 mg/L of Trichlorfon after 24 h and 48 h, respectively, while the antioxidant capacity against peroxyl radical levels was lower. Exposure to 22 mg/L of Trichlorfon for 24 h reduced brain cell viability compared to the control group, together with 11 and 22 mg/L of Trichlorfon for 48 h. Also, brain AChE, Na+ and K+-ATPase activities were reduced in those fish exposed to Trichlorfon compared to the control group. Thus, the rupture of BBB can be considered an important pathway involved in Trichlorfon-induced neurotoxic effects, which contributes to brain oxidative damage and important changes on brain neurotransmitters.
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disturbance of energetic homeostasis and oxidative damage provoked by Trichlorfon as relevant toxicological mechanisms using silver catfish as experimental model
Chemico-Biological Interactions, 2019Co-Authors: Matheus D Baldissera, Carine F Souza, Sharine N Descovi, Renato Zanella, Osmar D Prestes, Aleksandro S Da Silva, Bernardo Baldisserotto, Antonio Francisco Igor Magalhaes De Matos, Anderson Gris, Ricardo E MendesAbstract:Abstract Recent evidences have suggested the involvement of phosphoryl transfer, catalyzed by creatine kinase (CK), adenylate kinase (AK) and pyruvate kinase (PK), to metabolic alterations and impairment of bioenergetics homeostasis linked to adenosine triphosphate (ATP) production, and utilization during exposure to pesticides. It is recognized that sublethal concentrations of Trichlorfon alter hepatic and branchial metabolism, but the pathways involved in this process remains unknown. Thus, the aim of this study was to evaluate whether phosphoryl transfer network can be a pathway involved in the hepatic and branchial metabolic alterations during exposure to sublethal concentrations of Trichlorfon using silver catfish Rhamdia quelen as experimental model. Hepatic and branchial CK (cytosolic and mitochondrial isoforms) and PK activities were inhibited after 48 h of exposure to 11 and 22 mg/L Trichlorfon compared to control group, while AK activity did not differ between groups. In addition, sodium-potassium pump (Na+, K+-ATPase) activity was lower after 48 h of exposure to 22 mg/L Trichlorfon compared to control group. Thiobarbituric acid reactive substances (TBARS) were higher in liver samples after 24 h of exposure to 22 mg/L Trichlorfon compared to control group, as well as after 48 h of exposure to 11 and 22 mg/L Trichlorfon in liver and gills. Finally, hepatic and branchial non-protein thiol (NPSH) levels were lower after 48 h of exposure to 11 and 22 mg/L Trichlorfon. All evaluated parameters did not recover after 48 h in clean water. Based on these evidence, the impairment of phosphoryl transfer network can be considered a pathway involved in the hepatic and branchial metabolic alterations during exposure to sublethal concentrations of Trichlorfon. Moreover, alterations on CK and PK activities provoke an impairment on Na+, K+-ATPase activity, which can be mediated by lipid oxidative damage and reduction of NPSH content.
Matheus D Baldissera - One of the best experts on this subject based on the ideXlab platform.
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protective role of rutin dietary supplementation mediated by purinergic signaling in spleen of silver catfish rhamdia quelen exposed to organophosphate pesticide Trichlorfon
Comparative Biochemistry and Physiology C-toxicology & Pharmacology, 2021Co-Authors: Matheus D Baldissera, Carine F Souza, Aleksandro S Da Silva, Altevir Rossato Viana, Bernardo BaldisserottoAbstract:Abstract Evidence suggests the involvement of purinergic signaling, a mechanism mediated by extracellular nucleotides and nucleosides, with the impairment of immune and inflammatory responses in silver catfish (Rhamdia quelen) exposed to Trichlorfon. Plant-derived substances have been considered potent anti-inflammatory agents due to effects on the purinergic system, such as the use of the flavonoid rutin. The aim of this study was to determine whether a diet containing rutin is able to prevent or reduce Trichlorfon-induced impairment of immune responses through alteration of the purinergic pathway. Spleen adenosine triphosphate (ATP) levels were significantly higher in silver catfish exposed to 11 mg/L Trichlorfon for 48 h compared to the control group, while adenosine (Ado) levels were significantly lower. Spleen ectonucleoside triphosphate diphosphohydrolase (NTPDase) activity was significantly lower in silver catfish exposed to Trichlorfon compared to control group, while adenosine deaminase activity was significantly higher. Spleen metabolites of nitric oxide, interleukin-1, and IL-6 were significantly higher in silver catfish exposed to Trichlorfon compared to control group. Diet with 3 mg rutin/kg diet was able to prevent all the alterations elicited by Trichlorfon, except restoring spleen ATP levels. The purinergic exposure signaling is involved in impairment of immune and inflammatory responses in fish exposed to Trichlorfon due to reduction in ATP hydrolyses and by an increase in Ado deamination, leading to release of pro-inflammatory mediators. Use of rutin-added diet exerted an essential role in protecting the silver catfish spleen from Trichlorfon-induced impairment on immune and inflammatory responses, preventing all alterations on splenic purinergic signaling.
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behavioral impairment and neurotoxic responses of silver catfish rhamdia quelen exposed to organophosphate pesticide Trichlorfon protective effects of diet containing rutin
Comparative Biochemistry and Physiology C-toxicology & Pharmacology, 2021Co-Authors: Matheus D Baldissera, Carine F Souza, Renato Zanella, Osmar D Prestes, Aleksandro S Da Silva, Adriana Dillenburg Meinhart, Bernardo BaldisserottoAbstract:Abstract Trichlorfon is an organophosphate pesticide used extensively for controlling ectoparasites in aquaculture. Studies have found that Trichlorfon caused environmental pollution and severe neurotoxic effects in several freshwater species. Feed additives such as flavonoids may reduce or prevent pesticide-induced toxicity in fish. The aim of the present study was to determine whether acute exposure to Trichlorfon impairs behavior and causes oxidative damage in brains of silver catfish (Rhamdia quelen). We also sought to determine whether rutin would be capable of preventing or reducing these effects. Silver catfish were divided into four groups: groups A and C received basal feed, while groups B and D received feed containing 3 mg rutin/kg diet for 21 days. After 21 days, groups C and D were exposed for 48 h to a nominal concentration of 11 mg Trichlorfon/L water. Fish exposed to Trichlorfon showed significantly longer distances travelled and swimming performances than did unexposed fish. Cerebral levels of reactive oxygen species and lipid peroxidation were significantly higher in fish exposed to Trichlorfon than in unexposed fish, while cerebral superoxide dismutase, catalase, glutathione peroxidase, and acetylcholinesterase (AChE) activities were significantly lower. Taken together, our findings suggest that dietary supplementation rutin completely prevented all alterations elicited by Trichlorfon, except for cerebral AChE activity; the latter remained significantly lower compared to the unexposed group. In summary, rutin prevents Trichlorfon-induced neurotoxicity in silver catfish.
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protective effects of diet containing rutin against Trichlorfon induced muscle bioenergetics disruption and impairment on fatty acid profile of silver catfish rhamdia quelen
Ecotoxicology and Environmental Safety, 2020Co-Authors: Matheus D Baldissera, Carine F Souza, Adriana Dillenburg Meinhart, Belisa Parmeggiani, Raquel G Vendrusculo, Lucila C Ribeiro, Daniela K Muenchen, Carla C Zeppenfeld, Roger Wagner, Renato ZanellaAbstract:Abstract Trichlorfon is an organophosphate insecticide that is widely used on fish farms to control parasitic infections. It has been detected in freshwater ecosystems as well as in fishery products. There is a growing body of evidence to suggest that certain feed additives may reduce or prevent pesticide-induced toxicity in fish. The aim of the present study was to determine whether acute exposure to Trichlorfon would alter bioenergetic homeostasis and alter fatty acid profiles in muscles of silver catfish (Rhamdia quelen). We also sought to determine whether rutin prevents or reduces these effects. Cytosolic and mitochondrial creatine kinase (CK) and activities of complexes II-III and IV in muscle were significantly inhibited by exposure to 11 mg/L Trichlorfon for 48 h compared to effects in the unexposed group. Total content of polyunsaturated fatty acids (omega-3 and omega-6) were significantly lower in muscle of silver catfish exposed to 11 mg/L Trichlorfon for 48 h than in the unexposed group. Addition of 3 mg rutin/kg feed increased CK activity and prevented inhibition of complex IV activity, as well as preventing all alterations of muscle fatty acid profiles elicited by exposure to Trichlorfon. No significant differences were observed between groups with respect to muscle adenylate kinase or pyruvate kinase activities, as well as total content of saturated and monounsaturated fatty acids. Our findings suggest that exposure (48 h) to 11 mg Trichlorfon/L water inhibits cytosolic and mitochondrial CK activity in muscle. Trichlorfon also affects activities of complexes II-III and IV in respiratory chain, with important consequences for adenosine triphosphate production. The pesticide alters fatty acid profiles in the fish and endangers human consumers of the product. The most important finding of the present study is that inclusion of rutin improves bioenergetic homeostasis and muscle fatty acid profiles, suggesting that it reduces Trichlorfon-induced muscle damage.
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organophosphate pesticide Trichlorfon induced neurotoxic effects in freshwater silver catfish rhamdia quelen via disruption of blood brain barrier implications on oxidative status cell viability and brain neurotransmitters
Comparative Biochemistry and Physiology C-toxicology & Pharmacology, 2019Co-Authors: Matheus D Baldissera, Carine F Souza, Sharine N Descovi, Renato Zanella, Osmar D Prestes, Aleksandro S Da Silva, Bernardo BaldisserottoAbstract:Abstract The aim of this study was to evaluate whether rupture on blood-brain barrier (BBB) can be a pathway for Trichlorfon-induced neurotoxic effects, and to investigate its implications on oxidative status, cell viability and brain neurotransmitters in silver catfish (Rhamdia quelen). The BBB permeability was increased in fish exposed for 24 h to 22 mg/L of Trichlorfon compared to the control group, as well as in those exposed to 11 and 22 mg/L of Trichlorfon for 48 h. Compared to the control group, brain reactive oxygen species and lipid peroxide levels were higher when exposed to 22 mg/L of Trichlorfon and 11 and 22 mg/L of Trichlorfon after 24 h and 48 h, respectively, while the antioxidant capacity against peroxyl radical levels was lower. Exposure to 22 mg/L of Trichlorfon for 24 h reduced brain cell viability compared to the control group, together with 11 and 22 mg/L of Trichlorfon for 48 h. Also, brain AChE, Na+ and K+-ATPase activities were reduced in those fish exposed to Trichlorfon compared to the control group. Thus, the rupture of BBB can be considered an important pathway involved in Trichlorfon-induced neurotoxic effects, which contributes to brain oxidative damage and important changes on brain neurotransmitters.
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disturbance of energetic homeostasis and oxidative damage provoked by Trichlorfon as relevant toxicological mechanisms using silver catfish as experimental model
Chemico-Biological Interactions, 2019Co-Authors: Matheus D Baldissera, Carine F Souza, Sharine N Descovi, Renato Zanella, Osmar D Prestes, Aleksandro S Da Silva, Bernardo Baldisserotto, Antonio Francisco Igor Magalhaes De Matos, Anderson Gris, Ricardo E MendesAbstract:Abstract Recent evidences have suggested the involvement of phosphoryl transfer, catalyzed by creatine kinase (CK), adenylate kinase (AK) and pyruvate kinase (PK), to metabolic alterations and impairment of bioenergetics homeostasis linked to adenosine triphosphate (ATP) production, and utilization during exposure to pesticides. It is recognized that sublethal concentrations of Trichlorfon alter hepatic and branchial metabolism, but the pathways involved in this process remains unknown. Thus, the aim of this study was to evaluate whether phosphoryl transfer network can be a pathway involved in the hepatic and branchial metabolic alterations during exposure to sublethal concentrations of Trichlorfon using silver catfish Rhamdia quelen as experimental model. Hepatic and branchial CK (cytosolic and mitochondrial isoforms) and PK activities were inhibited after 48 h of exposure to 11 and 22 mg/L Trichlorfon compared to control group, while AK activity did not differ between groups. In addition, sodium-potassium pump (Na+, K+-ATPase) activity was lower after 48 h of exposure to 22 mg/L Trichlorfon compared to control group. Thiobarbituric acid reactive substances (TBARS) were higher in liver samples after 24 h of exposure to 22 mg/L Trichlorfon compared to control group, as well as after 48 h of exposure to 11 and 22 mg/L Trichlorfon in liver and gills. Finally, hepatic and branchial non-protein thiol (NPSH) levels were lower after 48 h of exposure to 11 and 22 mg/L Trichlorfon. All evaluated parameters did not recover after 48 h in clean water. Based on these evidence, the impairment of phosphoryl transfer network can be considered a pathway involved in the hepatic and branchial metabolic alterations during exposure to sublethal concentrations of Trichlorfon. Moreover, alterations on CK and PK activities provoke an impairment on Na+, K+-ATPase activity, which can be mediated by lipid oxidative damage and reduction of NPSH content.
Carine F Souza - One of the best experts on this subject based on the ideXlab platform.
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protective role of rutin dietary supplementation mediated by purinergic signaling in spleen of silver catfish rhamdia quelen exposed to organophosphate pesticide Trichlorfon
Comparative Biochemistry and Physiology C-toxicology & Pharmacology, 2021Co-Authors: Matheus D Baldissera, Carine F Souza, Aleksandro S Da Silva, Altevir Rossato Viana, Bernardo BaldisserottoAbstract:Abstract Evidence suggests the involvement of purinergic signaling, a mechanism mediated by extracellular nucleotides and nucleosides, with the impairment of immune and inflammatory responses in silver catfish (Rhamdia quelen) exposed to Trichlorfon. Plant-derived substances have been considered potent anti-inflammatory agents due to effects on the purinergic system, such as the use of the flavonoid rutin. The aim of this study was to determine whether a diet containing rutin is able to prevent or reduce Trichlorfon-induced impairment of immune responses through alteration of the purinergic pathway. Spleen adenosine triphosphate (ATP) levels were significantly higher in silver catfish exposed to 11 mg/L Trichlorfon for 48 h compared to the control group, while adenosine (Ado) levels were significantly lower. Spleen ectonucleoside triphosphate diphosphohydrolase (NTPDase) activity was significantly lower in silver catfish exposed to Trichlorfon compared to control group, while adenosine deaminase activity was significantly higher. Spleen metabolites of nitric oxide, interleukin-1, and IL-6 were significantly higher in silver catfish exposed to Trichlorfon compared to control group. Diet with 3 mg rutin/kg diet was able to prevent all the alterations elicited by Trichlorfon, except restoring spleen ATP levels. The purinergic exposure signaling is involved in impairment of immune and inflammatory responses in fish exposed to Trichlorfon due to reduction in ATP hydrolyses and by an increase in Ado deamination, leading to release of pro-inflammatory mediators. Use of rutin-added diet exerted an essential role in protecting the silver catfish spleen from Trichlorfon-induced impairment on immune and inflammatory responses, preventing all alterations on splenic purinergic signaling.
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behavioral impairment and neurotoxic responses of silver catfish rhamdia quelen exposed to organophosphate pesticide Trichlorfon protective effects of diet containing rutin
Comparative Biochemistry and Physiology C-toxicology & Pharmacology, 2021Co-Authors: Matheus D Baldissera, Carine F Souza, Renato Zanella, Osmar D Prestes, Aleksandro S Da Silva, Adriana Dillenburg Meinhart, Bernardo BaldisserottoAbstract:Abstract Trichlorfon is an organophosphate pesticide used extensively for controlling ectoparasites in aquaculture. Studies have found that Trichlorfon caused environmental pollution and severe neurotoxic effects in several freshwater species. Feed additives such as flavonoids may reduce or prevent pesticide-induced toxicity in fish. The aim of the present study was to determine whether acute exposure to Trichlorfon impairs behavior and causes oxidative damage in brains of silver catfish (Rhamdia quelen). We also sought to determine whether rutin would be capable of preventing or reducing these effects. Silver catfish were divided into four groups: groups A and C received basal feed, while groups B and D received feed containing 3 mg rutin/kg diet for 21 days. After 21 days, groups C and D were exposed for 48 h to a nominal concentration of 11 mg Trichlorfon/L water. Fish exposed to Trichlorfon showed significantly longer distances travelled and swimming performances than did unexposed fish. Cerebral levels of reactive oxygen species and lipid peroxidation were significantly higher in fish exposed to Trichlorfon than in unexposed fish, while cerebral superoxide dismutase, catalase, glutathione peroxidase, and acetylcholinesterase (AChE) activities were significantly lower. Taken together, our findings suggest that dietary supplementation rutin completely prevented all alterations elicited by Trichlorfon, except for cerebral AChE activity; the latter remained significantly lower compared to the unexposed group. In summary, rutin prevents Trichlorfon-induced neurotoxicity in silver catfish.
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protective effects of diet containing rutin against Trichlorfon induced muscle bioenergetics disruption and impairment on fatty acid profile of silver catfish rhamdia quelen
Ecotoxicology and Environmental Safety, 2020Co-Authors: Matheus D Baldissera, Carine F Souza, Adriana Dillenburg Meinhart, Belisa Parmeggiani, Raquel G Vendrusculo, Lucila C Ribeiro, Daniela K Muenchen, Carla C Zeppenfeld, Roger Wagner, Renato ZanellaAbstract:Abstract Trichlorfon is an organophosphate insecticide that is widely used on fish farms to control parasitic infections. It has been detected in freshwater ecosystems as well as in fishery products. There is a growing body of evidence to suggest that certain feed additives may reduce or prevent pesticide-induced toxicity in fish. The aim of the present study was to determine whether acute exposure to Trichlorfon would alter bioenergetic homeostasis and alter fatty acid profiles in muscles of silver catfish (Rhamdia quelen). We also sought to determine whether rutin prevents or reduces these effects. Cytosolic and mitochondrial creatine kinase (CK) and activities of complexes II-III and IV in muscle were significantly inhibited by exposure to 11 mg/L Trichlorfon for 48 h compared to effects in the unexposed group. Total content of polyunsaturated fatty acids (omega-3 and omega-6) were significantly lower in muscle of silver catfish exposed to 11 mg/L Trichlorfon for 48 h than in the unexposed group. Addition of 3 mg rutin/kg feed increased CK activity and prevented inhibition of complex IV activity, as well as preventing all alterations of muscle fatty acid profiles elicited by exposure to Trichlorfon. No significant differences were observed between groups with respect to muscle adenylate kinase or pyruvate kinase activities, as well as total content of saturated and monounsaturated fatty acids. Our findings suggest that exposure (48 h) to 11 mg Trichlorfon/L water inhibits cytosolic and mitochondrial CK activity in muscle. Trichlorfon also affects activities of complexes II-III and IV in respiratory chain, with important consequences for adenosine triphosphate production. The pesticide alters fatty acid profiles in the fish and endangers human consumers of the product. The most important finding of the present study is that inclusion of rutin improves bioenergetic homeostasis and muscle fatty acid profiles, suggesting that it reduces Trichlorfon-induced muscle damage.
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organophosphate pesticide Trichlorfon induced neurotoxic effects in freshwater silver catfish rhamdia quelen via disruption of blood brain barrier implications on oxidative status cell viability and brain neurotransmitters
Comparative Biochemistry and Physiology C-toxicology & Pharmacology, 2019Co-Authors: Matheus D Baldissera, Carine F Souza, Sharine N Descovi, Renato Zanella, Osmar D Prestes, Aleksandro S Da Silva, Bernardo BaldisserottoAbstract:Abstract The aim of this study was to evaluate whether rupture on blood-brain barrier (BBB) can be a pathway for Trichlorfon-induced neurotoxic effects, and to investigate its implications on oxidative status, cell viability and brain neurotransmitters in silver catfish (Rhamdia quelen). The BBB permeability was increased in fish exposed for 24 h to 22 mg/L of Trichlorfon compared to the control group, as well as in those exposed to 11 and 22 mg/L of Trichlorfon for 48 h. Compared to the control group, brain reactive oxygen species and lipid peroxide levels were higher when exposed to 22 mg/L of Trichlorfon and 11 and 22 mg/L of Trichlorfon after 24 h and 48 h, respectively, while the antioxidant capacity against peroxyl radical levels was lower. Exposure to 22 mg/L of Trichlorfon for 24 h reduced brain cell viability compared to the control group, together with 11 and 22 mg/L of Trichlorfon for 48 h. Also, brain AChE, Na+ and K+-ATPase activities were reduced in those fish exposed to Trichlorfon compared to the control group. Thus, the rupture of BBB can be considered an important pathway involved in Trichlorfon-induced neurotoxic effects, which contributes to brain oxidative damage and important changes on brain neurotransmitters.
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disturbance of energetic homeostasis and oxidative damage provoked by Trichlorfon as relevant toxicological mechanisms using silver catfish as experimental model
Chemico-Biological Interactions, 2019Co-Authors: Matheus D Baldissera, Carine F Souza, Sharine N Descovi, Renato Zanella, Osmar D Prestes, Aleksandro S Da Silva, Bernardo Baldisserotto, Antonio Francisco Igor Magalhaes De Matos, Anderson Gris, Ricardo E MendesAbstract:Abstract Recent evidences have suggested the involvement of phosphoryl transfer, catalyzed by creatine kinase (CK), adenylate kinase (AK) and pyruvate kinase (PK), to metabolic alterations and impairment of bioenergetics homeostasis linked to adenosine triphosphate (ATP) production, and utilization during exposure to pesticides. It is recognized that sublethal concentrations of Trichlorfon alter hepatic and branchial metabolism, but the pathways involved in this process remains unknown. Thus, the aim of this study was to evaluate whether phosphoryl transfer network can be a pathway involved in the hepatic and branchial metabolic alterations during exposure to sublethal concentrations of Trichlorfon using silver catfish Rhamdia quelen as experimental model. Hepatic and branchial CK (cytosolic and mitochondrial isoforms) and PK activities were inhibited after 48 h of exposure to 11 and 22 mg/L Trichlorfon compared to control group, while AK activity did not differ between groups. In addition, sodium-potassium pump (Na+, K+-ATPase) activity was lower after 48 h of exposure to 22 mg/L Trichlorfon compared to control group. Thiobarbituric acid reactive substances (TBARS) were higher in liver samples after 24 h of exposure to 22 mg/L Trichlorfon compared to control group, as well as after 48 h of exposure to 11 and 22 mg/L Trichlorfon in liver and gills. Finally, hepatic and branchial non-protein thiol (NPSH) levels were lower after 48 h of exposure to 11 and 22 mg/L Trichlorfon. All evaluated parameters did not recover after 48 h in clean water. Based on these evidence, the impairment of phosphoryl transfer network can be considered a pathway involved in the hepatic and branchial metabolic alterations during exposure to sublethal concentrations of Trichlorfon. Moreover, alterations on CK and PK activities provoke an impairment on Na+, K+-ATPase activity, which can be mediated by lipid oxidative damage and reduction of NPSH content.
Renato Zanella - One of the best experts on this subject based on the ideXlab platform.
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behavioral impairment and neurotoxic responses of silver catfish rhamdia quelen exposed to organophosphate pesticide Trichlorfon protective effects of diet containing rutin
Comparative Biochemistry and Physiology C-toxicology & Pharmacology, 2021Co-Authors: Matheus D Baldissera, Carine F Souza, Renato Zanella, Osmar D Prestes, Aleksandro S Da Silva, Adriana Dillenburg Meinhart, Bernardo BaldisserottoAbstract:Abstract Trichlorfon is an organophosphate pesticide used extensively for controlling ectoparasites in aquaculture. Studies have found that Trichlorfon caused environmental pollution and severe neurotoxic effects in several freshwater species. Feed additives such as flavonoids may reduce or prevent pesticide-induced toxicity in fish. The aim of the present study was to determine whether acute exposure to Trichlorfon impairs behavior and causes oxidative damage in brains of silver catfish (Rhamdia quelen). We also sought to determine whether rutin would be capable of preventing or reducing these effects. Silver catfish were divided into four groups: groups A and C received basal feed, while groups B and D received feed containing 3 mg rutin/kg diet for 21 days. After 21 days, groups C and D were exposed for 48 h to a nominal concentration of 11 mg Trichlorfon/L water. Fish exposed to Trichlorfon showed significantly longer distances travelled and swimming performances than did unexposed fish. Cerebral levels of reactive oxygen species and lipid peroxidation were significantly higher in fish exposed to Trichlorfon than in unexposed fish, while cerebral superoxide dismutase, catalase, glutathione peroxidase, and acetylcholinesterase (AChE) activities were significantly lower. Taken together, our findings suggest that dietary supplementation rutin completely prevented all alterations elicited by Trichlorfon, except for cerebral AChE activity; the latter remained significantly lower compared to the unexposed group. In summary, rutin prevents Trichlorfon-induced neurotoxicity in silver catfish.
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protective effects of diet containing rutin against Trichlorfon induced muscle bioenergetics disruption and impairment on fatty acid profile of silver catfish rhamdia quelen
Ecotoxicology and Environmental Safety, 2020Co-Authors: Matheus D Baldissera, Carine F Souza, Adriana Dillenburg Meinhart, Belisa Parmeggiani, Raquel G Vendrusculo, Lucila C Ribeiro, Daniela K Muenchen, Carla C Zeppenfeld, Roger Wagner, Renato ZanellaAbstract:Abstract Trichlorfon is an organophosphate insecticide that is widely used on fish farms to control parasitic infections. It has been detected in freshwater ecosystems as well as in fishery products. There is a growing body of evidence to suggest that certain feed additives may reduce or prevent pesticide-induced toxicity in fish. The aim of the present study was to determine whether acute exposure to Trichlorfon would alter bioenergetic homeostasis and alter fatty acid profiles in muscles of silver catfish (Rhamdia quelen). We also sought to determine whether rutin prevents or reduces these effects. Cytosolic and mitochondrial creatine kinase (CK) and activities of complexes II-III and IV in muscle were significantly inhibited by exposure to 11 mg/L Trichlorfon for 48 h compared to effects in the unexposed group. Total content of polyunsaturated fatty acids (omega-3 and omega-6) were significantly lower in muscle of silver catfish exposed to 11 mg/L Trichlorfon for 48 h than in the unexposed group. Addition of 3 mg rutin/kg feed increased CK activity and prevented inhibition of complex IV activity, as well as preventing all alterations of muscle fatty acid profiles elicited by exposure to Trichlorfon. No significant differences were observed between groups with respect to muscle adenylate kinase or pyruvate kinase activities, as well as total content of saturated and monounsaturated fatty acids. Our findings suggest that exposure (48 h) to 11 mg Trichlorfon/L water inhibits cytosolic and mitochondrial CK activity in muscle. Trichlorfon also affects activities of complexes II-III and IV in respiratory chain, with important consequences for adenosine triphosphate production. The pesticide alters fatty acid profiles in the fish and endangers human consumers of the product. The most important finding of the present study is that inclusion of rutin improves bioenergetic homeostasis and muscle fatty acid profiles, suggesting that it reduces Trichlorfon-induced muscle damage.
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organophosphate pesticide Trichlorfon induced neurotoxic effects in freshwater silver catfish rhamdia quelen via disruption of blood brain barrier implications on oxidative status cell viability and brain neurotransmitters
Comparative Biochemistry and Physiology C-toxicology & Pharmacology, 2019Co-Authors: Matheus D Baldissera, Carine F Souza, Sharine N Descovi, Renato Zanella, Osmar D Prestes, Aleksandro S Da Silva, Bernardo BaldisserottoAbstract:Abstract The aim of this study was to evaluate whether rupture on blood-brain barrier (BBB) can be a pathway for Trichlorfon-induced neurotoxic effects, and to investigate its implications on oxidative status, cell viability and brain neurotransmitters in silver catfish (Rhamdia quelen). The BBB permeability was increased in fish exposed for 24 h to 22 mg/L of Trichlorfon compared to the control group, as well as in those exposed to 11 and 22 mg/L of Trichlorfon for 48 h. Compared to the control group, brain reactive oxygen species and lipid peroxide levels were higher when exposed to 22 mg/L of Trichlorfon and 11 and 22 mg/L of Trichlorfon after 24 h and 48 h, respectively, while the antioxidant capacity against peroxyl radical levels was lower. Exposure to 22 mg/L of Trichlorfon for 24 h reduced brain cell viability compared to the control group, together with 11 and 22 mg/L of Trichlorfon for 48 h. Also, brain AChE, Na+ and K+-ATPase activities were reduced in those fish exposed to Trichlorfon compared to the control group. Thus, the rupture of BBB can be considered an important pathway involved in Trichlorfon-induced neurotoxic effects, which contributes to brain oxidative damage and important changes on brain neurotransmitters.
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disturbance of energetic homeostasis and oxidative damage provoked by Trichlorfon as relevant toxicological mechanisms using silver catfish as experimental model
Chemico-Biological Interactions, 2019Co-Authors: Matheus D Baldissera, Carine F Souza, Sharine N Descovi, Renato Zanella, Osmar D Prestes, Aleksandro S Da Silva, Bernardo Baldisserotto, Antonio Francisco Igor Magalhaes De Matos, Anderson Gris, Ricardo E MendesAbstract:Abstract Recent evidences have suggested the involvement of phosphoryl transfer, catalyzed by creatine kinase (CK), adenylate kinase (AK) and pyruvate kinase (PK), to metabolic alterations and impairment of bioenergetics homeostasis linked to adenosine triphosphate (ATP) production, and utilization during exposure to pesticides. It is recognized that sublethal concentrations of Trichlorfon alter hepatic and branchial metabolism, but the pathways involved in this process remains unknown. Thus, the aim of this study was to evaluate whether phosphoryl transfer network can be a pathway involved in the hepatic and branchial metabolic alterations during exposure to sublethal concentrations of Trichlorfon using silver catfish Rhamdia quelen as experimental model. Hepatic and branchial CK (cytosolic and mitochondrial isoforms) and PK activities were inhibited after 48 h of exposure to 11 and 22 mg/L Trichlorfon compared to control group, while AK activity did not differ between groups. In addition, sodium-potassium pump (Na+, K+-ATPase) activity was lower after 48 h of exposure to 22 mg/L Trichlorfon compared to control group. Thiobarbituric acid reactive substances (TBARS) were higher in liver samples after 24 h of exposure to 22 mg/L Trichlorfon compared to control group, as well as after 48 h of exposure to 11 and 22 mg/L Trichlorfon in liver and gills. Finally, hepatic and branchial non-protein thiol (NPSH) levels were lower after 48 h of exposure to 11 and 22 mg/L Trichlorfon. All evaluated parameters did not recover after 48 h in clean water. Based on these evidence, the impairment of phosphoryl transfer network can be considered a pathway involved in the hepatic and branchial metabolic alterations during exposure to sublethal concentrations of Trichlorfon. Moreover, alterations on CK and PK activities provoke an impairment on Na+, K+-ATPase activity, which can be mediated by lipid oxidative damage and reduction of NPSH content.
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protective role of rutin dietary supplementation mediated by purinergic signaling in spleen of silver catfish rhamdia quelen exposed to organophosphate pesticide Trichlorfon
Comparative Biochemistry and Physiology C-toxicology & Pharmacology, 2021Co-Authors: Matheus D Baldissera, Carine F Souza, Aleksandro S Da Silva, Altevir Rossato Viana, Bernardo BaldisserottoAbstract:Abstract Evidence suggests the involvement of purinergic signaling, a mechanism mediated by extracellular nucleotides and nucleosides, with the impairment of immune and inflammatory responses in silver catfish (Rhamdia quelen) exposed to Trichlorfon. Plant-derived substances have been considered potent anti-inflammatory agents due to effects on the purinergic system, such as the use of the flavonoid rutin. The aim of this study was to determine whether a diet containing rutin is able to prevent or reduce Trichlorfon-induced impairment of immune responses through alteration of the purinergic pathway. Spleen adenosine triphosphate (ATP) levels were significantly higher in silver catfish exposed to 11 mg/L Trichlorfon for 48 h compared to the control group, while adenosine (Ado) levels were significantly lower. Spleen ectonucleoside triphosphate diphosphohydrolase (NTPDase) activity was significantly lower in silver catfish exposed to Trichlorfon compared to control group, while adenosine deaminase activity was significantly higher. Spleen metabolites of nitric oxide, interleukin-1, and IL-6 were significantly higher in silver catfish exposed to Trichlorfon compared to control group. Diet with 3 mg rutin/kg diet was able to prevent all the alterations elicited by Trichlorfon, except restoring spleen ATP levels. The purinergic exposure signaling is involved in impairment of immune and inflammatory responses in fish exposed to Trichlorfon due to reduction in ATP hydrolyses and by an increase in Ado deamination, leading to release of pro-inflammatory mediators. Use of rutin-added diet exerted an essential role in protecting the silver catfish spleen from Trichlorfon-induced impairment on immune and inflammatory responses, preventing all alterations on splenic purinergic signaling.
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behavioral impairment and neurotoxic responses of silver catfish rhamdia quelen exposed to organophosphate pesticide Trichlorfon protective effects of diet containing rutin
Comparative Biochemistry and Physiology C-toxicology & Pharmacology, 2021Co-Authors: Matheus D Baldissera, Carine F Souza, Renato Zanella, Osmar D Prestes, Aleksandro S Da Silva, Adriana Dillenburg Meinhart, Bernardo BaldisserottoAbstract:Abstract Trichlorfon is an organophosphate pesticide used extensively for controlling ectoparasites in aquaculture. Studies have found that Trichlorfon caused environmental pollution and severe neurotoxic effects in several freshwater species. Feed additives such as flavonoids may reduce or prevent pesticide-induced toxicity in fish. The aim of the present study was to determine whether acute exposure to Trichlorfon impairs behavior and causes oxidative damage in brains of silver catfish (Rhamdia quelen). We also sought to determine whether rutin would be capable of preventing or reducing these effects. Silver catfish were divided into four groups: groups A and C received basal feed, while groups B and D received feed containing 3 mg rutin/kg diet for 21 days. After 21 days, groups C and D were exposed for 48 h to a nominal concentration of 11 mg Trichlorfon/L water. Fish exposed to Trichlorfon showed significantly longer distances travelled and swimming performances than did unexposed fish. Cerebral levels of reactive oxygen species and lipid peroxidation were significantly higher in fish exposed to Trichlorfon than in unexposed fish, while cerebral superoxide dismutase, catalase, glutathione peroxidase, and acetylcholinesterase (AChE) activities were significantly lower. Taken together, our findings suggest that dietary supplementation rutin completely prevented all alterations elicited by Trichlorfon, except for cerebral AChE activity; the latter remained significantly lower compared to the unexposed group. In summary, rutin prevents Trichlorfon-induced neurotoxicity in silver catfish.
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organophosphate pesticide Trichlorfon induced neurotoxic effects in freshwater silver catfish rhamdia quelen via disruption of blood brain barrier implications on oxidative status cell viability and brain neurotransmitters
Comparative Biochemistry and Physiology C-toxicology & Pharmacology, 2019Co-Authors: Matheus D Baldissera, Carine F Souza, Sharine N Descovi, Renato Zanella, Osmar D Prestes, Aleksandro S Da Silva, Bernardo BaldisserottoAbstract:Abstract The aim of this study was to evaluate whether rupture on blood-brain barrier (BBB) can be a pathway for Trichlorfon-induced neurotoxic effects, and to investigate its implications on oxidative status, cell viability and brain neurotransmitters in silver catfish (Rhamdia quelen). The BBB permeability was increased in fish exposed for 24 h to 22 mg/L of Trichlorfon compared to the control group, as well as in those exposed to 11 and 22 mg/L of Trichlorfon for 48 h. Compared to the control group, brain reactive oxygen species and lipid peroxide levels were higher when exposed to 22 mg/L of Trichlorfon and 11 and 22 mg/L of Trichlorfon after 24 h and 48 h, respectively, while the antioxidant capacity against peroxyl radical levels was lower. Exposure to 22 mg/L of Trichlorfon for 24 h reduced brain cell viability compared to the control group, together with 11 and 22 mg/L of Trichlorfon for 48 h. Also, brain AChE, Na+ and K+-ATPase activities were reduced in those fish exposed to Trichlorfon compared to the control group. Thus, the rupture of BBB can be considered an important pathway involved in Trichlorfon-induced neurotoxic effects, which contributes to brain oxidative damage and important changes on brain neurotransmitters.
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disturbance of energetic homeostasis and oxidative damage provoked by Trichlorfon as relevant toxicological mechanisms using silver catfish as experimental model
Chemico-Biological Interactions, 2019Co-Authors: Matheus D Baldissera, Carine F Souza, Sharine N Descovi, Renato Zanella, Osmar D Prestes, Aleksandro S Da Silva, Bernardo Baldisserotto, Antonio Francisco Igor Magalhaes De Matos, Anderson Gris, Ricardo E MendesAbstract:Abstract Recent evidences have suggested the involvement of phosphoryl transfer, catalyzed by creatine kinase (CK), adenylate kinase (AK) and pyruvate kinase (PK), to metabolic alterations and impairment of bioenergetics homeostasis linked to adenosine triphosphate (ATP) production, and utilization during exposure to pesticides. It is recognized that sublethal concentrations of Trichlorfon alter hepatic and branchial metabolism, but the pathways involved in this process remains unknown. Thus, the aim of this study was to evaluate whether phosphoryl transfer network can be a pathway involved in the hepatic and branchial metabolic alterations during exposure to sublethal concentrations of Trichlorfon using silver catfish Rhamdia quelen as experimental model. Hepatic and branchial CK (cytosolic and mitochondrial isoforms) and PK activities were inhibited after 48 h of exposure to 11 and 22 mg/L Trichlorfon compared to control group, while AK activity did not differ between groups. In addition, sodium-potassium pump (Na+, K+-ATPase) activity was lower after 48 h of exposure to 22 mg/L Trichlorfon compared to control group. Thiobarbituric acid reactive substances (TBARS) were higher in liver samples after 24 h of exposure to 22 mg/L Trichlorfon compared to control group, as well as after 48 h of exposure to 11 and 22 mg/L Trichlorfon in liver and gills. Finally, hepatic and branchial non-protein thiol (NPSH) levels were lower after 48 h of exposure to 11 and 22 mg/L Trichlorfon. All evaluated parameters did not recover after 48 h in clean water. Based on these evidence, the impairment of phosphoryl transfer network can be considered a pathway involved in the hepatic and branchial metabolic alterations during exposure to sublethal concentrations of Trichlorfon. Moreover, alterations on CK and PK activities provoke an impairment on Na+, K+-ATPase activity, which can be mediated by lipid oxidative damage and reduction of NPSH content.
