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Athar H Chishti - One of the best experts on this subject based on the ideXlab platform.
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combined deletion of mouse dematin headpiece and β adducin exerts a novel effect on the spectrin actin junctions leading to Erythrocyte Fragility and hemolytic anemia
Journal of Biological Chemistry, 2006Co-Authors: Huiqing Chen, Anwar A Khan, Fei Liu, Diana M Gilligan, Luanne L Peters, Joanne B Messick, Wanda M Haschekhock, Agnes E Ostafin, Athar H ChishtiAbstract:Dematin and adducin are actin-binding proteins of the Erythrocyte "junctional complex." Individually, they exert modest effects on Erythrocyte shape and membrane stability, and their homologues are expressed widely in non-erythroid cells. Here we report generation and characterization of double knock-out mice lacking beta-adducin and the headpiece domain of dematin. The combined mutations result in altered Erythrocyte morphology, increased membrane instability, and severe hemolysis. Peripheral blood analysis shows evidence of severe hemolytic anemia with reduced number of Erythrocytes/hematocrit/hemoglobin and an approximately 12-fold increase in the number of circulating reticulocytes. The presence of a variety of misshapen and fragmented Erythrocytes correlates with increased osmotic Fragility and reduced in vivo life span. Despite the apparently normal protein composition of the mutant Erythrocyte membrane, the retention of the spectrin-actin complex in the membrane under low ionic strength conditions is significantly reduced by the double mutation. Atomic force microscopy reveals an increase in grain size and a decrease in filament number of the mutant membrane cytoskeleton, although the volume parameter is similar to wild type Erythrocytes. Aggregated, disassembled, and irregular features are visualized in the mutant membrane, consistent with the presence of large protein aggregates. Importantly, purified dematin binds to the stripped inside-out vesicles in a saturable manner, and dematin-membrane binding is abolished upon pretreatment of membrane vesicles with trypsin. Together, these results reveal an essential role of dematin and adducin in the maintenance of Erythrocyte shape and membrane stability, and they suggest that the dematin-membrane interaction could link the junctional complex to the plasma membrane in erythroid cells.
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combined deletion of mouse dematin headpiece and β adducin exerts a novel effect on the spectrin actin junctions leading to Erythrocyte Fragility and hemolytic anemia
Journal of Biological Chemistry, 2006Co-Authors: Huiqing Chen, Anwar A Khan, Fei Liu, Diana M Gilligan, Luanne L Peters, Joanne B Messick, Wanda M Haschekhock, Agnes E Ostafin, Athar H ChishtiAbstract:Abstract Dematin and adducin are actin-binding proteins of the Erythrocyte “junctional complex.” Individually, they exert modest effects on Erythrocyte shape and membrane stability, and their homologues are expressed widely in non-erythroid cells. Here we report generation and characterization of double knock-out mice lacking β-adducin and the headpiece domain of dematin. The combined mutations result in altered Erythrocyte morphology, increased membrane instability, and severe hemolysis. Peripheral blood analysis shows evidence of severe hemolytic anemia with reduced number of Erythrocytes/hematocrit/hemoglobin and an ∼12-fold increase in the number of circulating reticulocytes. The presence of a variety of misshapen and fragmented Erythrocytes correlates with increased osmotic Fragility and reduced in vivo life span. Despite the apparently normal protein composition of the mutant Erythrocyte membrane, the retention of the spectrin-actin complex in the membrane under low ionic strength conditions is significantly reduced by the double mutation. Atomic force microscopy reveals an increase in grain size and a decrease in filament number of the mutant membrane cytoskeleton, although the volume parameter is similar to wild type Erythrocytes. Aggregated, disassembled, and irregular features are visualized in the mutant membrane, consistent with the presence of large protein aggregates. Importantly, purified dematin binds to the stripped inside-out vesicles in a saturable manner, and dematin-membrane binding is abolished upon pretreatment of membrane vesicles with trypsin. Together, these results reveal an essential role of dematin and adducin in the maintenance of Erythrocyte shape and membrane stability, and they suggest that the dematin-membrane interaction could link the junctional complex to the plasma membrane in erythroid cells.
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simultaneous loss of mouse dematin and beta adducin results in severe Erythrocyte Fragility and hemolytic anemia
Blood, 2005Co-Authors: Anwar A Khan, Huiqing Chen, Fei Liu, Diana M Gilligan, Luanne L Peters, Joanne B Messick, Wanda M Haschekhock, Agnes E Ostafin, Athar H ChishtiAbstract:Abstract The mechanical strength and stability of the Erythrocyte membrane are regulated by a network of proteins that participate in both horizontal and vertical interactions. The actin-containing junctional complexes, located at the tail ends of spectrin molecules, serve as the critical regulatory nodes for the maintenance of membrane stability. Dematin and beta-adducin, two actin-binding proteins of the junctional complex, are known to play essential roles in the regulation of Erythrocyte shape and membrane stability, as revealed recently by the development of mouse knockout models. Here, we show that simultaneous loss of functional dematin (headpiece domain deletion) and beta-adducin results in severe Fragility and abnormal shape of Erythrocytes, despite the presence of major skeletal proteins. Adducin/Dematin Double Knockout (ADKO) mice are viable and can be distinguished at birth by their pallor with pronounced spleomegaly and regenerative hematopoiesis. Hematological evaluations show a reduction of Erythrocytes, reduced hematocrit and hemoglobin, and a ~52% increase in the number of reticulocytes. The presence of a variety of misshapen and fragmented Erythrocytes in the ADKO mice correlates with increased osmotic Fragility and reduced Erythrocyte life span in vivo. Despite an apparently normal composition of ghosts and skeletal proteins, the retention of spectrin in the ADKO Erythrocyte plasma membrane is significantly compromised. Atomic force microscopy (AFM) revealed similar volume parameters in the four genotypes examined, but an increased grain size, and a decreased filament number in the ADKO Erythrocyte membrane. In addition, highly aggregated, disassembled, and irregular features were visualized by AFM in the ADKO Erythrocyte membrane. Staining of filamentous actin provided further evidence for the existence of large protein aggregates in the ADKO Erythrocyte membrane. Together, these results demonstrate a crucial function of dematin and beta-adducin in the maintenance of Erythrocyte shape and membrane stability, and more importantly, suggest the existence of an alternate mechanism for the linkage of junctional complexes to the plasma membrane.
Huiqing Chen - One of the best experts on this subject based on the ideXlab platform.
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combined deletion of mouse dematin headpiece and β adducin exerts a novel effect on the spectrin actin junctions leading to Erythrocyte Fragility and hemolytic anemia
Journal of Biological Chemistry, 2006Co-Authors: Huiqing Chen, Anwar A Khan, Fei Liu, Diana M Gilligan, Luanne L Peters, Joanne B Messick, Wanda M Haschekhock, Agnes E Ostafin, Athar H ChishtiAbstract:Dematin and adducin are actin-binding proteins of the Erythrocyte "junctional complex." Individually, they exert modest effects on Erythrocyte shape and membrane stability, and their homologues are expressed widely in non-erythroid cells. Here we report generation and characterization of double knock-out mice lacking beta-adducin and the headpiece domain of dematin. The combined mutations result in altered Erythrocyte morphology, increased membrane instability, and severe hemolysis. Peripheral blood analysis shows evidence of severe hemolytic anemia with reduced number of Erythrocytes/hematocrit/hemoglobin and an approximately 12-fold increase in the number of circulating reticulocytes. The presence of a variety of misshapen and fragmented Erythrocytes correlates with increased osmotic Fragility and reduced in vivo life span. Despite the apparently normal protein composition of the mutant Erythrocyte membrane, the retention of the spectrin-actin complex in the membrane under low ionic strength conditions is significantly reduced by the double mutation. Atomic force microscopy reveals an increase in grain size and a decrease in filament number of the mutant membrane cytoskeleton, although the volume parameter is similar to wild type Erythrocytes. Aggregated, disassembled, and irregular features are visualized in the mutant membrane, consistent with the presence of large protein aggregates. Importantly, purified dematin binds to the stripped inside-out vesicles in a saturable manner, and dematin-membrane binding is abolished upon pretreatment of membrane vesicles with trypsin. Together, these results reveal an essential role of dematin and adducin in the maintenance of Erythrocyte shape and membrane stability, and they suggest that the dematin-membrane interaction could link the junctional complex to the plasma membrane in erythroid cells.
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combined deletion of mouse dematin headpiece and β adducin exerts a novel effect on the spectrin actin junctions leading to Erythrocyte Fragility and hemolytic anemia
Journal of Biological Chemistry, 2006Co-Authors: Huiqing Chen, Anwar A Khan, Fei Liu, Diana M Gilligan, Luanne L Peters, Joanne B Messick, Wanda M Haschekhock, Agnes E Ostafin, Athar H ChishtiAbstract:Abstract Dematin and adducin are actin-binding proteins of the Erythrocyte “junctional complex.” Individually, they exert modest effects on Erythrocyte shape and membrane stability, and their homologues are expressed widely in non-erythroid cells. Here we report generation and characterization of double knock-out mice lacking β-adducin and the headpiece domain of dematin. The combined mutations result in altered Erythrocyte morphology, increased membrane instability, and severe hemolysis. Peripheral blood analysis shows evidence of severe hemolytic anemia with reduced number of Erythrocytes/hematocrit/hemoglobin and an ∼12-fold increase in the number of circulating reticulocytes. The presence of a variety of misshapen and fragmented Erythrocytes correlates with increased osmotic Fragility and reduced in vivo life span. Despite the apparently normal protein composition of the mutant Erythrocyte membrane, the retention of the spectrin-actin complex in the membrane under low ionic strength conditions is significantly reduced by the double mutation. Atomic force microscopy reveals an increase in grain size and a decrease in filament number of the mutant membrane cytoskeleton, although the volume parameter is similar to wild type Erythrocytes. Aggregated, disassembled, and irregular features are visualized in the mutant membrane, consistent with the presence of large protein aggregates. Importantly, purified dematin binds to the stripped inside-out vesicles in a saturable manner, and dematin-membrane binding is abolished upon pretreatment of membrane vesicles with trypsin. Together, these results reveal an essential role of dematin and adducin in the maintenance of Erythrocyte shape and membrane stability, and they suggest that the dematin-membrane interaction could link the junctional complex to the plasma membrane in erythroid cells.
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simultaneous loss of mouse dematin and beta adducin results in severe Erythrocyte Fragility and hemolytic anemia
Blood, 2005Co-Authors: Anwar A Khan, Huiqing Chen, Fei Liu, Diana M Gilligan, Luanne L Peters, Joanne B Messick, Wanda M Haschekhock, Agnes E Ostafin, Athar H ChishtiAbstract:Abstract The mechanical strength and stability of the Erythrocyte membrane are regulated by a network of proteins that participate in both horizontal and vertical interactions. The actin-containing junctional complexes, located at the tail ends of spectrin molecules, serve as the critical regulatory nodes for the maintenance of membrane stability. Dematin and beta-adducin, two actin-binding proteins of the junctional complex, are known to play essential roles in the regulation of Erythrocyte shape and membrane stability, as revealed recently by the development of mouse knockout models. Here, we show that simultaneous loss of functional dematin (headpiece domain deletion) and beta-adducin results in severe Fragility and abnormal shape of Erythrocytes, despite the presence of major skeletal proteins. Adducin/Dematin Double Knockout (ADKO) mice are viable and can be distinguished at birth by their pallor with pronounced spleomegaly and regenerative hematopoiesis. Hematological evaluations show a reduction of Erythrocytes, reduced hematocrit and hemoglobin, and a ~52% increase in the number of reticulocytes. The presence of a variety of misshapen and fragmented Erythrocytes in the ADKO mice correlates with increased osmotic Fragility and reduced Erythrocyte life span in vivo. Despite an apparently normal composition of ghosts and skeletal proteins, the retention of spectrin in the ADKO Erythrocyte plasma membrane is significantly compromised. Atomic force microscopy (AFM) revealed similar volume parameters in the four genotypes examined, but an increased grain size, and a decreased filament number in the ADKO Erythrocyte membrane. In addition, highly aggregated, disassembled, and irregular features were visualized by AFM in the ADKO Erythrocyte membrane. Staining of filamentous actin provided further evidence for the existence of large protein aggregates in the ADKO Erythrocyte membrane. Together, these results demonstrate a crucial function of dematin and beta-adducin in the maintenance of Erythrocyte shape and membrane stability, and more importantly, suggest the existence of an alternate mechanism for the linkage of junctional complexes to the plasma membrane.
Suleiman Folorunsho Ambali - One of the best experts on this subject based on the ideXlab platform.
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Erythrocyte osmotic Fragility and lipid peroxidation following chronic co exposure of rats to chlorpyrifos and deltamethrin and the beneficial effect of alpha lipoic acid
Toxicology reports, 2014Co-Authors: Chidiebere Uchendu, Suleiman Folorunsho Ambali, J O Ayo, King A N Esievo, Angela J UmosenAbstract:The present study aimed to evaluate the effect of chronic co-exposure to chlorpyrifos (CPF) and deltamethrin (DLT) on Erythrocyte osmotic Fragility, lipid peroxidation and the ameliorative effect of alpha-lipoic acid (ALA) on Erythrocyte Fragility. Thirty-six male Wistar rats divided into six groups of six rats each were used for the study. Groups I (S/oil) and II (ALA) were given soya oil (2 ml/kg) and ALA (60 mg/kg), respectively. Rats in group III (DLT) and IV (CPF) were exposed to DLT (6.25 mg/kg) and CPF (4.75 mg/kg) (1/20th of the previously determined LD50 of 125 mg/kg and 95 mg/kg, respectively, over a period of 48 h). Rats in group V (CPF + DLT) were co-exposed to CPF (4.75 mg/kg) and DLT (6.25 mg/kg), while those in group VI (ALA + CPF + DLT) were pretreated with ALA (60 mg/kg) and then co-exposed to CPF and DLT, 45 min later. The treatments were administered by gavage once daily for a period of 16 weeks. Blood collected at the end of the experimental period were analyzed for Erythrocyte osmotic Fragility and malondialdehyde (MDA) concentration. The study showed that chronic co-exposure to CPF and DLT resulted in an increase in Erythrocyte Fragility and MDA concentration which were ameliorated by supplementation with alpha-lipoic acid. The study concluded that repeated co-exposure to CPF and DLT elevated Erythrocyte Fragility probably due to increased lipid peroxidation, and pretreatment with alpha-lipoic acid ameliorated these alterations.
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ameliorative effect of vitamin c on chronic chlorpyrifos induced Erythrocyte osmotic Fragility in wistar rats
Human & Experimental Toxicology, 2011Co-Authors: Suleiman Folorunsho Ambali, J O Ayo, Samuel A Ojo, King A N EsievoAbstract:Chronic exposure to chlorpyrifos (CPF) has been shown to cause increased lipoperoxidative changes in the Erythrocyte membranes. The relationship between chronic CPF-induced lipoperoxidative changes and Erythrocyte Fragility has not been elucidated. The aim of the present study is to evaluate the role of lipoperoxidation on CPF-induced Erythrocyte Fragility and the ameliorative effect of vitamin C. Twenty animals divided at random into four groups of five animals each served as subject for this study. Rats in group I served as the control group and were given only soya oil at a dose of 2 mL/kg body weight (b.w.). Rats in group II were dosed with vitamin C (100 mg/kg b.w.) and then supplemented with soya oil (2 mL/kg b.w.), while those in group III were administered with CPF only at a dose of 10.6 mg/kg b.w. (~one-eighth of the previously determined median lethal dose [LD(50)]). Rats in group IV were pretreated with 100 mg/kg b.w. of vitamin C, and then dosed with CPF at a dose of 10.6 mg/kg b.w., 30 min later. The different treatment regimens were orally administered daily for a period of 17 weeks. Blood collected from the animals at the end of the test period were analyzed for Erythrocyte osmotic Fragility and malonaldehyde (MDA) concentration as an index of lipid peroxidation. The study showed that CPF caused significant increase in Erythrocyte Fragility and MDA concentration, which were ameliorated by pretreatment with vitamin C. In conclusion, the study showed that CPF-evoked Erythrocyte Fragility due to increased lipoperoxidative changes was ameliorated by pretreatment with vitamin C.
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comparative effects of vitamin c and acetyl l carnitine on subacute chlorpyrifos induced Erythrocyte osmotic Fragility in wistar rats
Advances in Applied Science Research, 2011Co-Authors: Chidiebere Uchendu, Suleiman Folorunsho Ambali, Surakat L Yakub, Oluwole I Lasisi, Angela J UmosenAbstract:Lipid peroxidation which can be measured indirectly by Erythrocyte osmotic Fragility is a molecular mechanism implicated in chlorpyrifos poisoning. The aim of the present study was to evaluate the comparative effects of vitamin C and acetyl-L-carnitine on subacute CPF-induced Erythrocyte osmotic Fragility in Wistar rats. Forty-nine adult male Wistar rats divided into 7 groups of 7 animals each were used as experimental subjects. Rats in groups I (S/oil), II (VC), III (ALC) and IV (CPF) were exposed to soya oil only (2 ml/kg), vitamin C (100 mg/kg), acetyl-Lcarnitine (300 mg/kg) and chlorpyrifos only (8.5 mg/kg~ 1/10th of the LD50), respectively. Groups V (VC+CPF) and VI (ALC+CPF) were pretreated with vitamin C (100 mg/kg) and acetyl-Lcarnitine (300 mg/kg), respectively, and then dosed with CPF (8.5 mg/kg) 30 min later. While group VII (VC+ALC+CPF) was pretreated with the combination of VC (100 mg/kg) and ALC (300 mg/kg) and then dosed with CPF (8.5 mg/kg), 30 min later. These regimens were administered orally once daily for a period of 28 days. At the end of the study, the rats were sacrificed and Erythrocyte analyzed for Erythrocyte osmotic Fragility. The study showed that subacute CPF exposure caused increase in Erythrocyte osmotic Fragility, which was significantly decreased (P 0.05) by ALC and the combination of VC and ALC. In conclusion, the study showed that CPF-evoked Erythrocyte Fragility was best ameliorated by pretreatment with vitamin C alone.
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vitamin e protects wistar rats from chlorpyrifos induced increase in Erythrocyte osmotic Fragility
Food and Chemical Toxicology, 2010Co-Authors: Suleiman Folorunsho Ambali, J O Ayo, Samuel A Ojo, King A N EsievoAbstract:The aim of the present study was to evaluate the effect of chronic chlorpyrifos (CPF) exposure on Erythrocyte osmotic Fragility, the role of lipid peroxidation and the ameliorative effect of vitamin E on the Erythrocyte Fragility. Twenty young adult male Wistar rats divided into four groups of five animals each served as subjects for this study. Groups I (control) and II were exposed to soya oil (2 ml/kg) and vitamin E (75 mg/kg), respectively. Rats in group III were exposed to CPF (10.6 mg/kg 1/8th of the previously determined LD50 of 85 mg/kg over a period of 48 h), while those in group IV were pretreated with vitamin E (75 mg/kg) and then exposed to CPF, 30 min later. The regimens were administered orally by gavage once daily for a period of 17 weeks. Blood samples collected at the end of the test period were analyzed for Erythrocyte osmotic Fragility, while the washed Erythrocytes were used to evaluate malondialdehyde (MDA) concentration, as an index of lipid peroxidation. The study showed that repeated CPF exposure caused increased Erythrocyte Fragility and MDA concentration. Pretreatment with vitamin E ameliorated CPF-induced increase in Erythrocyte Fragility and lipoperoxidative changes in Wistar rats.
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ameliorative effect of zinc on chlorpyrifos induced Erythrocyte Fragility in wistar rats
2010Co-Authors: Suleiman Folorunsho Ambali, Ahmad Tijjani Abubakar, A GiwaAbstract:Oxidative stress has been implicated in the molecular mechanism of chlorpyrifos (CPF) poisoning. The present study was aimed at evaluating the ameliorative effect of zinc, an antioxidant trace element, on lipoperoxidative changes and Erythrocyte Fragility induced by subchronic CPF exposure in Wistar rats. Twenty adult Wistar rats divided into 4 groups of 5 animals each were used as experimental subjects. Rats in groups I (S/oil group) and II (CPF group) were exposed to soya oil only (2 ml/kg) and CPF only (10.6 mg/kg~ 1/8 th LD 50 ), respectively. Group III (Zn group) were dosed with zinc only (50 mg/kg) while in group IV (Zn+CPF), Zn (50 mg/kg) were co-administered with CPF (10.6 mg/kg). These regimens were administered orally once daily for a period of 8 weeks. At the end of the study, the rats were sacrificed and Erythrocytes analysed for Erythrocyte osmotic Fragility and malonaldehyde (MDA) concentration as an index of lipoperoxidative changes. Erythrocyte Fragility was significantly increased ( P < 0.01) in CPF group compared to S/oil, Zn and Zn+CPF groups, respectively. Similarly, the CPF group showed a significant increase (P < 0.01) in MDA concentration compared to S/oil, Zn and Zn+CPF groups, respectively.The present study has shown that repeated exposure of rats to CPF increased Erythrocyte Fragility partly due to oxidative hemolysis resulting from increased lipoperoxidative changes. (New York Science Journal 2010;3(5):117-122). (ISSN 1554 - 0200).
King A N Esievo - One of the best experts on this subject based on the ideXlab platform.
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Erythrocyte osmotic Fragility and lipid peroxidation following chronic co exposure of rats to chlorpyrifos and deltamethrin and the beneficial effect of alpha lipoic acid
Toxicology reports, 2014Co-Authors: Chidiebere Uchendu, Suleiman Folorunsho Ambali, J O Ayo, King A N Esievo, Angela J UmosenAbstract:The present study aimed to evaluate the effect of chronic co-exposure to chlorpyrifos (CPF) and deltamethrin (DLT) on Erythrocyte osmotic Fragility, lipid peroxidation and the ameliorative effect of alpha-lipoic acid (ALA) on Erythrocyte Fragility. Thirty-six male Wistar rats divided into six groups of six rats each were used for the study. Groups I (S/oil) and II (ALA) were given soya oil (2 ml/kg) and ALA (60 mg/kg), respectively. Rats in group III (DLT) and IV (CPF) were exposed to DLT (6.25 mg/kg) and CPF (4.75 mg/kg) (1/20th of the previously determined LD50 of 125 mg/kg and 95 mg/kg, respectively, over a period of 48 h). Rats in group V (CPF + DLT) were co-exposed to CPF (4.75 mg/kg) and DLT (6.25 mg/kg), while those in group VI (ALA + CPF + DLT) were pretreated with ALA (60 mg/kg) and then co-exposed to CPF and DLT, 45 min later. The treatments were administered by gavage once daily for a period of 16 weeks. Blood collected at the end of the experimental period were analyzed for Erythrocyte osmotic Fragility and malondialdehyde (MDA) concentration. The study showed that chronic co-exposure to CPF and DLT resulted in an increase in Erythrocyte Fragility and MDA concentration which were ameliorated by supplementation with alpha-lipoic acid. The study concluded that repeated co-exposure to CPF and DLT elevated Erythrocyte Fragility probably due to increased lipid peroxidation, and pretreatment with alpha-lipoic acid ameliorated these alterations.
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ameliorative effect of vitamin c on chronic chlorpyrifos induced Erythrocyte osmotic Fragility in wistar rats
Human & Experimental Toxicology, 2011Co-Authors: Suleiman Folorunsho Ambali, J O Ayo, Samuel A Ojo, King A N EsievoAbstract:Chronic exposure to chlorpyrifos (CPF) has been shown to cause increased lipoperoxidative changes in the Erythrocyte membranes. The relationship between chronic CPF-induced lipoperoxidative changes and Erythrocyte Fragility has not been elucidated. The aim of the present study is to evaluate the role of lipoperoxidation on CPF-induced Erythrocyte Fragility and the ameliorative effect of vitamin C. Twenty animals divided at random into four groups of five animals each served as subject for this study. Rats in group I served as the control group and were given only soya oil at a dose of 2 mL/kg body weight (b.w.). Rats in group II were dosed with vitamin C (100 mg/kg b.w.) and then supplemented with soya oil (2 mL/kg b.w.), while those in group III were administered with CPF only at a dose of 10.6 mg/kg b.w. (~one-eighth of the previously determined median lethal dose [LD(50)]). Rats in group IV were pretreated with 100 mg/kg b.w. of vitamin C, and then dosed with CPF at a dose of 10.6 mg/kg b.w., 30 min later. The different treatment regimens were orally administered daily for a period of 17 weeks. Blood collected from the animals at the end of the test period were analyzed for Erythrocyte osmotic Fragility and malonaldehyde (MDA) concentration as an index of lipid peroxidation. The study showed that CPF caused significant increase in Erythrocyte Fragility and MDA concentration, which were ameliorated by pretreatment with vitamin C. In conclusion, the study showed that CPF-evoked Erythrocyte Fragility due to increased lipoperoxidative changes was ameliorated by pretreatment with vitamin C.
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vitamin e protects wistar rats from chlorpyrifos induced increase in Erythrocyte osmotic Fragility
Food and Chemical Toxicology, 2010Co-Authors: Suleiman Folorunsho Ambali, J O Ayo, Samuel A Ojo, King A N EsievoAbstract:The aim of the present study was to evaluate the effect of chronic chlorpyrifos (CPF) exposure on Erythrocyte osmotic Fragility, the role of lipid peroxidation and the ameliorative effect of vitamin E on the Erythrocyte Fragility. Twenty young adult male Wistar rats divided into four groups of five animals each served as subjects for this study. Groups I (control) and II were exposed to soya oil (2 ml/kg) and vitamin E (75 mg/kg), respectively. Rats in group III were exposed to CPF (10.6 mg/kg 1/8th of the previously determined LD50 of 85 mg/kg over a period of 48 h), while those in group IV were pretreated with vitamin E (75 mg/kg) and then exposed to CPF, 30 min later. The regimens were administered orally by gavage once daily for a period of 17 weeks. Blood samples collected at the end of the test period were analyzed for Erythrocyte osmotic Fragility, while the washed Erythrocytes were used to evaluate malondialdehyde (MDA) concentration, as an index of lipid peroxidation. The study showed that repeated CPF exposure caused increased Erythrocyte Fragility and MDA concentration. Pretreatment with vitamin E ameliorated CPF-induced increase in Erythrocyte Fragility and lipoperoxidative changes in Wistar rats.
M C Calhoun - One of the best experts on this subject based on the ideXlab platform.
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the effects of varying gossypol intake from whole cottonseed and cottonseed meal on lactation and blood parameters in lactating dairy cows
Journal of Dairy Science, 2004Co-Authors: H Mena, M Tarazon, J E P Santos, J.t. Huber, M C CalhounAbstract:Effects of varying amounts of gossypol from whole Upland cottonseed (WCS) and cottonseed meal (CSM) were evaluated in 40 midlactation Holstein cows. After 14 d of pretreatment, cows were assigned to 1 of the 5 treatments for 84 d: control (no gossypol), 931 mg/kg total gossypol (TG) and 850 mg/kg free gossypol (FG) from WCS (moderate TG and high FG); 924 mg/kg TG and 91 mg/kg FG from CSM (moderate TG and low FG), 945 mg/kg TG and 479 mg/kg FG with equal amounts of TG from WCS and CSM (moderate TG and FG), or 1894 mg/kg TG and 960 mg/kg FG with equal amounts of TG from WCS and CSM (high TG and FG). Concentrations of plasma gossypol (PG) and its isomers were directly proportional to FG intake. Concentrations of PG reached a plateau after 28 d on treatment, and they were highest in cows receiving a diet with high TG and FG. Erythrocyte Fragility differed among treatments and increased with increasing FG intake. Plasma gossypol returned to negligible concentrations 28 d after withdrawal of cottonseed products from the high TG and FG diet. Serum vitamin A was similar among treatments, but vitamin E increased with increasing FG intake. Serum enzymes were generally unaffected by treatments, but urea N increased in diets higher in TG and FG. Intake of dry matter was higher for the diet high in TG and FG than for the control diet, but was similar for other treatments. Cows receiving the high TG and FG diet produced more milk and 3.5% fat-corrected milk, with no changes in milk composition. Feeding a diet containing 1894 mg/kg TG and 960 mg/kg FG for 84 d increased PG concentrations and Erythrocyte Fragility and resulted in minor changes in blood metabolites and enzymes, but no detrimental effect on lactation performance was observed. Indicators of liver, kidney, and muscle cell viability suggest that the higher amounts of gossypol consumed in this study had only minor effects on those tissues in lactating dairy cows.
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the effects of feeding varying amounts of gossypol from whole cottonseed and cottonseed meal in lactating dairy cows
Journal of Dairy Science, 2001Co-Authors: H Mena, J M Simas, M Tarazon, J E P Santos, J.t. Huber, M C CalhounAbstract:Effects of feeding varying amounts of total gossypol from whole cottonseed and cottonseed meal were evaluated in 30 lactating Holstein cows. After a 14-d pretreatment period, cows were assigned for 42 d to one of five treatments: control (diet A); 1040 mg/kg of total gossypol, and 989 mg/kg of free gossypol from whole cottonseed (diet B); 900 mg/kg of total gossypol and 64 mg/kg of free gossypol from cottonseed meal (diet C); 960 mg/kg of total gossypol and 531 mg/kg of free gossypol with equal amounts of total gossypol from whole cottonseed and cottonseed meal (diet D); or 1922 mg/kg of total gossypol and 1050 mg/kg of free gossypol with equal amounts of total gossypol from whole cottonseed and cottonseed meal (diet E). Concentrations of plasma gossypol and its isomers were directly proportional to free gossypol intake. Plasma gossypol concentrations plateaued after 35 d on treatment, and they were highest in cows receiving diet E. At 42 d on treatment, Erythrocyte Fragility was higher in the cows receiving the diet E, but it did not differ among other treatments. Dry matter intakes were similar for all groups. Cows receiving diet E produced more milk and 3.5% fat-corrected milk, but milk protein content decreased. Feeding diets containing 1900 mg/kg of total gossypol and 1050 mg/kg of free gossypol for 42 d resulted in increased plasma gossypol concentrations and Erythrocyte Fragility, but no detrimental impact on lactation performance were observed.