The Experts below are selected from a list of 135 Experts worldwide ranked by ideXlab platform
Patrice Couture - One of the best experts on this subject based on the ideXlab platform.
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temporal variations in kidney metal concentrations and their implications for retinoid metabolism and oxidative stress response in wild yellow perch perca flavescens
Aquatic Toxicology, 2018Co-Authors: Michel A Defo, Louis Bernatchez, Peter G C Campbell, Patrice CoutureAbstract:The objective of this study was to determine if temporal variations in tissue metal concentrations are related to biomarkers of retinoid metabolism and oxidative stress responses in juvenile yellow perch (Perca flavescens). To this end, kidney metal (Cd, Cu and Zn) concentrations were measured in fish sampled in spring and fall 2012 in four lakes representing a wide range of water and sediment metal contamination in the Rouyn-Noranda (Quebec) region. Lakes Opasatica and Helene were considered as reference lakes while lakes Dufault and Marlon were metal-contaminated. Kidney concentrations of Cd, Cu and Zn varied widely between spring and fall in fish from both clean and metal-contaminated lakes. An inter-lake difference in renal metal concentrations was only observed for Cd, with fish from Lake Marlon consistently displaying higher concentrations. In the spring, the concentrations of liver Dehydroretinol, dehydroretinyl palmitate and total vitamin A esters were higher in fish sampled in the most contaminated lake. Strong temporal variations in the concentrations of these metabolites, as well as in the percentage of liver free Dehydroretinol and the epidermal retinol dehydrogenase 2 transcription levels, were observed in fish living in the most metal-impacted lake, with generally higher values in the spring. In contrast to liver, in muscle, no clear seasonal variations in the concentrations of Dehydroretinol, dehydroretinyl stearate or in the percentage of free Dehydroretinol were observed in fish captured in the most contaminated lake. Temporal variations of traditional biomarkers of oxidative stress response were also observed in the most metal-impacted lake. For example, the transcription level of the gene encoding Cu/Zn superoxide dismutase-1 in liver and muscle catalase activity of perch sampled in the most contaminated lake were higher in spring than in fall. Positive relationships were found between kidney Cd concentrations and the transcription level of the gene encoding glucose 6-phosphate dehydrogenase, and all forms of retinoid concentrations in liver in spring, except with the percentage of free Dehydroretinol where the correlation was negative. Our results translate to a state of stress caused by Cd and illustrate that temporal variations in tissue metal concentrations affect retinoid metabolism and antioxidant capacities in juvenile wild yellow perch. Overall this study contributes to highlight the importance of considering temporal variations when investigating the consequences of metal contamination on the physiology of wild fish.
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Waterborne cadmium and nickel impact oxidative stress responses and retinoid metabolism in yellow perch.
Aquatic toxicology (Amsterdam Netherlands), 2014Co-Authors: Michel A Defo, Louis Bernatchez, Peter G C Campbell, Patrice CoutureAbstract:In this experiment, we studied the transcriptional and functional (enzymatic) responses of yellow perch (Perca flavescens) to metal stress, with a focus on oxidative stress and vitamin A metabolism. Juvenile yellow perch were exposed to two environmentally relevant concentrations of waterborne cadmium (Cd) and nickel (Ni) for a period of 6 weeks. Kidney Cd and Ni bioaccumulation significantly increased with increasing metal exposure. The major retinoid metabolites analyzed in liver and muscle decreased with metal exposure except at high Cd exposure where no variation was reported in liver. A decrease in free plasma Dehydroretinol was also observed with metal exposure. In the liver of Cd-exposed fish, both epidermal retinol dehydrogenase 2 transcription level and corresponding enzyme activities retinyl ester hydrolase and lecithin dehydroretinyl acyl transferase increased. In contrast, muscle epidermal retinol dehydrogenase 2 transcription level decreased with Cd exposure. Among antioxidant defences, liver transcription levels of catalase, microsomal glutathione-S-transferase-3 and glucose-6-phosphate dehydrogenase were generally enhanced in Cd-exposed fish and this up-regulation was accompanied by an increase in the activities of corresponding enzymes, except for microsomal glutathione-S-transferase. No consistent pattern in antioxidant defence responses was observed between molecular and biochemical response when fish were exposed to Ni, suggesting a non-synchronous response of antioxidant defence in fish exposed to waterborne Ni. There was a general lack of consistency between muscle transcription level and enzyme activities analyzed. The overall findings from this investigation highlight the usefulness of transcriptional and biochemical endpoints in the identification of oxidative stress and vitamin A metabolism impairment biomarkers and the potential use of multi-level biological approaches when assessing environmental risk in fish.
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Evidence for metabolic imbalance of vitamin A2 in wild fish chronically exposed to metals
Ecotoxicology and environmental safety, 2012Co-Authors: Michel A Defo, Louis Bernatchez, Peter G C Campbell, Fabien Pierron, Philip A. Spear, Patrice CoutureAbstract:In a recent study on indigenous yellow perch chronically exposed to metals, we reported a negative correlation between liver metal concentration and liver transcription levels of genes encoding for enzymes involved in the metabolism of retinoids. We therefore speculated that metals, and especially the non-essential metal Cd, could alter the metabolism of retinoids in wild fish. Thus the present field study investigates the impact of in situ metal exposure on retinoid storage. A total of 55 yellow perch (Perca flavescens) were sampled in six lakes representing a metal contamination gradient (8≤N≤10 per lake). Our results show that yellow perch from Cd-contaminated lakes had significantly higher concentrations of liver Dehydroretinol and dehydroretinyl esters than did fish from reference lakes. However, the increase in retinyl ester stores with increasing Cd concentrations was quantitatively much more important than the increase in free Dehydroretinol. As a result, a significant decrease in the percentage of hepatic free Dehydroretinol with increasing renal Cd concentrations was observed. These results suggest that the enzymes and the binding proteins involved in vitamin A homeostasis are inhibited by the presence of Cd. Alternatively, the increase in tissue vitamin A (antioxidant) levels could serve to better counteract the oxidative stress engendered by Cd exposure. Overall our findings illustrate that vitamin A(2) homeostasis can be altered as a consequence of chronic exposure to low Cd concentrations. Thus, in the context of environmental risk assessment, the percentage of liver free Dehydroretinol can be considered as a biomarker of for in situ Cd exposure.
Michel A Defo - One of the best experts on this subject based on the ideXlab platform.
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temporal variations in kidney metal concentrations and their implications for retinoid metabolism and oxidative stress response in wild yellow perch perca flavescens
Aquatic Toxicology, 2018Co-Authors: Michel A Defo, Louis Bernatchez, Peter G C Campbell, Patrice CoutureAbstract:The objective of this study was to determine if temporal variations in tissue metal concentrations are related to biomarkers of retinoid metabolism and oxidative stress responses in juvenile yellow perch (Perca flavescens). To this end, kidney metal (Cd, Cu and Zn) concentrations were measured in fish sampled in spring and fall 2012 in four lakes representing a wide range of water and sediment metal contamination in the Rouyn-Noranda (Quebec) region. Lakes Opasatica and Helene were considered as reference lakes while lakes Dufault and Marlon were metal-contaminated. Kidney concentrations of Cd, Cu and Zn varied widely between spring and fall in fish from both clean and metal-contaminated lakes. An inter-lake difference in renal metal concentrations was only observed for Cd, with fish from Lake Marlon consistently displaying higher concentrations. In the spring, the concentrations of liver Dehydroretinol, dehydroretinyl palmitate and total vitamin A esters were higher in fish sampled in the most contaminated lake. Strong temporal variations in the concentrations of these metabolites, as well as in the percentage of liver free Dehydroretinol and the epidermal retinol dehydrogenase 2 transcription levels, were observed in fish living in the most metal-impacted lake, with generally higher values in the spring. In contrast to liver, in muscle, no clear seasonal variations in the concentrations of Dehydroretinol, dehydroretinyl stearate or in the percentage of free Dehydroretinol were observed in fish captured in the most contaminated lake. Temporal variations of traditional biomarkers of oxidative stress response were also observed in the most metal-impacted lake. For example, the transcription level of the gene encoding Cu/Zn superoxide dismutase-1 in liver and muscle catalase activity of perch sampled in the most contaminated lake were higher in spring than in fall. Positive relationships were found between kidney Cd concentrations and the transcription level of the gene encoding glucose 6-phosphate dehydrogenase, and all forms of retinoid concentrations in liver in spring, except with the percentage of free Dehydroretinol where the correlation was negative. Our results translate to a state of stress caused by Cd and illustrate that temporal variations in tissue metal concentrations affect retinoid metabolism and antioxidant capacities in juvenile wild yellow perch. Overall this study contributes to highlight the importance of considering temporal variations when investigating the consequences of metal contamination on the physiology of wild fish.
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Waterborne cadmium and nickel impact oxidative stress responses and retinoid metabolism in yellow perch.
Aquatic toxicology (Amsterdam Netherlands), 2014Co-Authors: Michel A Defo, Louis Bernatchez, Peter G C Campbell, Patrice CoutureAbstract:In this experiment, we studied the transcriptional and functional (enzymatic) responses of yellow perch (Perca flavescens) to metal stress, with a focus on oxidative stress and vitamin A metabolism. Juvenile yellow perch were exposed to two environmentally relevant concentrations of waterborne cadmium (Cd) and nickel (Ni) for a period of 6 weeks. Kidney Cd and Ni bioaccumulation significantly increased with increasing metal exposure. The major retinoid metabolites analyzed in liver and muscle decreased with metal exposure except at high Cd exposure where no variation was reported in liver. A decrease in free plasma Dehydroretinol was also observed with metal exposure. In the liver of Cd-exposed fish, both epidermal retinol dehydrogenase 2 transcription level and corresponding enzyme activities retinyl ester hydrolase and lecithin dehydroretinyl acyl transferase increased. In contrast, muscle epidermal retinol dehydrogenase 2 transcription level decreased with Cd exposure. Among antioxidant defences, liver transcription levels of catalase, microsomal glutathione-S-transferase-3 and glucose-6-phosphate dehydrogenase were generally enhanced in Cd-exposed fish and this up-regulation was accompanied by an increase in the activities of corresponding enzymes, except for microsomal glutathione-S-transferase. No consistent pattern in antioxidant defence responses was observed between molecular and biochemical response when fish were exposed to Ni, suggesting a non-synchronous response of antioxidant defence in fish exposed to waterborne Ni. There was a general lack of consistency between muscle transcription level and enzyme activities analyzed. The overall findings from this investigation highlight the usefulness of transcriptional and biochemical endpoints in the identification of oxidative stress and vitamin A metabolism impairment biomarkers and the potential use of multi-level biological approaches when assessing environmental risk in fish.
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Evidence for metabolic imbalance of vitamin A2 in wild fish chronically exposed to metals
Ecotoxicology and environmental safety, 2012Co-Authors: Michel A Defo, Louis Bernatchez, Peter G C Campbell, Fabien Pierron, Philip A. Spear, Patrice CoutureAbstract:In a recent study on indigenous yellow perch chronically exposed to metals, we reported a negative correlation between liver metal concentration and liver transcription levels of genes encoding for enzymes involved in the metabolism of retinoids. We therefore speculated that metals, and especially the non-essential metal Cd, could alter the metabolism of retinoids in wild fish. Thus the present field study investigates the impact of in situ metal exposure on retinoid storage. A total of 55 yellow perch (Perca flavescens) were sampled in six lakes representing a metal contamination gradient (8≤N≤10 per lake). Our results show that yellow perch from Cd-contaminated lakes had significantly higher concentrations of liver Dehydroretinol and dehydroretinyl esters than did fish from reference lakes. However, the increase in retinyl ester stores with increasing Cd concentrations was quantitatively much more important than the increase in free Dehydroretinol. As a result, a significant decrease in the percentage of hepatic free Dehydroretinol with increasing renal Cd concentrations was observed. These results suggest that the enzymes and the binding proteins involved in vitamin A homeostasis are inhibited by the presence of Cd. Alternatively, the increase in tissue vitamin A (antioxidant) levels could serve to better counteract the oxidative stress engendered by Cd exposure. Overall our findings illustrate that vitamin A(2) homeostasis can be altered as a consequence of chronic exposure to low Cd concentrations. Thus, in the context of environmental risk assessment, the percentage of liver free Dehydroretinol can be considered as a biomarker of for in situ Cd exposure.
Peter G C Campbell - One of the best experts on this subject based on the ideXlab platform.
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temporal variations in kidney metal concentrations and their implications for retinoid metabolism and oxidative stress response in wild yellow perch perca flavescens
Aquatic Toxicology, 2018Co-Authors: Michel A Defo, Louis Bernatchez, Peter G C Campbell, Patrice CoutureAbstract:The objective of this study was to determine if temporal variations in tissue metal concentrations are related to biomarkers of retinoid metabolism and oxidative stress responses in juvenile yellow perch (Perca flavescens). To this end, kidney metal (Cd, Cu and Zn) concentrations were measured in fish sampled in spring and fall 2012 in four lakes representing a wide range of water and sediment metal contamination in the Rouyn-Noranda (Quebec) region. Lakes Opasatica and Helene were considered as reference lakes while lakes Dufault and Marlon were metal-contaminated. Kidney concentrations of Cd, Cu and Zn varied widely between spring and fall in fish from both clean and metal-contaminated lakes. An inter-lake difference in renal metal concentrations was only observed for Cd, with fish from Lake Marlon consistently displaying higher concentrations. In the spring, the concentrations of liver Dehydroretinol, dehydroretinyl palmitate and total vitamin A esters were higher in fish sampled in the most contaminated lake. Strong temporal variations in the concentrations of these metabolites, as well as in the percentage of liver free Dehydroretinol and the epidermal retinol dehydrogenase 2 transcription levels, were observed in fish living in the most metal-impacted lake, with generally higher values in the spring. In contrast to liver, in muscle, no clear seasonal variations in the concentrations of Dehydroretinol, dehydroretinyl stearate or in the percentage of free Dehydroretinol were observed in fish captured in the most contaminated lake. Temporal variations of traditional biomarkers of oxidative stress response were also observed in the most metal-impacted lake. For example, the transcription level of the gene encoding Cu/Zn superoxide dismutase-1 in liver and muscle catalase activity of perch sampled in the most contaminated lake were higher in spring than in fall. Positive relationships were found between kidney Cd concentrations and the transcription level of the gene encoding glucose 6-phosphate dehydrogenase, and all forms of retinoid concentrations in liver in spring, except with the percentage of free Dehydroretinol where the correlation was negative. Our results translate to a state of stress caused by Cd and illustrate that temporal variations in tissue metal concentrations affect retinoid metabolism and antioxidant capacities in juvenile wild yellow perch. Overall this study contributes to highlight the importance of considering temporal variations when investigating the consequences of metal contamination on the physiology of wild fish.
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Waterborne cadmium and nickel impact oxidative stress responses and retinoid metabolism in yellow perch.
Aquatic toxicology (Amsterdam Netherlands), 2014Co-Authors: Michel A Defo, Louis Bernatchez, Peter G C Campbell, Patrice CoutureAbstract:In this experiment, we studied the transcriptional and functional (enzymatic) responses of yellow perch (Perca flavescens) to metal stress, with a focus on oxidative stress and vitamin A metabolism. Juvenile yellow perch were exposed to two environmentally relevant concentrations of waterborne cadmium (Cd) and nickel (Ni) for a period of 6 weeks. Kidney Cd and Ni bioaccumulation significantly increased with increasing metal exposure. The major retinoid metabolites analyzed in liver and muscle decreased with metal exposure except at high Cd exposure where no variation was reported in liver. A decrease in free plasma Dehydroretinol was also observed with metal exposure. In the liver of Cd-exposed fish, both epidermal retinol dehydrogenase 2 transcription level and corresponding enzyme activities retinyl ester hydrolase and lecithin dehydroretinyl acyl transferase increased. In contrast, muscle epidermal retinol dehydrogenase 2 transcription level decreased with Cd exposure. Among antioxidant defences, liver transcription levels of catalase, microsomal glutathione-S-transferase-3 and glucose-6-phosphate dehydrogenase were generally enhanced in Cd-exposed fish and this up-regulation was accompanied by an increase in the activities of corresponding enzymes, except for microsomal glutathione-S-transferase. No consistent pattern in antioxidant defence responses was observed between molecular and biochemical response when fish were exposed to Ni, suggesting a non-synchronous response of antioxidant defence in fish exposed to waterborne Ni. There was a general lack of consistency between muscle transcription level and enzyme activities analyzed. The overall findings from this investigation highlight the usefulness of transcriptional and biochemical endpoints in the identification of oxidative stress and vitamin A metabolism impairment biomarkers and the potential use of multi-level biological approaches when assessing environmental risk in fish.
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Evidence for metabolic imbalance of vitamin A2 in wild fish chronically exposed to metals
Ecotoxicology and environmental safety, 2012Co-Authors: Michel A Defo, Louis Bernatchez, Peter G C Campbell, Fabien Pierron, Philip A. Spear, Patrice CoutureAbstract:In a recent study on indigenous yellow perch chronically exposed to metals, we reported a negative correlation between liver metal concentration and liver transcription levels of genes encoding for enzymes involved in the metabolism of retinoids. We therefore speculated that metals, and especially the non-essential metal Cd, could alter the metabolism of retinoids in wild fish. Thus the present field study investigates the impact of in situ metal exposure on retinoid storage. A total of 55 yellow perch (Perca flavescens) were sampled in six lakes representing a metal contamination gradient (8≤N≤10 per lake). Our results show that yellow perch from Cd-contaminated lakes had significantly higher concentrations of liver Dehydroretinol and dehydroretinyl esters than did fish from reference lakes. However, the increase in retinyl ester stores with increasing Cd concentrations was quantitatively much more important than the increase in free Dehydroretinol. As a result, a significant decrease in the percentage of hepatic free Dehydroretinol with increasing renal Cd concentrations was observed. These results suggest that the enzymes and the binding proteins involved in vitamin A homeostasis are inhibited by the presence of Cd. Alternatively, the increase in tissue vitamin A (antioxidant) levels could serve to better counteract the oxidative stress engendered by Cd exposure. Overall our findings illustrate that vitamin A(2) homeostasis can be altered as a consequence of chronic exposure to low Cd concentrations. Thus, in the context of environmental risk assessment, the percentage of liver free Dehydroretinol can be considered as a biomarker of for in situ Cd exposure.
Louis Bernatchez - One of the best experts on this subject based on the ideXlab platform.
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temporal variations in kidney metal concentrations and their implications for retinoid metabolism and oxidative stress response in wild yellow perch perca flavescens
Aquatic Toxicology, 2018Co-Authors: Michel A Defo, Louis Bernatchez, Peter G C Campbell, Patrice CoutureAbstract:The objective of this study was to determine if temporal variations in tissue metal concentrations are related to biomarkers of retinoid metabolism and oxidative stress responses in juvenile yellow perch (Perca flavescens). To this end, kidney metal (Cd, Cu and Zn) concentrations were measured in fish sampled in spring and fall 2012 in four lakes representing a wide range of water and sediment metal contamination in the Rouyn-Noranda (Quebec) region. Lakes Opasatica and Helene were considered as reference lakes while lakes Dufault and Marlon were metal-contaminated. Kidney concentrations of Cd, Cu and Zn varied widely between spring and fall in fish from both clean and metal-contaminated lakes. An inter-lake difference in renal metal concentrations was only observed for Cd, with fish from Lake Marlon consistently displaying higher concentrations. In the spring, the concentrations of liver Dehydroretinol, dehydroretinyl palmitate and total vitamin A esters were higher in fish sampled in the most contaminated lake. Strong temporal variations in the concentrations of these metabolites, as well as in the percentage of liver free Dehydroretinol and the epidermal retinol dehydrogenase 2 transcription levels, were observed in fish living in the most metal-impacted lake, with generally higher values in the spring. In contrast to liver, in muscle, no clear seasonal variations in the concentrations of Dehydroretinol, dehydroretinyl stearate or in the percentage of free Dehydroretinol were observed in fish captured in the most contaminated lake. Temporal variations of traditional biomarkers of oxidative stress response were also observed in the most metal-impacted lake. For example, the transcription level of the gene encoding Cu/Zn superoxide dismutase-1 in liver and muscle catalase activity of perch sampled in the most contaminated lake were higher in spring than in fall. Positive relationships were found between kidney Cd concentrations and the transcription level of the gene encoding glucose 6-phosphate dehydrogenase, and all forms of retinoid concentrations in liver in spring, except with the percentage of free Dehydroretinol where the correlation was negative. Our results translate to a state of stress caused by Cd and illustrate that temporal variations in tissue metal concentrations affect retinoid metabolism and antioxidant capacities in juvenile wild yellow perch. Overall this study contributes to highlight the importance of considering temporal variations when investigating the consequences of metal contamination on the physiology of wild fish.
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Waterborne cadmium and nickel impact oxidative stress responses and retinoid metabolism in yellow perch.
Aquatic toxicology (Amsterdam Netherlands), 2014Co-Authors: Michel A Defo, Louis Bernatchez, Peter G C Campbell, Patrice CoutureAbstract:In this experiment, we studied the transcriptional and functional (enzymatic) responses of yellow perch (Perca flavescens) to metal stress, with a focus on oxidative stress and vitamin A metabolism. Juvenile yellow perch were exposed to two environmentally relevant concentrations of waterborne cadmium (Cd) and nickel (Ni) for a period of 6 weeks. Kidney Cd and Ni bioaccumulation significantly increased with increasing metal exposure. The major retinoid metabolites analyzed in liver and muscle decreased with metal exposure except at high Cd exposure where no variation was reported in liver. A decrease in free plasma Dehydroretinol was also observed with metal exposure. In the liver of Cd-exposed fish, both epidermal retinol dehydrogenase 2 transcription level and corresponding enzyme activities retinyl ester hydrolase and lecithin dehydroretinyl acyl transferase increased. In contrast, muscle epidermal retinol dehydrogenase 2 transcription level decreased with Cd exposure. Among antioxidant defences, liver transcription levels of catalase, microsomal glutathione-S-transferase-3 and glucose-6-phosphate dehydrogenase were generally enhanced in Cd-exposed fish and this up-regulation was accompanied by an increase in the activities of corresponding enzymes, except for microsomal glutathione-S-transferase. No consistent pattern in antioxidant defence responses was observed between molecular and biochemical response when fish were exposed to Ni, suggesting a non-synchronous response of antioxidant defence in fish exposed to waterborne Ni. There was a general lack of consistency between muscle transcription level and enzyme activities analyzed. The overall findings from this investigation highlight the usefulness of transcriptional and biochemical endpoints in the identification of oxidative stress and vitamin A metabolism impairment biomarkers and the potential use of multi-level biological approaches when assessing environmental risk in fish.
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Evidence for metabolic imbalance of vitamin A2 in wild fish chronically exposed to metals
Ecotoxicology and environmental safety, 2012Co-Authors: Michel A Defo, Louis Bernatchez, Peter G C Campbell, Fabien Pierron, Philip A. Spear, Patrice CoutureAbstract:In a recent study on indigenous yellow perch chronically exposed to metals, we reported a negative correlation between liver metal concentration and liver transcription levels of genes encoding for enzymes involved in the metabolism of retinoids. We therefore speculated that metals, and especially the non-essential metal Cd, could alter the metabolism of retinoids in wild fish. Thus the present field study investigates the impact of in situ metal exposure on retinoid storage. A total of 55 yellow perch (Perca flavescens) were sampled in six lakes representing a metal contamination gradient (8≤N≤10 per lake). Our results show that yellow perch from Cd-contaminated lakes had significantly higher concentrations of liver Dehydroretinol and dehydroretinyl esters than did fish from reference lakes. However, the increase in retinyl ester stores with increasing Cd concentrations was quantitatively much more important than the increase in free Dehydroretinol. As a result, a significant decrease in the percentage of hepatic free Dehydroretinol with increasing renal Cd concentrations was observed. These results suggest that the enzymes and the binding proteins involved in vitamin A homeostasis are inhibited by the presence of Cd. Alternatively, the increase in tissue vitamin A (antioxidant) levels could serve to better counteract the oxidative stress engendered by Cd exposure. Overall our findings illustrate that vitamin A(2) homeostasis can be altered as a consequence of chronic exposure to low Cd concentrations. Thus, in the context of environmental risk assessment, the percentage of liver free Dehydroretinol can be considered as a biomarker of for in situ Cd exposure.
Marcia Simon - One of the best experts on this subject based on the ideXlab platform.
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UVA/B exposure promotes the biosynthesis of Dehydroretinol in cultured human keratinocytes
Molecular and Cellular Biochemistry, 2012Co-Authors: Juliana I. Tafrova, Adriana Pinkas-sarafova, Erik Stolarzewicz, Kathlyn A. Parker, Marcia SimonAbstract:Retinol and its metabolites modulate epithelial differentiation and serve as cellular UV sensors through changes in retinoid status. Of note is the Dehydroretinol family which may serve functions distinct from parental retinol. This study focuses on the metabolism of this family and its potential participation in the response of normal epidermal human keratinocytes to UV irradiation. There were three findings. First, keratinocytes contain two pools of dehydroretinyl esters, one of which is shielded from UVB-, but not from UVA-induced decomposition. Second, using a novel in vitro assay we demonstrated that both UVA and UVB promote Dehydroretinol biosynthesis in keratinocytes, but only UVB exposure promotes retinoid ester accretion by enhancing the activity of at least one acyl transferase. Finally, Dehydroretinol sufficiency reduces UVA/B driven apoptosis more effectively than retinol sufficiency. This may in part be due to differences in the expression of Fas ligand, which we found to be upregulated by retinoic acid, but not dehydroretinoic acid. These observations implicate a role of Dehydroretinol and its metabolites in UVA/B adaptation. Thus, the keratinocyte response to UV is jointly shaped by both the retinoids and dehydroretinoids.
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uva b exposure promotes the biosynthesis of Dehydroretinol in cultured human keratinocytes
Molecular and Cellular Biochemistry, 2012Co-Authors: Juliana I. Tafrova, Erik Stolarzewicz, Kathlyn A. Parker, Adriana Pinkassarafova, Marcia SimonAbstract:Retinol and its metabolites modulate epithelial differentiation and serve as cellular UV sensors through changes in retinoid status. Of note is the Dehydroretinol family which may serve functions distinct from parental retinol. This study focuses on the metabolism of this family and its potential participation in the response of normal epidermal human keratinocytes to UV irradiation. There were three findings. First, keratinocytes contain two pools of dehydroretinyl esters, one of which is shielded from UVB-, but not from UVA-induced decomposition. Second, using a novel in vitro assay we demonstrated that both UVA and UVB promote Dehydroretinol biosynthesis in keratinocytes, but only UVB exposure promotes retinoid ester accretion by enhancing the activity of at least one acyl transferase. Finally, Dehydroretinol sufficiency reduces UVA/B driven apoptosis more effectively than retinol sufficiency. This may in part be due to differences in the expression of Fas ligand, which we found to be upregulated by retinoic acid, but not dehydroretinoic acid. These observations implicate a role of Dehydroretinol and its metabolites in UVA/B adaptation. Thus, the keratinocyte response to UV is jointly shaped by both the retinoids and dehydroretinoids.