abhishek Yadav - Academia.edu (original) (raw)
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Papers by abhishek Yadav
Ecotoxicology and Environmental Safety, 2011
We investigated the effects of silymarin and naringenin in counteracting arsenic-induced hepatic ... more We investigated the effects of silymarin and naringenin in counteracting arsenic-induced hepatic oxidative stress post exposure. Male wistar rats were chronically exposed to sodium arsenite for eight months followed by oral treatment with silymarin and naringenin (50 mg/kg each) for 15 consecutive days to evaluate hepatic damage and antioxidant potential. Our results demonstrate a significant decrease in hepatic GSH levels, SOD and catalase activities and an increase in GST and TBARS levels after arsenic administration. Silymarin or naringenin administration increased GSH levels and was beneficial in the recovery of altered SOD and catalase activity besides significantly reducing blood and tissue arsenic concentration. Our results point to the antioxidant potential of these flavonoids, which might be of benefit in the clinical recovery of subject exposed to arsenic. These flavonoids can be incorporated into the diet or co-supplemented during chelation treatment, and thus may afford a protective effect against arsenite-induced cytotoxicity.
Molecular & Cellular Toxicology, 2011
Flavonoids have been extensively studied and reported to possess widespread biological activities... more Flavonoids have been extensively studied and reported to possess widespread biological activities, including antioxidant and chelating properties. They have been proposed to exert beneficial effects in a multitude of diseased states generated due to oxidative stress. Therapeutic efficacy of oral administration of Silymarin and Quercetin after fluoride exposure (50 ppm in drinking water for 45 days) was investigated in rats. Animals exposed to fluoride showed a marked enhancement in reactive oxygen species (ROS), a significant decrease in reduced glutathione (GSH) in blood. In brain and kidney also, a significant elevation in ROS and Thiobarbituric Acid Substances (TBARS) level was noted accompanied by a significant decline in reduced/oxidized glutathione (GSH: GSSG) ratio. Furthermore, significant protection was observed in altered neurotransmitters level following the administration of Silymarin and Quercetin. Interestingly, both the flavonoids were able to reduce the level of fluoride from blood and kidney suggesting that the two flavonoids have the ability to bind fluoride ion too. It can be concluded from the results that, posttreatment with these flavonoids not only significantly protects against fluoride-induced oxidative stress but reduce its burden too from blood and tissues.
Toxicology and Applied Pharmacology, 2011
Arsenicosis, due to contaminated drinking water, is a serious health hazard in terms of morbidity... more Arsenicosis, due to contaminated drinking water, is a serious health hazard in terms of morbidity and mortality. Arsenic induced free radicals generated are known to cause cellular apoptosis through mitochondrial driven pathway. In the present study, we investigated the effect of arsenic interactions with various complexes of the electron transport chain and attempted to evaluate if there was any complex preference of arsenic that could trigger apoptosis. We also evaluated if chelation with monoisoamyl dimercaptosuccinic acid (MiADMSA) could reverse these detrimental effects. Our results indicate that arsenic exposure induced free radical generation in rat neuronal cells, which diminished mitochondrial potential and enzyme activities of all the complexes of the electron transport chain. Moreover, these complexes showed differential responses towards arsenic. These early events along with diminished ATP levels could be co-related with the later events of cytosolic migration of cytochrome c, altered bax/bcl(2) ratio, and increased caspase 3 activity. Although MiADMSA could reverse most of these arsenic-induced altered variables to various extents, DNA damage remained unaffected. Our study for the first time demonstrates the differential effect of arsenic on the complexes leading to deficits in bioenergetics leading to apoptosis in rat brain. However, more in depth studies are warranted for better understanding of arsenic interactions with the mitochondria.
Ecotoxicology and Environmental Safety, 2011
We investigated the effects of silymarin and naringenin in counteracting arsenic-induced hepatic ... more We investigated the effects of silymarin and naringenin in counteracting arsenic-induced hepatic oxidative stress post exposure. Male wistar rats were chronically exposed to sodium arsenite for eight months followed by oral treatment with silymarin and naringenin (50 mg/kg each) for 15 consecutive days to evaluate hepatic damage and antioxidant potential. Our results demonstrate a significant decrease in hepatic GSH levels, SOD and catalase activities and an increase in GST and TBARS levels after arsenic administration. Silymarin or naringenin administration increased GSH levels and was beneficial in the recovery of altered SOD and catalase activity besides significantly reducing blood and tissue arsenic concentration. Our results point to the antioxidant potential of these flavonoids, which might be of benefit in the clinical recovery of subject exposed to arsenic. These flavonoids can be incorporated into the diet or co-supplemented during chelation treatment, and thus may afford a protective effect against arsenite-induced cytotoxicity.
Molecular & Cellular Toxicology, 2011
Flavonoids have been extensively studied and reported to possess widespread biological activities... more Flavonoids have been extensively studied and reported to possess widespread biological activities, including antioxidant and chelating properties. They have been proposed to exert beneficial effects in a multitude of diseased states generated due to oxidative stress. Therapeutic efficacy of oral administration of Silymarin and Quercetin after fluoride exposure (50 ppm in drinking water for 45 days) was investigated in rats. Animals exposed to fluoride showed a marked enhancement in reactive oxygen species (ROS), a significant decrease in reduced glutathione (GSH) in blood. In brain and kidney also, a significant elevation in ROS and Thiobarbituric Acid Substances (TBARS) level was noted accompanied by a significant decline in reduced/oxidized glutathione (GSH: GSSG) ratio. Furthermore, significant protection was observed in altered neurotransmitters level following the administration of Silymarin and Quercetin. Interestingly, both the flavonoids were able to reduce the level of fluoride from blood and kidney suggesting that the two flavonoids have the ability to bind fluoride ion too. It can be concluded from the results that, posttreatment with these flavonoids not only significantly protects against fluoride-induced oxidative stress but reduce its burden too from blood and tissues.
Toxicology and Applied Pharmacology, 2011
Arsenicosis, due to contaminated drinking water, is a serious health hazard in terms of morbidity... more Arsenicosis, due to contaminated drinking water, is a serious health hazard in terms of morbidity and mortality. Arsenic induced free radicals generated are known to cause cellular apoptosis through mitochondrial driven pathway. In the present study, we investigated the effect of arsenic interactions with various complexes of the electron transport chain and attempted to evaluate if there was any complex preference of arsenic that could trigger apoptosis. We also evaluated if chelation with monoisoamyl dimercaptosuccinic acid (MiADMSA) could reverse these detrimental effects. Our results indicate that arsenic exposure induced free radical generation in rat neuronal cells, which diminished mitochondrial potential and enzyme activities of all the complexes of the electron transport chain. Moreover, these complexes showed differential responses towards arsenic. These early events along with diminished ATP levels could be co-related with the later events of cytosolic migration of cytochrome c, altered bax/bcl(2) ratio, and increased caspase 3 activity. Although MiADMSA could reverse most of these arsenic-induced altered variables to various extents, DNA damage remained unaffected. Our study for the first time demonstrates the differential effect of arsenic on the complexes leading to deficits in bioenergetics leading to apoptosis in rat brain. However, more in depth studies are warranted for better understanding of arsenic interactions with the mitochondria.