Permethrin-induced oxidative damage in liver of rainbow trout [Oncorhynchus mykiss] and its attenuation by vitamin C

The objective of this study was to investigate the propensity of permethrin [PTN] to induce oxidative stress and changes in enzyme activities in liver of rainbow trout and its possible attenuation by vitamin C. Forty-eight fish were randomly assigned to 1 of 6 treatment groups and their livers were used for liver perfusion method: control [0 microgL-1 permethrin and 0 mgL-1 vitamin C], PTN-0.16 [0.16 microgL-1 permethrin], PTN-0.32 [0.32 microgL-1 permethrin], PTN-0.64 [0.64 microgL-1 permethrin], Vit. C [17.2 mgL-1 vitamin C], and PTN-0.64 + Vit. C [0.64 microgL-1 permethrin and 17.2 mgL-1 vitamin C]. Results obtained showed that permethrin significantly [P<0.05] increased ALT, AST and LDH activities in the liver perfusion medium and malondialdehyde [MDA] level in liver tissue. The values of reduced glutathione [GSH] and total antioxidant capacity [FRAP] in the liver tissue were significantly decreased due to permethrin administration. Pearson's correlation analysis revealed a positive correlation between MDA concentration and ALT, AST and LDH activities in the permethrin groups, suggesting that the enhanced lipid peroxidation may be linked to hepatic damage caused by permethrin. On the other hand, treatment with vitamin C in the PTN-0.64 + Vit. C group increased the values of GSH and FRAP, and decreased the level of MDA and the activities of hepatic enzymes, when compared to the PTN-0.64 group. The present study revealed that vitamin C could ameliorate permethrin-induced oxidative damage by decreasing lipid peroxidation and altering antioxidant defense system in liver of rainbow trout

pretreatment effects of pentoxifylline on aflatoxin B1-induced oxidative damage in perfused rat liver

This study was conducted to investigate the hepatoprotective and antioxidant effects of pentoxifylline [PTX] against aflatoxin Bl [AFB1] exposure in perfused rat livers by evaluating damage marker enzymes, antioxidant defense systems [glutathione, GSH] and lipid peroxidation [malondialdehyde, MDA]. Sixteen rats were divided randomly into four experimental groups: control, PTX, AFB1 and AFB1 + PTX. Rats in the control group were infused with Krebs-Henseleit bicarbonate buffer. Rats in the AFB1 -treated group received approximately 1 ppm and the PTX- treated group received 100 mg/kg intraperitoneally 24 h before surgery. Alanine aminotransferase and lactate dehydrogenase levels were increased by AFB 1 and decreased by PTX. PTX also ameliorated the increased concentration of MDA caused by AFB1. PTX did not compensate for the decrease in GSH caused by AFB 1. These results imply that PTX has an antioxidant effect by inhibiting free radicals, and prior treatment with PTX ameliorates the effects of AFB 1 -induced lipid peroxidation but does not compensate GSH depots