The role of oxidative stress in α-amanitin-induced hepatotoxicity in an experimental mouse model.

Background/aim: This study aimed to evaluate oxidative stress markers of liver tissue in a mouse a-amanitin poisoning model with three different toxin levels. Materials and methods: The mice were randomly divided into Group 1 (control), Group 2 (0.2 mg/kg), Group 3 (0.6 mg/kg), and Group 4 (1.0 mg/kg). The toxin was injected intraperitoneally and 48 h of follow-up was performed before sacrifice. Results: Median superoxide dismutase activities of liver tissue in Groups 3 and 4 were significantly higher than in Group 1 (for both, P = 0.001). The catalase activity in Group 2 was significantly higher, but in Groups 3 and 4 it was significantly lower than in Group 1 (for all, P = 0.001). The glutathione peroxidase activities in Groups 2, 3, and 4 were significantly higher than in Group 1 (P = 0.006, P = 0.001, and P = 0.001, respectively). The malondialdehyde levels of Groups 3 and 4 were significantly higher than Group 1 (P = 0.015 and P = 0.003, respectively). The catalase activity had significant correlations with total antioxidant status and total oxidant status levels (r = 0.935 and r = -0.789, respectively; for both, P < 0.001). Conclusion: Our findings support a significant role for increased oxidative stress in a-amanitin-induced hepatotoxicity. [ABSTRACT FROM AUTHOR]