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

Dündar ZD, Ergin M, Kilinç İ et al.

Department of Emergency Medicine, Meram Faculty of Medicine, Necmettin Erbakan University, Konya, Turkey.

Turkish journal of medical sciences. 02 2017.

This study aimed to evaluate oxidative stress markers of liver tissue in a mouse α-amanitin poisoning model with three different toxin levels.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.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).Our findings support a significant role for increased oxidative stress in α-amanitin-induced hepatotoxicity. Pubmed

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