ALPHA-AMANITIN POISONING, NEPHROTOXICITY AND OXIDATIVE STRESS: AN EXPERIMENTAL MOUSE MODEL

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ERGIN MEHMET; DUNDAR ZERRIN DEFNE; KILINC IBRAHIM; COLAK TAMER; OLTULU PEMBE; SADIK GIRISGIN ABDULLAH

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Journal: Iranian Red Crescent Medical Journal Year:2015 | Volume:17 | Issue:8 Page(s): 0-0

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Title

ALPHA-AMANITIN POISONING, NEPHROTOXICITY AND OXIDATIVE STRESS: AN EXPERIMENTAL MOUSE MODEL

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Keywords

ALPHA-AMANITIN

OXIDATIVE STRESS

MYCOTOXINS

Abstract

Background: ALPHA-AMANITIN (a-AMA) plays a major role in Amanita phalloides poisoning, showing toxic effects on multi-organs, particularly on the liver and kidneys. Studies have shown a relationship between a-AMA-related injuries and reactive oxygen species.Objectives: We aimed to investigate whether there is renal injury and its relationship with OXIDATIVE STRESS after intraperitoneal injection of a-AMA in mice experimental poisoning models.Materials and Methods: There were 37 male BALB/c laboratory mice treated with a-AMA, according to the study groups: control group (n=7); low dose (0.2 mg/kg) (n=10); moderate dose (0.6 mg/kg) (n=10), and high dose (1 mg/kg) (n=10). The sample size was detected according to the ethical committee’s decision as well as similar studies in the literature. After a 48-hour follow-up period, all the subjects were sacrificed for pathological and biochemical assays. The study was held in Turkey.Results: a-AMA poisoning in mice results in inflammatory changes and necrosis in renal structures. There were statistically significant differences between the study groups regarding measured levels of catalase, superoxide dismutase, glutathione peroxidase, total antioxidant status (TAS), total oxidant status (TOS) and malonyl dialdehyde in renal homogenates of mice (P<0.001, P<0.001, P<0.001, P<0.001, P<0.001, and P=0.001, respectively). The TOS and TAS measurements helped to eliminate cumbersome analysis of diverse oxidant and antioxidant molecules. The TOS levels in renal homogenate of mice were significantly higher in all the intoxication groups compared to the control group (5.73, 7.02, 7.77, and 9.65 mmol trolox eq/g protein and P=0.002, P=0.001, and P=0.001, respectively). The TAS levels in moderate and high-dose groups were significantly lower than all the other groups treated with α-AMA (0.130, 0.152, 0.065, and 0.087 mmol trolox eq/g protein and P=0.031, P=0.001, and P=0.001, respectively).Conclusions: Our results indicated that a-AMA poisoning in mice led to inflammatory changes and necrosis in renal structures. Biochemical analysis showed a shift in the oxidative/anti-oxidative balance towards the oxidative status.

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APA: Copy

ERGIN, MEHMET, DUNDAR, ZERRIN DEFNE, KILINC, IBRAHIM, COLAK, TAMER, OLTULU, PEMBE, & SADIK GIRISGIN, ABDULLAH. (2015). ALPHA-AMANITIN POISONING, NEPHROTOXICITY AND OXIDATIVE STRESS: AN EXPERIMENTAL MOUSE MODEL. IRANIAN RED CRESCENT MEDICAL JOURNAL (IRCMJ), 17(8), 0-0. SID. https://sid.ir/paper/293111/en

Vancouver: Copy

ERGIN MEHMET, DUNDAR ZERRIN DEFNE, KILINC IBRAHIM, COLAK TAMER, OLTULU PEMBE, SADIK GIRISGIN ABDULLAH. ALPHA-AMANITIN POISONING, NEPHROTOXICITY AND OXIDATIVE STRESS: AN EXPERIMENTAL MOUSE MODEL. IRANIAN RED CRESCENT MEDICAL JOURNAL (IRCMJ)[Internet]. 2015;17(8):0-0. Available from: https://sid.ir/paper/293111/en

IEEE: Copy

MEHMET ERGIN, ZERRIN DEFNE DUNDAR, IBRAHIM KILINC, TAMER COLAK, PEMBE OLTULU, and ABDULLAH SADIK GIRISGIN, “ALPHA-AMANITIN POISONING, NEPHROTOXICITY AND OXIDATIVE STRESS: AN EXPERIMENTAL MOUSE MODEL,” IRANIAN RED CRESCENT MEDICAL JOURNAL (IRCMJ), vol. 17, no. 8, pp. 0–0, 2015, [Online]. Available: https://sid.ir/paper/293111/en

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