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Alpha-Amanitin Poisoning, Nephrotoxicity and Oxidative Stress: An Experimental Mouse Model
Mehmet Ergin1, Zerrin Defne Dundar1, Ibrahim Kilinc2
1Department of Emergency Medicine, Meram Medicine School, Necmettin Erbakan University, Konya, Turkey.
Background:
Alpha-amanitin (α-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 α-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 α-AMA in mice experimental poisoning models.
Materials And Methods:
There were 37 male BALB/c laboratory mice treated with α-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:
α-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 α-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.
Insights
Alpha-amanitin poisoning causes kidney damage in mice, characterized by inflammation and necrosis. This study demonstrates a significant shift towards oxidative stress in the kidneys following alpha-amanitin exposure.
Area of Science:
- Toxicology
- Nephrology
- Biochemistry
Background:
- Alpha-amanitin (α-AMA) is a key toxin in Amanita phalloides poisoning, affecting multiple organs, especially the liver and kidneys.
- Previous research suggests a link between α-AMA-induced injuries and reactive oxygen species (ROS).
Purpose of the Study:
- To investigate renal injury in mice experimentally poisoned with α-AMA.
- To determine the relationship between α-AMA-induced renal injury and oxidative stress.
Main Methods:
- 37 male BALB/c mice were divided into control and α-AMA intoxication groups (low, moderate, high doses).
- Mice were monitored for 48 hours post-injection.
- Pathological and biochemical analyses of renal tissues were performed.
Main Results:
- α-AMA poisoning induced inflammatory changes and necrosis in mouse renal structures.
- Significant differences were observed in renal levels of catalase, superoxide dismutase, glutathione peroxidase, TAS, TOS, and MDA.
- TOS levels were significantly elevated, and TAS levels were significantly reduced in α-AMA-treated groups compared to controls.
Conclusions:
- α-AMA poisoning causes renal damage, including inflammation and necrosis in mice.
- The study confirms a shift in the oxidative-antioxidative balance towards oxidative stress in the kidneys following α-AMA exposure.
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