Repository of Research and Investigative Information

Repository of Research and Investigative Information

دانشگاه علوم پزشکی و خدمات بهداشتی درمانی زنجان

Toxicity of depleted uranium on isolated liver mitochondria: a revised mechanistic vision for justification of clinical complication of depleted uranium (DU) on liver

(2013) Toxicity of depleted uranium on isolated liver mitochondria: a revised mechanistic vision for justification of clinical complication of depleted uranium (DU) on liver. Toxicological and Environmental Chemistry. pp. 1221-1234.

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Abstract

Depleted uranium (DU) is widely used in military anti-armor weapons. Recent evidence suggested that oxidative stress and mitochondrial dysfunction may contribute to DU-induced toxicity. However, the underlying mechanisms of DU toxicity in mitochondria are not well understood. In this study, liver mitochondria were obtained from Wistar rats treated with DU in the form of uranyl acetate (UA) (0.5, 1 or 2mg/kg i.p.) using differential centrifugation. For in vitro experiments, control rat liver mitochondria were incubated with different concentrations of UA (50, 100 or 200M) for 1 hr. Mitochondrial reactive oxygen species (ROS) production, collapse of mitochondrial membrane potential, and mitochondrial swelling were examined by flow cytometry. Mitochondrial sources of ROS formation were determined using specific substrates and inhibitors. Extent of lipid peroxidation (LPO) and glutathione (GSH) oxidation, and also complex II and IV activities were detected via spectroscopy. Further, the concentration of ATP and ATP/ADP ratio was measured using luciferase enzyme and release of cytochrome c from mitochondria which was detected by ELISA kit. UA induced succinate-supported mitochondrial ROS production, elevated LPO levels, GSH oxidation, and mitochondrial complex II inhibition. UA also induced mitochondrial permeability transition and increase in cytochrome c release which subsequently disturbed oxidative phosphorylation and reduced the mitochondrial ATP concentration. Data suggest that mitochondrial oxidative stress and uncoupling of oxidative phosphorylation may play key roles in DU-induced hepatic toxicity.

Item Type: Article
Page Range: pp. 1221-1234
Journal or Publication Title: Toxicological and Environmental Chemistry
Abstract and Indexing: ISI
Quartile : Q4
Volume: 95
Number: 7
Publisher: scopus
Depositing User: خانم مریم زرقانی
URI: http://repository.zums.ac.ir/id/eprint/1919

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