Effects of exposure to BDE-99 on oxidative status of liver and kidney in adult rats

• Published in: Toxicology (Amsterdam) 2010-04, Vol.271 (1), p.51-56
• Main Authors: Albina, Maria L, Alonso, Virginia, Linares, Victoria, Bellés, Montserrat, Sirvent, Juan J, Domingo, José L, Sánchez, Domènec J
• Format: Article
• Language: English
• Subjects: Adult rats; Adults; Animals; BDE-99; Biological and medical sciences; Catalase - metabolism; Damage; Emergency; Ethers; Glutathione; Glutathione - metabolism; Glutathione Disulfide - metabolism; Glutathione Peroxidase - metabolism; Glutathione Reductase - metabolism; Glutathione Transferase - metabolism; Halogenated Diphenyl Ethers - toxicity; Hepatotoxicity; Histocytochemistry; Kidney - drug effects; Kidney - enzymology; Kidney - metabolism; Kidneys; Liver; Liver - drug effects; Liver - enzymology; Liver - metabolism; Male; Medical sciences; Nephrotoxicity; Oxidative stress; Oxidative Stress - drug effects; Random Allocation; Rats; Rats, Sprague-Dawley; Sod; Statistics, Nonparametric; Superoxide Dismutase - metabolism; Thiobarbituric Acid Reactive Substances - metabolism; Toxicology
• ISSN: 0300-483X; 1879-3185
• DOI: 10.1016/j.tox.2010.03.006

Abstract Little is known about the potential toxicity of polybrominated diphenyl ethers (PBDEs) on hepatic and renal tissues. In this study, we investigated the modifications in endogenous antioxidant capacity and oxidative damage in liver and kidney of rats by exposure to one of the most persistent PBDE congeners, the 2,2′,4,4′,5-pentabromodiphenyl ether (BDE-99). Adult male rats (10 per group) received BDE-99 by gavage at a single dose of 0, 0.6, and 1.2 mg/kg body weight. Forty-five days after exposure, liver and kidney were removed and processed to examine the following oxidative stress (OS) markers: reduced glutathione (GSH), oxidized glutathione (GSSG), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), superoxide dismutase (SOD), catalase (CAT), and thiobarbituric acid reactive substances (TBARS). In liver, BDE-99 significantly increased SOD activity, GSSG levels, and GSSG/GSH ratio, while GSH levels decreased. Moreover, CAT activity was only reduced at the highest BDE-99 dose. In kidney, CAT activity was significantly decreased, while GSSG/GSH ratio significantly increased following BDE-99 exposure at 1.2 mg/kg body weight. Histological examination of tissues showed phagolysosomes in the kidneys of BDE-99-exposed rats. The results of this investigation suggest that acute oral BDE-99 exposure causes renal and liver impairment, being oxidative damage a potential mechanism for nephrotoxicity and hepatotoxicity.