Changes in the brain antioxidant profile after chronic vanadium administration in mice

Abstract

Vanadium is known to induce reactive oxygen species (ROS) in biological systems. Exposure to vanadium has been linked to neurological defects affecting the central nervous system (CNS) early in life and culminates later to neurodegeneration. This study was designed to evaluate the effects of chronic vanadium exposure on antioxidant profile in mice, and progressive changes after withdrawal from treatment. A total of 85 male BALB/c mice (4 weeks old) were used for the experiment and were divided into three groups of vanadium exposed (3 mg/kg i.p at 3–18 months treatment), matched controls, and animals exposed to vanadium for three months and thereafter vanadium was withdrawn. Vanadium exposure caused significant increases (p<0.05) in levels of malondialdehyde (MDA), hydrogen peroxide (H₂O₂) generation and nitric oxide with a concomitant decrease (p<0.05) in the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase and a decline in the level of reduced glutathione (GSH) after 6 months of vanadium exposure in the brain. This trend continued in all vanadium-exposed groups (9, 12, 15 and 18 months) relative to the matched controls. Withdrawal after 3 months of vanadium exposure significantly reversed oxidative stress in intoxicated mice from 9 to 15 months after vanadium withdrawal. We have shown that chronic administration of vanadium led to oxidative stress in the brain which is reversible only after a long period of vanadium withdrawal.

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