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

• Published in: Metabolic brain disease Vol. 33; no. 2; pp. 377 - 385
• Main Authors: Folarin, O. R., Adaramoye, O. A., Akanni, O. O., Olopade, J. O.
• Format: Journal Article
• Language: English
• Published: New York Springer US 01-04-2018; Springer Nature B.V
• Subjects: Animals; Antioxidants; Antioxidants - pharmacology; Biochemistry; Biomedical and Life Sciences; Biomedicine; Brain; Brain - drug effects; Brain - metabolism; Central nervous system; Exposure; Glutathione; Glutathione peroxidase; Glutathione Peroxidase - drug effects; Glutathione Peroxidase - metabolism; Glutathione transferase; Hydrogen peroxide; Hydrogen Peroxide - pharmacology; Male; Malondialdehyde; Metabolic Diseases; Mice; Mice, Inbred BALB C; Neurodegeneration; Neurology; Neurosciences; Nitric oxide; Oncology; Original Article; Oxidative stress; Oxidative Stress - drug effects; Peroxidase; Reactive oxygen species; Reactive Oxygen Species - metabolism; Rodents; Superoxide dismutase; Superoxide Dismutase - drug effects; Superoxide Dismutase - metabolism; Vanadium; Vanadium - administration & dosage; Vanadium - pharmacology; Brain; Reactive oxygen species; Neurodegeneration; Vanadium
• ISSN: 0885-7490; 1573-7365
• DOI: 10.1007/s11011-017-0070-9

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3–18 months treatment), matched controls, and animals exposed to vanadium for three months and thereafter vanadium was withdrawn.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 (H
2
O
2
) 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.