Ajiboye John Adebayo, Oyagbemi Ademola Adetokunbo, Akintunde Jacob Kehinde, Akinyinka Ebunoluwa Olamide and Arojojoye oluwatosin
Isoniazid, a broad-spectrum antibiotic employed clinically in the treatment of bacterial infections, is known to cause a number of biochemical dysfunctions and suspected to induce memory decline with age to animals and humans. The present study therefore evaluates the oxidative damage in brain albino male rats. Isoniazid was administered orally at the dose regimen level of 5.0 mg/kg body weight per day in three equal divided doses of 10, 20, 30mg/kg (12 h interval) for 60 days. Control rats were given distilled water for the same period. Administration of Isoniazid significantly decreased the activity of superoxide dismutase. The activity of gamma-glutamyltranspeptidase, the activity of alanine-amino transferase (ALT) and alkaline phosphatase (ALP) as well as the formation of malondialdehyde (MDA) increased (p<0.05) compared to the corresponding control. The toxic effects of Isoniazid to the brain antioxidant defence systems were significantly increased. Collectively, the results suggest that therapeutic dose of Isoniazid elicits brain lesions in male rats through induction of oxidative damage and via the inhibitory effect on protein synthesis.