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Benzene is known to cause myelotoxicity which impacts secondary complications mediated by oxidative stress on the heart and erythrocyte. Gallic acid is an antioxidant which has not been evaluated for protective effect against cardiovascular complications of benzene-induced myelotoxicity. Therefore, this study was carried out to evaluate the effects of gallic acid on the concentrations of selected oxidative stress biomarkers and activities of antioxidant enzymes in the erythrocyte and heart of mice with benzene-induced myelotoxicity. Thirty-six male mice were randomized into six groups of six mice each. Group A served as the normal control receiving distilled water while the remaining groups were orally administered 150 mg/kg body weight of benzene for fourteen days. Distilled water, 50 mg/kg body weight of ascorbic acid, 25, 50, and 100 mg/kg body weight of gallic acid were simultaneously administered to mice of groups B (negative control), C, D, E, and F respectively for fourteen days. Concentrations of oxidative stress biomarkers and activities of antioxidant enzymes in target tissues were then determined. Results revealed significant elevation (p<0.05) in the concentrations of malondialdehyde, nitric oxide and protein carbonyl, as well as significant decrease (p<0.05) in the concentrations of reduced glutathione, protein, and activities of catalase, glutathione peroxidase, glutathione-S-transferase and superoxide dismutase in the heart and erythrocyte of negative control compared to normal control. However, treatment with gallic acid at various doses significantly reverted (p<0.05) the observed alterations in these parameters, comparing favourably with ascorbic acid (reference drug). These results suggest that gallic acid protected the heart and erythrocyte against lipid and protein oxidation, and enhanced antioxidant defense system of mice with benzene-induced myelotoxicity. Keywords: myelotoxicity; oxidative stress; gallic acid; ascorbic acid; benzene; antioxidant enzymes; biomarkers; lipid peroxidation; protein oxidation.