Hydroquinone is pharmacologically active metabolite of arbutin, is released from arbutin by the action of enzyme β-glucosidase and alkali conditions in human organism. Hydroquinone has shown carcinogenic properties in chronic toxicity studies in rodents where it has been shown that hydroquinone stimulate benign liver and kidney tumors as well as mononuclear leukemia. The purpose of this study is to determine the effect of hydroquinone on the oxidative stress level by spectrophotometric measurements of superoxide dismutase and catalase activity, as well as the determination of lipid peroxidation by measuring the concentration of malondialdehyde and the possible genotoxic effect using a standard comet assay in alkaline conditions. This research was carried out on kidney, liver and brain of Lewis breed rats of both gender treated with hydroquinone in concentration of 200 mg/kg during 28 days. The results indicate that hydroquinone slightly increases a level of lipid peroxidation but does not affect the activity of the antioxidant enzymes catalase and superoxide dismutase. Hydroquinone shows a statistically relevant increase of primary DNA damage in male rats kidney cells for parameters the tail intensity and tail moment. There was a statistically relevant increase in DNA damage for all three parameters of the comet assay on female rats liver cells. But since they measured levels of damage do not exceed 10% DNA in comet tail, hydroquinone shows low genotoxic potential. Based on the indicated results it can be concluded that the permitted daily dose of hydroquinone is not toxic to the cells of the kidneys, liver and brain.