Chromium(VI) induces oxidative stress in the mouse brain

Potassium dichromate was given to female Swiss mice (25 mg/kg per day) oral ly in water for 1-3 days. Brain homogenates were prepared to evaluate the o ccurrence of oxidative stress in this organ through the measurement of the antioxidant defense levels, and the extent of lipid peroxidation. In additi on, mitochondrial fractions were isolated from brain homogenates to determi ne the production of reactive oxygen species in this subcellular fraction. The administration of potassium dichromate for 3 days caused increases of 7 2 and 74% in superoxide dismutase and catalase activities, respectively, in the homogenates. The treatment with this metal for 3 days increased brain homogenate chemiluminescence and thiobarbituric acid-reactive substances by 34 and 29%, respectively. The brain contents of the non-enzymatic antioxid ants a-tocopherol and sulfhydryl groups decreased by 35 and 32%, respective ly. Ascorbic acid levels were not modified by the administration of potassi um dichromate. Finally, there was a significant increment in the mitochondr ial production of oxidants in the brain of treated mice as compared with co ntrols. These results suggest that chromium(VI) produces an increased forma tion of reactive oxygen species and brain lipid peroxidation. The increase in the antioxidant enzyme activities reflects an adaptive response against oxidative stress, while the reduction in the levels of non-enzymatic antiox idants might be due to their reaction with reactive oxygen species generate d during the metabolism of chromium(IV). (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.