Benzo(a)pyrene-induced acute neurotoxicity in the F-344 rat: role of oxidative stress

摘要: Given the link between neurotoxicity and exposure to pollutants, potential behavioral of benzo(a)pyrene [B(a)P] was investigated. Studies have established that B(a)P requires metabolic activation highly reactive species elicit many its adverse effects. This study investigated perturbation nervous system function by correlating changes with metabolism B(a)P, antioxidant enzyme levels lipid peroxidation in selected brain regions. The neurobehavioral effects single oral doses (25-200 mg kg(-1) body weight) on motor activity were examined male F-344 rats at 2, 4, 6, 12, 24, 48, 72 96 h post treatment. Parent metabolites measured above mentioned time points reverse phase HPLC. several enzymes (superoxide dismutase, catalase glutathione peroxidase) malondialdehyde determined 6 both striatum hippocampus exposed rats. Suppression (up 70%) reached a maximum h, but reversible all dose groups. kinetics disposition data show strong onset duration Benzo(a)pyrene caused 15-70% inhibition superoxide dismutase peroxidase an enhancement 68%) treatment, respectively. These findings suggest B(a)P-induced acute toxicity may occur through oxidative stress due scavenging system.