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

Given the link between neurotoxicity and exposure to pollutants, the potential behavioral neurotoxicity of benzo(a)pyrene [B(a)P] was investigated. Studies have established that B(a)P requires metabolic activation to highly reactive species to elicit many of its adverse effects. This study investigated the perturbation of nervous system function by correlating behavioral changes with the metabolism of B(a)P, antioxidant enzyme levels and lipid peroxidation in selected brain regions.

Fluoranthene-induced neurobehavioral toxicity in F-344 rats.

Fluroanthene (FLA) is a nonalternant representative of polycyclic aromatic hydrocarbon (PAH) family of toxic chemicals that are widely distributed in the environment. The effects of single acute doses of FLA on locomotor activities and the functional observational battery (FOB) were investigated in 8-week-old male and female F-344 rats. FLA was dissolved in peanut oil and administered by oral gavage as single doses of 0, 100, 200 and 400 mg/kg.

Modulation of neurotoxic behavior in F-344 rats by temporal disposition of benzo(a)pyrene.

The behavioral changes caused by benzo(a)pyrene (BaP), a polycyclic aromatic hydrocarbon (PAH) compound, were monitored, and also its metabolite levels in cerebellum and cortex were measured in BaP treated rats to see if any relationship existed between these two aspects. Rats were administered 0, 25, 50, 100, and 200 mg/kg of BaP in peanut oil by oral gavage. Plasma, and brain tissue (cerebellum and cortex) samples were collected at 0, 2, 4, 6, 12, 24, 48, 72 and 96 h post administration.

Nifedipine potentiates the toxic effects of cocaine in mice.

The calcium channel blockers (CCBs) have been shown to be effective in attenuating the behavioral effects of cocaine in rodents and subjective effects in cocaine-using volunteers. There have been reports indicating that, in the presence of toxic doses of cocaine, the CCBs could actually potentiate cocaine toxicity in rats. The present study was undertaken to make toxicological assessment of the potentiating effect of CCBs in mice.