Neurobehavioral and neurochemical effects of perinatal arsenite exposure in Sprague-Dawley rats.

Exposure to relatively high levels of inorganic arsenic (iAs) is associated with detrimental effects on human health, including cancer and diabetes. The effects of lower-level exposures are less clear, and gaps in the literature exist as to the effects of iAs exposure on neurodevelopment. The current study assessed the effects of perinatal iAs exposure on rodent neurodevelopment and behavior. Pregnant Sprague-Dawley (SD) rats were exposed to arsenite (AsIII) via oral gavage on gestational days (GD) 6 through 21, and pups were directly dosed via gavage on postnatal days (PND) 1 through 21. Dams and offspring received the same doses: 0.00, 0.10, 1.50, or 3.75 mg/kg/day. Male and female offspring underwent a battery of behavioral assessments from weaning until PND 180. Brain arsenic levels increased in a dose-dependent manner at both PND 1 and 21. Results from the behavioral tests show that pre- and postnatal AsIII exposure did not adversely affect offspring weight gain, adolescent motor and cognitive functions, or adult motor and cognitive functions in the SD rat. There were no differences in concentration of several brain proteins associated with blood-brain barrier permeability, dopamine functions, and inflammation.

S-Allylcysteine prevents amyloid-beta peptide-induced oxidative stress in rat hippocampus and ameliorates learning deficits.

The effects of S-allylcysteine on oxidative damage and spatial learning and memory deficits produced by an intrahippocampal injection of amyloid-beta peptide 25-35 (Abeta(25-35)) in rats were investigated. The formation of reactive oxygen species, lipid peroxidation and the activities of the antioxidant enzymes superoxide dismutase and glutathione peroxidase were all measured in hippocampus 120 min after Abeta(25-35) injection (1 microl of 100 microM solution), while learning and memory skills were evaluated 2 and 35 days after the infusion of Abeta(25-35) to rats, respectively. Abeta(25-35) increased both reactive oxygen species and lipid peroxidation, whereas pretreatment with S-allylcysteine (300 mg/kg, i.p.) 30 min before peptide injection decreased both of these markers. In addition, Abeta(25-35)-induced incorrect learning responses were prevented in most of trials by S-allylcysteine. In contrast, enzyme activities were found unchanged in all groups tested. Findings of this work: (i) support the participation of reactive oxygen species in Abeta(25-35)-induced hippocampal toxicity and learning deficits; and (ii) suggest that the protective effects of S-allylcysteine were related to its ability to scavenge reactive oxygen species.