Late-life Cardiac Injury in Rats following Early Life Exposure to Lead: Reversal Effect of Nutrient Metal Mixture.

Early-life exposure to lead (Pb) can lead to health effects in later life. The neurotoxic effects of Pb have been well documented but its effects on the heart are poorly elucidated. We examined the late life cardiac impairments resulting from developmental exposure to Pb.

Perinatal exposure to lead: reduction in alterations of brain mitochondrial antioxidant system with calcium supplement.

Lead (Pb) is a potent neurotoxicant that causes several neurochemical and behavioral alterations. Previous studies showed that the gestational and lactational exposure to Pb reduces the cholinergic and aminergic systems, and behavior of rats. The present study was designed to examine the protective effects of calcium supplementation against Pb-induced oxidative stress in cerebellum and hippocampus of brain at postnatal day (PND) 21, PND 28, PND 35, and PND 60.

Alterations in apoptotic caspases and antioxidant enzymes in arsenic exposed rat brain regions: reversal effect of essential metals and a chelating agent.

Arsenic (As) widely studied for its effects as a neurotoxicant. The present study was designed to evaluate the protective effect of calcium, zinc or monoisoamyl dimercaptosuccinic acid (MiADMSA), either individually or in combination on As induced oxidative stress and apoptosis in brain regions (cerebral cortex, hippocampus and cerebellum) of postnatal day (PND) 21, 28 and 3 months old rats. Arsenic exposure significantly decreased the activities of superoxide dismutase (SOD) isoforms, catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) with increase in glutathione s transferase (GST) while lipid peroxidation (LPx), arsenic levels, mRNA expression of caspase 3 and 9 were significantly increased in different brain regions.

Reversal effect of monoisoamyl dimercaptosuccinic acid (MiADMSA) for arsenic and lead induced perturbations in apoptosis and antioxidant enzymes in developing rat brain.

Oxidative stress (OS) has been implicated in the pathophysiology of many neurodegenerative disorders. Several studies have shown that exposure to arsenic (As) and lead (Pb) produces oxidative stress, one of the most noted molecular mechanisms for the neurotoxicity of these metals. In the present study, we examined the effect of combined exposure to these metals (As and Pb) on the activity levels of antioxidant enzymes and apoptotic marker enzymes in brain regions (cerebral cortex, hippocampus and cerebellum) of rats at postnatal day (PND) 21, 28 and 3 months age and compared the toxicity levels with individual metals (As or Pb).