Attenuation of Lead-Induced Neurotoxicity by Omega-3 Fatty Acid in Rats

Abstract

Background: Lead is widely distributed in the environment and has been found to be associated with various health problems including neurodegenerative diseases. Purpose: In view of the increasing health risk caused by lead, this study has been carried out to investigate the neuroprotective effect of omega-3 fatty acid (omega-3FA) in lead-induced neurotoxicity in rats. Methods: Biochemical parameters including oxidative stress in brain regions, lead levels in blood and brain regions and histopathological examination of brain regions of rats were carried out in the present study. Results: Rats exposed to lead (lead acetate 7.5 mg/kg body weight p.o. for 14 days) caused a significant increase in the levels of lipid peroxidation, protein carbonyl content, ROS production and decreased the activities of glutathione peroxidase, superoxide dismutase and catalase in the cerebellum and cerebral cortex, respectively, as compared to controls. Abnormal histopathological changes and increase in the levels of lead in blood and brain were also observed as compared to controls. Co-treatment of lead with omega-3FA (750 mg/kg body weight p.o. for 14 days) decreased the levels of lipid peroxidation, protein carbonyl content, ROS production and increased the activities of glutathione peroxidase, superoxide dismutase and catalase and showed protection in the histopathological study as compared to rats treated with lead alone. Conclusions: The result of the present study shows that lead-induced oxidative stress and histopathological alteration in the brain region were significantly protected with co-treatment of lead and omega-3FA. This could be due to its strong antioxidant potential and metal-binding property.

Histopathological effects of experimental exposure to lead on nervous system in albino female rats

“…Additionally, hemorrhage, neurophagia and glial nodules were observed. These finding are agreement with those reported by (11,13,14) which they exposed mice, rats and guinea pigs to lead and observed Vascular lesions additionally to encephalpathic injury of lead mediated at the neuronal level.…”

“…It is a potent neurotoxic agent, affecting nervous system (2,3). The brain tissue is vulnerable to the effects of lead injury (11,12). Lead is capable to pass through the endothelium of the blood brain barrier because it can replace for ions of the calcium and be taken up by Ca +2 -ATPase pumps, thus interfering with synapse formation.…”

Preclinical assessment of Alzheimer's disease using novel designed 99mTc‐labeled RGD‐based pro‐apoptotic cyclic peptide as a promising SPECT agent

“…LAT intoxication may also result in biochemical alterations and multiple neurological disorders such as AD, nerve damage, PD, damage to neuronal mitochondria, and finally leads to programmed cell death. [ 35 ] In our study, the results of serum and biochemical parameters obtained from animal samples suggested that LAT exposure is associated with increased AST, ALT, LDH, CPK, and ALP levels. Furthermore, an upregulation was also observed in oxidative stress (ROS), lipid peroxidation, protein carbonyl content, and apoptosis inducing factor Bax levels; on the other hand, a downregulation pattern was observed for superoxide dismutase, catalase, and glutathione peroxidase activities which highlighted the incidence of neurotoxicity.…”

“…[ 33,34 ] These outcomes are in agreement with the results reported in literature which suggests that LAT can accumulate in brain regions by crossing blood–brain barrier and express its toxic effects to cause AD. [ 33,35 ]…”

Syzygium Cumini Leaves Extract from West Sumatra Indonesia Alleviate Oxidative Stress by Decreasing Malondialdehyde Level and Enhancing Catalase Activity in Rat Induced by Lead Acetate

“…12,27 Exposure to lead acetate can increase free radicals in the body. 16,[28][29][30] Increased free radicals lead to a rise in lipid peroxidation, [31][32][33] one of the remaining lipid peroxidations often found is Malondialdehyde. [17][18][19] Previous research has shown that exposure to lead acetate leads to elevated levels of blood Malondialdehyde.…”