Effect of selenium on lead-induced neurotoxicity in different brain regions of adult rats.
The different effects of lead exposure in young children and adults, and inconsistencies between in vivo and in vitro studies as well as between experimental and clinical data suggest that lead toxicity may have different mechanisms. During the developmental phase, lead neurotoxicity results in permanent dysfunction, but its neuropharmacological toxicity as seen in adults might involve its interaction with micronutrients such as calcium and zinc. Lead administered orally in a dose of 20 mg/kg for 8 weeks was found to inhibit the enzyme activity of succinic dehydrogenase, acetylcholine esterase and Na+/K+ ATPase both in the cerebrum and in the cerebellum. Selenium also affected these enzymes when administered in a dose of 0.5 ppm for 8 weeks. When lead and selenium were administered simultaneously the inhibition of the three enzyme activities was considerably alleviated. However, when selenium (0.5 ppm) was given only for 15 days after exposure to lead, the activity of the enzymes was much reduced when compared with control.
Nehru
B
B
Department of Biophysics, Panjab University, Chandigarh, India.
Iyer
A
A
D000704:Analysis of Variance; D000818:Animals; D001921:Brain / Q000187:drug effects*; D002800:Cholinesterase Inhibitors / Q000633:toxicity; D004347:Drug Interactions; D007854:Lead / Q000633:toxicity*; D009474:Neurons / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012643:Selenium / Q000494:pharmacology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors; D013385:Succinate Dehydrogenase / Q000037:antagonists & inhibitors; D009435:Synaptic Transmission / Q000187:drug effects
D002800:Cholinesterase Inhibitors; D007854:Lead; D013385:Succinate Dehydrogenase; D000254:Sodium-Potassium-Exchanging ATPase; D012643:Selenium