Nehru B, Iyer A
Department of Biophysics, Panjab University, Chandigarh, India.
J Environ Pathol Toxicol Oncol. 1994;13(4):265-8.
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.
铅暴露对幼儿和成人的影响不同，体内研究与体外研究之间以及实验数据与临床数据之间存在不一致，这表明铅毒性可能具有不同的机制。在发育阶段，铅神经毒性会导致永久性功能障碍，但在成年人中所见的神经药理毒性可能涉及其与钙和锌等微量营养素的相互作用。发现以20mg/kg的剂量口服给予铅8周会抑制大脑和小脑中琥珀酸脱氢酶、乙酰胆碱酯酶和Na+/K+ATP酶的酶活性。以0.5ppm的剂量给予硒8周时也会影响这些酶。当同时给予铅和硒时，三种酶活性的抑制作用会大大减轻。然而，当在接触铅后仅给予硒（0.5ppm）15天时，与对照组相比，酶的活性会大大降低。
