铅对发育中的脑脂质过氧化作用的影响

新生大鼠吸吮饮用含Pb~(2+)300 ppm和1000ppm水的母鼠乳汁(约含Pb~(2+)10～25ppm)连续21 d后,血铅和脑铅含量有显著增高,其血和脑ALAD活性亦有不同程度的抑制,说明Pb~(2+)容易由母体乳汁传递给新生大鼠引起铅中毒。另外还看到,新生大鼠脑匀浆、脑线粒体和微粒体的膜MDA含量及脂质过氧化荧光物质量比对照明显增加,血浆SOD活性抑制,均提示Pb~(2+)引起膜损伤(一是促进膜脂质过氧化作用;二是抑制SOD活性),因而出现Pb~(2+)对中枢神经系统的神经毒性。

Effect of lead acetate on lipid peroxidation of developing rat brain

Newborn rats were exposed to Pb2+ from the maternal milk during their postnatal development period up to 21 days of age.Lead content were significantly increased and marked inhibition of ALAD activity were observed in blood and whole brain,indicating lead poisoning of newborn rats.Lipid peroxidation was monitored by measuring the production of thiobarbituric acid reactive substances (ma-londialdehyde,MDA)and fluorescent products formed by crosslinking two primary amines with MDA.The rate of lipid peroxidation was enhanced in brain homogenate,mitochondrial and microsomal membranesof newborn rats after lead intoxication,while a significant inhibition of plasma suporoxide dismutase (SOD)activity was accompanied by an increase of the Pb2+ concentration in the whole blood of lead poisoned newborn rats.Results suggest that the increased lipid peroxidation in brain subcellular membranes and inhibition of SOD activity by ex posure to lead may play a significant role in lead-induced neurotoxicity.