Muñoz J J, Roca C, Santos J L, Arroyo M, de Salamanca R E
Porphyria Research Unit, University Hospital Doce de Octubre, Madrid, Spain.
Pharmacol Toxicol. 1993 Oct;73(4):189-91. doi: 10.1111/j.1600-0773.1993.tb01562.x.
Two alternatives for the treatment of lead intoxication, administration of zinc or a thiol donor, S-adenosyl-L-methionine (SAM), were analysed. Rats were exposed to lead (Pb)-acetate (60 mg/l) in drinking water during 90 days; one group also received SO4Zn in water (40 mg/l), while another received both Pb and SAM (5 mg/24 hr intraperitoneally. Erythrocytic delta-aminolaevulinic dehydratase (ALA-D) activity was significantly reduced (P < 0.001) both in rats receiving Pb alone and in rats receiving Pb and each of the other two treatments. The high erythrocytic uroporphyrinogen synthetase (URO-S) activity noticed in Pb administered rats, was significantly (P < 0.001) reduced in animals treated either with zinc or with SAM. Hepatic ALA-D activity tended to decrease while renal enzyme activity was not modified by the low level Pb exposure used in this work. Interestingly, SAM treated rats in both tissues exhibited significantly (P < 0.01) higher activities of the enzyme. It is argued that SAM treatment causes a surplus of thiols that allows the full expression of ALA-D catalytic activity.
分析了治疗铅中毒的两种替代方法，即给予锌或硫醇供体S-腺苷-L-甲硫氨酸（SAM）。大鼠在90天内饮用含醋酸铅（60 mg/l）的水；一组还在水中接受硫酸锌（40 mg/l），而另一组同时接受铅和SAM（5 mg/24小时腹腔注射）。单独接受铅的大鼠以及接受铅和其他两种治疗方法之一的大鼠，其红细胞δ-氨基乙酰丙酸脱水酶（ALA-D）活性均显著降低（P < 0.001）。在给予铅的大鼠中观察到的高红细胞尿卟啉原合成酶（URO-S）活性，在用锌或SAM治疗的动物中显著降低（P < 0.001）。肝脏ALA-D活性有下降趋势，而本研究中使用的低水平铅暴露未改变肾脏酶活性。有趣的是，SAM处理的大鼠在两个组织中该酶的活性均显著更高（P < 0.01）。有人认为，SAM治疗会导致硫醇过剩，从而使ALA-D催化活性得以充分表达。
