氯化甲基汞抑制脑α_1-肾上腺素受体结合及恢复效应的体内及体外实验研究  

Experimental Study on Regeneration of Brain 1adrenergic Receptors in Vitro and in Vivo After Inhibition With Methylmercury Chloride in Rats

作　　者：詹立[1,2,3] 吴德生[1,2,3] 孙俊 

机构地区：[1]成都市卫生防疫站 [2]华西医科大学公共卫生学院 [3]华西医科大学口腔医学院

出　　处：《环境与健康杂志》1999年第3期136-138,共3页Journal of Environment and Health

基　　金：国家自然科学基金

摘　　要：为研究甲基汞对大鼠脑α１－肾上腺素受体的影响以及拮抗剂对甲基汞引起该受体特异结合抑制的恢复效果，本文应用放射性配体结合技术进行了体内外试验研究。结果显示：氯化甲基汞能明显抑制大鼠脑α１－肾上腺素受体与［３Ｈ］ｐｒａｚｏｓｉｎ的特异结合，ＩＣ５０为２．８９μｍｏｌ／Ｌ。二巯基丙磺酸钠、二巯基丁二酸钠，半胱氨酸能使被氯化甲基汞抑制的［３Ｈ］ｐｒｏｚｏｓｉｎ结合得到不同程度的恢复。表明甲基汞与巯基基团的结合是脑α１－肾上腺素受体受其抑制的分子机制。而含巯基的化合物能把与受体上巯基基团结合的甲基汞竞争下来，从而恢复α１－肾上腺素受体与配体的结合能力。The effects of methylmercury on 1adrenergic receptors and regeneration of functionally active 1adrenergic receptors by antogonists were studied with radioligand binding assay in vitro and in vivo.The results showed that methylmercury chloride significantly inhibited the binding of prazosin to 1adrenergic receptors of rat brain with an IC50value of 289 mol/L.In vivo methylmercury significantly reduced the binding rate of 1adrenergic receptors to prazosin.Regeneration of functionally active rat brain 1adrenergic receptors after inhibition with methylmercury was achieved by sodinm 2,3dimercapto1propanesulfon ate(DMPS),sodium dimercaptosuccinate(DMSA)and Cysteine in different degrees.Combination of these sulfhydryl groups with mythylmercurg was the molecular mechanism of inhibition of Author brain 1adrenergic receptors by methylmercury.Our results provided evidence that thiols chelated out mercuric cations competitivelg that tightly bounded to sulfhydryl groups in 1adrenergic receptor binding sites and regenerated prazosin binding activity.

关 键 词：甲基汞 脑肾上腺素受体 拮抗剂 恢复效应 

分 类 号：R338.2[医药卫生—人体生理学]