摘要
采用生化和细胞生物学方法研究了不同剂量甲基汞对细胞膜系统损伤作用及机理。结果红细胞膜、脑肝肾微粒体膜T-ATP酶、Mg ̄(++)-ATP酶、Na ̄+-K ̄+-ATP酶活性与对照组相比显著降低,并随剂量增加而下降。红细胞膜Na ̄+-K ̄+-ATP酶与脑肾微粒体膜Na ̄+-K ̄+-ATP酶活性呈正相关。红细胞膜、脑微粒体膜SH基含量均显著降低(P<0.01)。肾SH基含量与肾三种ATP酶均呈负相关,脑SH基含量与脑ATP酶呈正相关。红细胞膜、脑肝肾微粒体膜荧光偏振度增高,膜流动性下降,血浆中LDH活性增高而细胞内LDH活性则下降,通透性增强。脑肝的线粒体呼吸酶活性与对照组相比呈下降(P<0.05)。肝脾肾脑细胞 ̄3H-TdR掺入量(cpm值)受影响,DNA合成和UDS修复能力,在高剂量组受抑制,低剂量组则有刺激作用。骨髓细胞SCE频率,随着剂量增加SCE频率也随之增高(p<0.001)。细胞周期进程,从G_0/G_1期进入S期的脾细胞数增多,S期进入G_2/M期则脾细胞数显著减少、DNA合成已受到抑制。
amage to cell membrane system caused by methylmercury(Me-Hg)and its mechanism were studied with biochemical and cell biological methods experimentally. Results showed erythrocyte membrane and activities of T-ATPase, Mg ̄(++)-ATPase and Na ̄+-K ̄+-ATPase of microsome membrane in brain,liver and kidney of the exposed animals decreased more significantly than of controls with a dose-effect pattern. Activities of Mg ̄(++)-ATPase and Na ̄+-K ̄+-ATPase of erythrocyte membrane cor-related positively with those of microsome membrane in brain and kidney.Sulfhydryl content of ery-throcyte membrane and brain microsome membrane decreased singnificantly in the exposed animals(P<0.01). Sulfhydryl content correlated inversely with the activities of above three kinds of AT-Pase in kidney,but so did in brain positively. Fluorescent polarization of membranes of erythrocytes and rnicrosome in brain,liver and kidney increased , membrane fluidity decreased,LDH activities in-creased in plasma and decreased in cells and cell permeability increased in the exposed animals,Activ-ities of respiratory enzymes of mitochondrion in exposed animals were lower than those in controls(P<0.05). ̄3H-TdR incorporation was inhibited in spleen liver and brain in exposed animals. Abili-ties of DNA synthesis and UDS repair were inhibited with high-dose of Me-Hg,and stimulated with low-Jose,SCE frequency in bone marrow cells increased with dose of Me-Hg(P<0. 001). Propor-tion of splenocyte from G_0/G_1 to S phases increased and those from S to G_2/M phases lowered,and it suggested DNA synthesis had been inhibited.
出处
《中华预防医学杂志》
CAS
CSCD
北大核心
1995年第1期9-12,共4页
Chinese Journal of Preventive Medicine
基金
国家自然科学基金