摘要
利用不同浓度的重金属化合物溴化汞、三氯化铬、硫酸镉、氯化镍处理人羊膜FL/P4501A1细胞,其半数抑制浓度(IC50,mg/ml)分别为6.0260,37.5213,24.5491和45.3845。结果表明:不同的重金属化合物对FL/P4501A1细胞的毒性相差很大,溴化汞和硫酸镉的细胞毒性较大。FL/P4501A1细胞带有P4501A1基因,该基因产物为乙氧基异吩恶唑O—去乙基酶(ethoxyresorufinO-deethylase,EROD)。酶活性测定结果表明溴化汞、硫酸镉能抑制FL/1A1细胞自发产生的EROD活性;三氯化铬、溴化汞、氯化镍、硫酸镉能抑制去甲肾上腺素诱导FL/1A1细胞产生的EROD活性。P4501A1酶能激活多环芳烃,溴化汞和硫酸镉可通过降低P4501A1酶活性干扰多环芳烃的致癌作用。
Human amnion FL/P4501A1 cells were treated with various heavy metal compounds(HgBr 2,CrCl 3,CdSO 4,NiCl 2);the 50% inhibitory concentrations(IC 50 ,mg/ml) of HgBr 2,CrCl 3,CdSO 4,NiCl 2 were 6.0260,37.5213,24.5491,45.3845 respectively.The results showed that the cell toxicities of these heavy metal compounds on FL/P450 1A1 cell are different.The cell toxicities of HgBr 2 and CdSO 4 are more serious.FL/P450 1A1 cell carries P450 1A1 gene,the gene can produce ethoxyresorufin O-deethylase(EROD).The results of this enzyme activity assay show HgBr 2 and CdSO 4 can inhibit uninduced FL/P450 1A1 cell EROD activity;CrCl 3,HgBr 2,NiCl 2 and CdSO 4 can inhibit FL/P450 1A1 cell EROD activity induced by norepinephrine.P4501A1 enzyme can activate polycyclic aromatic hydrocarbons(PAHs),HgBr 2 and CdSO 4 may decrease the enzyme activity and interfere with the carcinogenesis of PAHs.
出处
《癌变.畸变.突变》
CAS
CSCD
1997年第5期305-310,共6页
Carcinogenesis,Teratogenesis & Mutagenesis
基金
国家自然科学基金