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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。
The half inhibitory concentration (IC50, mg / ml) of human amniotic FL / P4501A1 cells treated with different concentrations of heavy metal compounds such as mercuric chloride, chromium trichloride, cadmium sulfate and nickel chloride were 6.0260, 37.5213, 24.5491 and 45.3845. The results showed that the toxicity of different heavy metal compounds to FL / P4501A1 cells varied greatly, and the cytotoxicity of mercury bromide and cadmium sulfate was higher. FL / P4501A1 cells harbor the P4501A1 gene, which is ethoxyresorufinO-deethylase (EROD). The results of enzyme activity assay showed that mercuric bromide and cadmium sulfate could inhibit the spontaneous EROD activity of FL / 1A1 cells. Chromium trichloride, mercuric bromide, nickel chloride and cadmium sulfate could inhibit the production of FL / 1A1 cells induced by norepinephrine EROD activity. P4501A1 enzyme can activate polycyclic aromatic hydrocarbons, mercury bromide and cadmium sulfate interfere with the carcinogenic effects of PAHs by reducing P4501A1 enzyme activity.