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目的探讨甲基硝基亚硝基胍（ＭＮＮＧ）对胃粘膜上皮细胞的损伤作用．方法对ＭＮＮＧ在诱发体外培养的人胎胃粘膜上皮细胞的非程序ＤＮＡ合成、脂质过氧化和ｒａｓＰ２１蛋白进行观察．结果ＭＮＮＧ处理组各时相胃粘膜上皮细胞的增殖速率，非程序ＤＮＡ合成水平（１８３８ｃｐｍ±２０５ｃｐｍｖｓ７０５ｃｐｍ±１２５ｃｐｍ，Ｐ＜００１），质脂过氧化物（第２０天，７．４２ｎｍｏｌ／ｍｇ±０．６８ｎｍｄ／ｍｇｖｓ３．６２ｎｍｏｌ／ｍｇ±０．５４ｎｍｏｌ／ｍｇ蛋白Ｐ＜０．０１）和ｒａｓＰ２１蛋白含量（第４０天，１２１Ａ±０１２Ａｖｓ０５１Ａ±００７Ａ，Ｐ＜００１）．结论ＭＮＮＧ可诱发胃粘膜上皮细胞恶性转化，其作用机制可能是通过损伤细胞ＤＮＡ，诱发质脂过氧化或导致ｒａｓＰ２１异常表达所致．
5. Objective To investigate the effect of MNNG on gastric epithelial cells. Methods The non-program DNA synthesis, lipid peroxidation and rasP21 protein of human fetal gastric epithelial cells induced by MNNG were observed. Results The proliferation rate of gastric mucosal epithelial cells at various phases of the MNNG-treated group was unprogrammed DNA synthesis (1838 cpm±205 cpm, 705 cpm±125 cpm, P<001), lipid peroxide (20th) Days, 7.42 nmol/mg±0.68 nmd/mgvs 3.62 nmol/mg±0.54 nmol/mg protein P<0.01) and rasP21 protein content (day 40, 121A±012Avs051A±0 07A, P<001). Conclusion MNNG can induce the malignant transformation of gastric epithelial cells, which may be caused by the damage of cellular DNA, the induction of lipid peroxidation or the abnormal expression of rasP21.