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为探讨烟碱、高温及其联合作用对肝损伤的机制和敏感的检测指标，观察了烟碱（６．５ｍｇｋｇ－１ｄ－１灌胃，连续８天）或（和）高温（４２℃，６０分钟）处理大鼠肝线粒体、微粒体丙二醛（ＭＤＡ）、超氧化物歧化酶（ＳＯＤ）、谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）和血清谷胱甘肽Ｓ转移酶（ＧＳＴ）、铜蓝蛋白（Ｃｐ）、丙氨酸转氨酶（ＡＬＴ）及细胞超微结构变化。结果发现：烟碱、高温均可导致肝微粒体脂质过氧化、微粒体ＳＯＤ的活力被抑制，两者具有协同作用；提高胞浆Ｃｐ活力，联合作用呈抑制效应。烟碱可抑制线粒体ＧＳＨ－Ｐｘ和胞浆ＧＳＴ活力。血清ＧＳＴ升高可能是热应激肝细胞受损的敏感指标。
In order to explore the mechanism of liver injury induced by nicotine, high temperature and their combined effects and sensitive detection indexes, the effects of nicotine (6.5 mg kg-1d-1 for 8 days) or (and) high temperature (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and serum glutathione S-transferase (GST ), Ceruloplasmin (Cp), alanine aminotransferase (ALT) and cell ultrastructure changes. The results showed that both nicotine and high temperature could lead to the lipid peroxidation of liver microsome, the activity of microsome SOD was inhibited, and both had synergistic effects. The cytosolic Cp activity was increased and the combined effect was inhibited. Nicotine can inhibit mitochondrial GSH-Px and cytosolic GST activity. Elevated serum GST may be a sensitive indicator of heat-induced hepatocellular damage.