DL-半胱氨酸对CCL_4肝中毒小白鼠LDH和SOD活性的影响

小白鼠口服花生油溶四氯化碳（ＣＣＬ４）１３．９５ｇ／ｋｇ（公斤体重）至３６ｈ诱发肝中毒和口服ＣＣＬ４前１０～２０ｍｉｎ于腹腔注入ＤＬ－半胱氨酸１００ｍｇ／ｋｇ．用凝胶圆盘电泳法显示肝中毒和中毒前腹腔注入ＤＬ－半胱氨酸小白鼠的血清乳酸脱氢酶（ＬＤＨ）同工酶和肝匀浆超氧化物歧化酶（ＳＯＤ）的谱带变化．结果表明，中毒鼠血清呈现以ＬＤＨ５带占优势的肝损伤ＬＤＨ同工酶谱；中毒前腹腔注入ＤＬ－半胱氨酸的小白鼠，血清ＬＤＨ同工酶谱ＬＤＨ５显著缩减，其它同工酶带几乎未显现．ＣＣＬ４中毒的肝匀浆ＳＯＤ谱带与正常鼠比较明显变宽或呈现两条同工酶带；中毒前腹注ＤＬ－半胱氨酸的小鼠ＳＯＤ带与正常鼠略同，但有的仍呈现两条微弱的同工酶带．谱带的这些变化表明，ＣＣＬ４诱发肝细胞损伤可能与自由基生成和脂质过氧化有关，ＤＬ－半胱氨酸则可能具有阻断肝损伤的作用；ＣＣＬ４肝中毒在诱发自由基生成的同时又刺激了肝细胞ＳＯＤ活性增强

THE EFFECTS OF THE DL-CYSTEINE ON HEPATIC SUPEROXIDE DISMUTASE AND SERUM LACTATE DEHYDROGENASE ACTIVITY OF THE MICE WITH HEPATOTOXICITY BY CARBONTOTARCHLORIDE

The mice were induced hepatotoxicity by orally poured soluble CCL 4 of peanut oil 13.95g/kg (per kilogram of body weight) till 36 hours, and prior to the hepatotoxicity about 20-30 minutes and were intraperitonelly injected DL-cystine 100mg/kg. We used PAGE to analyse isoenzymes profile of serum LDH and hepatic SOD of above mice. The reaults demonstrated that the serum LDH isoenzymes were hepatotoic injury LDH profile, that is the LDH 5 was preponderant, in the hepatotoxic mice, while the LDH 5 was obviously red uced and other bends almost did not appeared in the mice injected DL-cystine prior to hepatotoxicity; and the hepatotoxic mice were shown obviously wider than the normal mice or were shown two bands, while the mice injected DL-cysteine prior to hepatotoxicity were almost the same as the normal mice though some of the them still were shown two light band. these changes of isoenzme profile illustrated that CCL 4 induced the formation of free radical and lipid peroxide with hepatic injury as well as stimulated SOD activity in hepatic cells. The DL-cysteine could block the formation of free radical and lipid peroxide.