Adam S E, Thorpe E
Br J Exp Pathol. 1970 Aug;51(4):394-403.
A single oral dose of carbon tetrachloride (CCl) of 1 ml./kg. was given to mice maintained at 10° and 20-22°. Cold exposure alone produced fatty changes and depletion of glycogen in the centrilobular zone and modified the liver damage induced by CCl between 5-24 hr after dosing, by increasing lipid accumulation, markedly depleting glycogen, by narrowing the lumina of the sinusoids in the necrotic areas and by producing a large number of ballooned cells in the mid lobular zone. Liver regeneration was rapid in mice kept at room temperature and was complete by 8 days. Depletion of glycogen and fatty infiltration in the centrilobular zone persisted in the liver of mice exposed to cold. The enzymes studied by histochemical techniques were non-specific alkaline phosphatase, adenosine triphosphatase, succinic tetrazolium reductase and glutamate dehydrogenase. Exposure to cold stimulated the sinusoidal alkaline phosphatase activity and depressed the activity of succinic and glutamate dehydrogenases. The early stages of carbon tetrachloride intoxication were accompanied by loss of activities of the latter 2 enzymes. This was more marked on exposure to cold whilst the depressed activity of canalicular adenosine triphosphatase in mice kept at room temperature was absent in those exposed to cold. Necrosis was followed by increased sinusoidal alkaline phosphatase activity and scattered cell reaction in mice kept at both temperatures. There was intense cellular and sinusoidal adenosine triphosphatase activity in mice kept at room temperature and a wider and less intense reaction in these sites in mice exposed to cold. Activities of succinic and glutamate dehydrogenases were diminished in necrotic areas which showed non-specific deposits due to adsorption of enzymes to lipid in mice in both environments. Liver regeneration stimulated the activities of all enzymes although those of succinic and glutamate dehydrogenases remained relatively low in mice exposed to cold environment.
给处于10°以及20 - 22°环境下的小鼠单次口服1 ml/kg的四氯化碳（CCl）。单独的寒冷暴露会导致小叶中心区出现脂肪变性和糖原消耗，并在给药后5 - 24小时内改变由CCl诱导的肝损伤，具体表现为脂质蓄积增加、糖原显著消耗、坏死区域的肝血窦管腔变窄以及小叶中区出现大量气球样细胞。室温饲养的小鼠肝脏再生迅速，8天内完成。暴露于寒冷环境的小鼠肝脏中，小叶中心区的糖原消耗和脂肪浸润持续存在。通过组织化学技术研究的酶有非特异性碱性磷酸酶、三磷酸腺苷酶、琥珀酸四氮唑还原酶和谷氨酸脱氢酶。寒冷暴露会刺激肝血窦碱性磷酸酶活性，同时降低琥珀酸和谷氨酸脱氢酶的活性。四氯化碳中毒的早期阶段伴随着后两种酶活性的丧失。在寒冷环境下这种情况更为明显，而室温饲养的小鼠肝小管三磷酸腺苷酶活性降低，寒冷环境下的小鼠则没有这种情况。在两种温度环境下饲养的小鼠中，坏死之后肝血窦碱性磷酸酶活性均增加且出现散在细胞反应。室温饲养的小鼠细胞和肝血窦三磷酸腺苷酶活性强烈，而寒冷环境下的小鼠在这些部位的反应范围更广但强度更低。在两种环境下的小鼠中，坏死区域的琥珀酸和谷氨酸脱氢酶活性均降低，这些区域因酶吸附于脂质而出现非特异性沉积物。肝脏再生会刺激所有酶的活性，尽管在寒冷环境下饲养的小鼠中，琥珀酸和谷氨酸脱氢酶的活性仍然相对较低。
