中文摘要：

研究壳寡糖（COS）、氨基葡萄糖（GlcNH2）和N-乙酰氨基葡萄糖（GlcNAc）对CCL4诱导的雄性昆明种小鼠肝毒性的保护作用，并探讨其可能机制，小鼠腹腔注射CCL4（20mg／kg体重）24h后，血清天门冬氨酸转氨酶（AST）和丙氨酸转氨酶（ALT）活性明显提高，引起肝脏脂质过氧化反应，巯基含量降低，总抗氧化能力（T-AOC）减弱，诱发基因毒性,提前连续12天分别灌胃给予COS，GlcNH2和GcNAc（1．5g/kg体重）能够显著诱导金属硫蛋白（MT）的表达，体内的抗氧化防御系统随之增强以抵抗CCL4诱导的氧化损伤,血清AST和ALT活性明显降低，肝脏丙二醛（MDA）生成被抑制，巯基含量，T-AOC明显恢复,但是，从DNA电泳结果反应出的基因毒性并未减轻,实验结果证明。提前给予COS，GlcNH2和GlcNAc对CCL4诱导的小鼠肝损伤能够起到有效的保护作用，其中，GlcNH2的作用效果最显著。

英文摘要：

The protective effects of chitosan oligosaccharide （COS）, D-glucosamine （GlcNH2） and N-acetyl-D-glucosamine （G1-cNAc） on carbon tetrachloride （CCL4） induced hepatotoxicity in male ICR mice were investigated and the possible mechanisms involved were discussed . CCL4 （20 mg/kg body weight） administration induces marked increase in serum AST and ALT activities, primes liver lipid peroxidation, depletes sulfhydryl content, impairs total antioxidant capabilities （T-AOC） and induces genotoxic- ity 24h after administration. Pretreatment with COS, GlcNH2, and GlcNAc （1.5 g/kg body weight） for 12 consecutive days prior to CCL4 challenge significantly induces metallothionein （MT） expression. Thus, the antioxidant defensive system in the body is strengthened to counteract the oxidative damage induced by the CCL4 administration. Serum AST and ALT activities are effectively decreased. Hepatic malondialdehyde （MDA） formation is inhibited, and sulfhydryl contents and T-AOC are markedly restored. Genotoxicity as reflected by DNA fragmentation, however, it is not mitigated by pretreatment with COS, GlcNH2, and GlcNAc. The results suggest that pretreatment with COS, GlcNH2, and GlcNAc can efficiently protect mice against CCL4-induced toxicity, of which GlcNH2 is the most effective.