Shon Yun-Hee, Park In-Kook, Moon Il-Soo, Chang Hyeun Wook, Park In-Kyung, Nam Kyung-Soo
Department of Pharmacology, College of Medicine and Intractable Disease Research Center, Dongguk University, Kyongju, Korea.
Biol Pharm Bull. 2002 Sep;25(9):1161-4. doi: 10.1248/bpb.25.1161.
The abilities of two types of chitosan oligosaccharides, chitosan oligosaccharide I (1-kDa<MW<3-kDa) and chitosan oligosaccharide II (3-kDa<MW<5-kDa), to prevent 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced oxidative stress were examined in ICR mice. Chitosan oligosaccharide I had no effect on TCDD-induced alterations in lipid peroxidation and glutathione S-transferase activity or liver weight change. However, mice treated with chitosan oligosaccharide II were protected from TCDD-induced lipid peroxidation, inhibition of glutathione peroxidase and glutathione S-transferase activities, and losses in body and liver weights. These results suggest that chitosan oligosaccharide might be a potential agent for combating TCDD-induced pathogenesis.
在ICR小鼠中检测了两种壳寡糖，即壳寡糖I（1 kDa＜分子量＜3 kDa）和壳寡糖II（3 kDa＜分子量＜5 kDa）预防2,3,7,8-四氯二苯并对二恶英（TCDD）诱导的氧化应激的能力。壳寡糖I对TCDD诱导的脂质过氧化、谷胱甘肽S-转移酶活性改变或肝脏重量变化没有影响。然而，用壳寡糖II处理的小鼠可免受TCDD诱导的脂质过氧化、谷胱甘肽过氧化物酶和谷胱甘肽S-转移酶活性抑制以及体重和肝脏重量损失的影响。这些结果表明，壳寡糖可能是对抗TCDD诱导的发病机制的潜在药物。
