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논문 기본 정보

자료유형
학술저널
저자정보
Lee, Jin-Young (Department of Biochemistry, College of Medicine, Inje University) Lee, Sang-Hun (Department of Bioscience and Biotechnology, Silla University) Kim, Hee-Jin (Department of Bioscience and Biotechnology, Silla University) Ha, Jong-Myung (Department of Bioscience and Biotechnology, Silla University) Lee, Sang-Hyun (Department of Bioscience and Biotechnology, Silla University) Lee, Jae-Hwa (Department of Bioscience and Biotechnology, Silla University) Ha, Bae-Jin (Department of Bioscience and Biotechnology, Silla University)
저널정보
대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제27권 제3호
발행연도
2004.1
수록면
340 - 345 (6page)

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Our work in this study was made in the microsomal fraction to evaluate the lipid peroxidation by measuring superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and malondialdehyde (MDA) and to elucidate the preventive role of CS in the $CCl_4$-induced oxidative stress. The excessive lipid peroxidation by free radicals derived from $CCl_4$ leads to the condition of oxidative stress which results in the accumulation of MDA. MDA is one of the end-products in the lipid peroxidation process and oxidative stress. MDA, lipid peroxide, produced in this oxidative stress causes various diseases related to aging and hepatotoxicity, etc. Normal cells have a number of enzymatic and nonenzymatic endogenous defense systems to protect themselves from reactive species. The enzymes in the defense systems, for example, are SOD, CAT, and GPx. They quickly eliminate reactive oxygen species (ROS) such as superoxide anion free radicalㆍO$^{[-10]}$ $_2$, hydrogen peroxide $H_2O$$_2$ and hydroxyl free radicalㆍOH. CS inhibited the accumulation of MDA and the deactivation of SOD, CAT and GPx in the dose-dependent and preventive manner. Our study suggests that CS might be a potential scavenger of free radicals in the oxidative stress originated from the lipid peroxidation of the liver cells of $CCl_4$-treated rats.

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