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[肝细胞癌组织中超氧化物歧化酶活性受损及脂质过氧化物含量降低]

[Impaired superoxide dismutase activity and decreased content of lipid peroxides in hepatocellular carcinoma tissue].

作者信息

Huang C C

机构信息

Changhai Hospital, Second Military Medical College, Shanghai.

出版信息

Zhonghua Wai Ke Za Zhi. 1991 Mar;29(3):195-7, 207.

PMID:1651838
Abstract

Superoxide dismutase (SOD) activity and content of lipid peroxides (LPO) in human hepatocellular carcinoma (HCC) tissue were studied. It was observed that SOD activity and LPO content in HCC tissue were lower than those in normal liver tissue (P less than 0.001 respectively). The contents of copper, zinc and manganese in HCC tissue were also lower than those in normal liver tissue (P less than 0.001, P less than 0.05). Furthermore, LPO content in necrotic HCC tissue was higher than that in non-necrotic HCC tissue (P less than 0.05). The results suggest that deficiency of copper, zinc and manganese in HCC tissue may be a contributing factor that leads to impairment of SOD activity. Decreased SOD activity in liver cancer cells was a negative feedback of the multiplication of cancer cells loss of lipid peroxidation explains the malignancy of HCC, and enhanced lipid peroxidation in liver cancer cells may cause the necrosis of cancer cells.

摘要

研究了人肝细胞癌(HCC)组织中超氧化物歧化酶(SOD)活性和脂质过氧化物(LPO)含量。观察到HCC组织中的SOD活性和LPO含量低于正常肝组织(P分别小于0.001)。HCC组织中铜、锌和锰的含量也低于正常肝组织(P小于0.001,P小于0.05)。此外,坏死HCC组织中的LPO含量高于非坏死HCC组织(P小于0.05)。结果表明,HCC组织中铜、锌和锰的缺乏可能是导致SOD活性受损的一个因素。肝癌细胞中SOD活性降低是癌细胞增殖的负反馈,脂质过氧化的丧失解释了HCC的恶性程度,而肝癌细胞中脂质过氧化增强可能导致癌细胞坏死。

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