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HYDROGEN PEROXIDE INDUCES APOPTOSIS IN HUMAN HEPATOMA CELLS AND ALTERS CELL REDOX STATUS
Author(s) -
Li Ji,
Huang ChungYang,
Zheng RongLiang,
Cui KaiRong,
Li JianFeng
Publication year - 2000
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1006/cbir.1999.0438
Subject(s) - apoptosis , lipid peroxidation , intracellular , hydrogen peroxide , chemistry , dna fragmentation , microbiology and biotechnology , downregulation and upregulation , cycloheximide , programmed cell death , biochemistry , biology , oxidative stress , protein biosynthesis , gene
Direct exposure of human hepatoma cell line SMMC‐7721 to hydrogen peroxide (H 2 O 2 ) can induce apoptosis. Apoptosis induced by H 2 O 2 was inhibited by cycloheximide, actinomycin D, 3‐aminobenzamide, EGTA or Zn 2+ . H 2 O 2 can increase the level of intracellular Ca 2+ , downregulate GSH levels, slightly induce lipid peroxidation, and lead to change in the ratio of reduced ion components to oxidized ion components of cells. Analysis of flow cytometry indicates that H 2 O 2 decreases the level of Bcl‐2. The data indicate that H 2 O 2 ‐induced apoptosis requires new mRNA and protein syntheses; H 2 O 2 can activate Ca 2+ /Mg 2+ ‐dependent endonuclease leading to internucleosomal DNA fragmentation and activation of poly (ADP‐ribose) polymerase interfering with the energy metabolism of the cell. The H 2 O 2 downregulation of GSH may be more important for apoptosis than H 2 O 2 induction of lipid peroxidation, and the H 2 O 2 induced changes in redox status of the cell may be among the original events which lead up to other biochemical changes.