Gallic acid induces vascular smooth muscle cell death via hydroxyl radical production

[1]  G. Takemura,et al.  Induction of apoptosis by gallic acid in lung cancer cells. , 1999, Anti-cancer drugs.

[2]  C. Borner,et al.  Apoptosis without caspases: an inefficient molecular guillotine? , 1999, Cell Death and Differentiation.

[3]  T. Aoyama,et al.  Significance of myocytes with positive DNA in situ nick end-labeling (TUNEL) in hearts with dilated cardiomyopathy: not apoptosis but DNA repair. , 1999, Circulation.

[4]  G. Gibbons,et al.  Determinants of vascular smooth muscle cell apoptosis after balloon angioplasty injury. Influence of redox state and cell phenotype. , 1999, Circulation research.

[5]  大野道也.  "Apoptotic"myocytes in infarct area in rabbit hearts may be oncotic myocytes with DNA fragmentation -Analysis by immunogold electron microscopy combined with in situ nick end-labeling , 1999 .

[6]  H. Takano,et al.  Radical intensity and cytotoxic activity of curcumin and gallic acid. , 1998, Anticancer research.

[7]  M. Inoue,et al.  Formation of reactive oxygen intermediates might be involved in the trypanocidal activity of gallic acid. , 1998, Biological & pharmaceutical bulletin.

[8]  GenzouTakemura,et al.  Role of Apoptosis in the Disappearance of Infiltrated and Proliferated Interstitial Cells After Myocardial Infarction , 1998 .

[9]  M. Inoue,et al.  Reactive oxygen species and intracellular Ca2+, common signals for apoptosis induced by gallic acid. , 1998, Biochemical pharmacology.

[10]  G. Roy,et al.  Derivatives of gallic acid induce apoptosis in tumoral cell lines and inhibit lymphocyte proliferation. , 1998, Archives of biochemistry and biophysics.

[11]  R. Dietz,et al.  Differential effect of hydrogen peroxide and superoxide anion on apoptosis and proliferation of vascular smooth muscle cells. , 1997, Circulation.

[12]  J. Weinberg,et al.  Internucleosomal DNA cleavage triggered by plasma membrane damage during necrotic cell death. Involvement of serine but not cysteine proteases. , 1997, The American journal of pathology.

[13]  H. Sakurai,et al.  Protective effects of hydroxybenzoic acids and their esters on cell damage induced by hydroxyl radicals and hydrogen peroxides. , 1997, Biological & pharmaceutical bulletin.

[14]  S. Patterson,et al.  Selective Activation of Caspases During Apoptotic Induction in HL-60 Cells , 1997, The Journal of Biological Chemistry.

[15]  H. Sakagami,et al.  Possible role of radical intensity and oxidation potential for gallic acid-induced apoptosis. , 1997, Anticancer research.

[16]  H. Sakagami,et al.  Prooxidant action of two antioxidants: ascorbic acid and gallic acid. , 1997, Anticancer research.

[17]  P. Hornsby,et al.  Presence of double-strand breaks with single-base 3' overhangs in cells undergoing apoptosis but not necrosis , 1996, The Journal of cell biology.

[18]  V. Ferrans,et al.  Reactive oxygen species are downstream mediators of p53-dependent apoptosis. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[19]  J. Orenstein,et al.  Fas mediates apoptosis in human monocytes by a reactive oxygen intermediate dependent pathway. , 1996, Journal of immunology.

[20]  M. Inoue,et al.  Selective induction of cell death in cancer cells by gallic acid. , 1995, Biological & pharmaceutical bulletin.

[21]  G. Kroemer,et al.  Sequential reduction of mitochondrial transmembrane potential and generation of reactive oxygen species in early programmed cell death , 1995, The Journal of experimental medicine.

[22]  G. Evan,et al.  Apoptosis of human vascular smooth muscle cells derived from normal vessels and coronary atherosclerotic plaques. , 1995, The Journal of clinical investigation.

[23]  M. Inoue,et al.  Antioxidant, gallic acid, induces apoptosis in HL-60RG cells. , 1994, Biochemical and biophysical research communications.

[24]  T. Onodera,et al.  Quantification of hydroxyl radical and its lack of relevance to myocardial injury during early reperfusion after graded ischemia in rat hearts. , 1992, Circulation research.

[25]  T. Onodera,et al.  Detection of hydroxyl radicals in the post-ischemic reperfused heart using salicylate as a trapping agent. , 1991, Journal of molecular and cellular cardiology.

[26]  M. Ingelman-Sundberg,et al.  Hydroxylation of salicylate as an assay for hydroxyl radicals: a cautionary note. , 1991, Free radical biology & medicine.

[27]  T. Okuda,et al.  Effects of the Interaction of Tannins with Co-existing Substances. VI. : Effects of Tannins and Related Polyphenols on Superoxide Anion Radical, and on 1, 1-Diphenyl-2-picrylhydrazyl Radical , 1989 .

[28]  V. Kagan.  Lipid Peroxidation In Biomembranes , 1988 .

[29]  B. Halliwell,et al.  Aromatic hydroxylation as a potential measure of hydroxyl-radical formation in vivo. Identification of hydroxylated derivatives of salicylate in human body fluids. , 1986, The Biochemical journal.

[30]  R. Floyd,et al.  Sensitive assay of hydroxyl free radical formation utilizing high pressure liquid chromatography with electrochemical detection of phenol and salicylate hydroxylation products. , 1984, Journal of biochemical and biophysical methods.

[31]  C. Winterbourn.  Comparison of superoxide with other reducing agents in the biological production of hydroxyl radicals. , 1979, The Biochemical journal.

[32]  大川 博,et al.  Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction , 1979 .

[33]  K. Puget,et al.  Iron containing superoxide dismutases from luminous bacteria. , 1974, Biochimie.

[34]  Fritz Haber,et al.  The catalytic decomposition of hydrogen peroxide by iron salts , 1934 .