Gallic acid, an antioxidant, exhibits antiapoptotic potential in normal human lymphocytes: A Bcl-2 independent mechanism

Summary Oxidative stress, produced as a consequence of normal metabolism or induced by extraneous stimuli, has been proved to be a mediator of cell death. The inherent antioxidant defense system and exogenous antioxidants can help the body to combat this oxidative stress-induced cell death. In this...

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Published in:Journal of Nutritional Science and Vitaminology 2003, Vol.49(4), pp.221-227
Main Authors: Sohi, K.K. (Postgraduate Inst. of Medical Education and Research, Chandigarh (India)), Mittal, N, Hundal, M.K, Khanduja, K.L
Format: Article
Language:English
Subjects:
ANTIOXIDANTS
Antioxidants - pharmacology
APOPTOSIS
Apoptosis - drug effects
Biological and medical sciences
Carcinogenesis, carcinogens and anticarcinogens
Cells, Cultured
DNA Fragmentation
Dose-Response Relationship, Drug
Foods and miscellaneous
Free Radical Scavengers - pharmacology
gallic acid
Gallic Acid - pharmacology
Genes, bcl-2 - physiology
Humans
Hydrogen Peroxide - pharmacology
Lipid Peroxidation - drug effects
LYMPHOCYTES
Lymphocytes - cytology
Lymphocytes - drug effects
MANKIND
Medical sciences
Oxidative Stress
reactive oxygen
Reactive Oxygen Species
species (ROS)
TANNINS
Tumors
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Summary:Summary Oxidative stress, produced as a consequence of normal metabolism or induced by extraneous stimuli, has been proved to be a mediator of cell death. The inherent antioxidant defense system and exogenous antioxidants can help the body to combat this oxidative stress-induced cell death. In this study, we explored the antiapoptotic potential of gallic acid, a dietary phenolic having antioxidative and anticarcinogenic properties, in normal human peripheral blood lymphocytes (PBLs). Incubation of PBLs With 100 microM H2O2 for 1.5-2.0 h induced phosphatidy1 serine externalisation, lipid peroxidation and high molecular weight DNA fragmentation. Pretreatment of lymphocytes with gallic acid for 18 h could effectively inhibit lipid peroxidation and apoptosis induced by oxidative stress. Treatment of PBLs with gallic acid failed to induce any change in the expression of Bcl-2, an antiapoptotic protein. It seems that the protection provided by gallic acid was due to its direct action in the scavenging of free radicals as it was found to be a stronger antiradical than trolox, a water- soluble analogue of vitamin E.
ISSN:0301-4800
1881-7742
DOI:10.3177/jnsv.49.221