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    Indian J Physiol Pharmacol. 2008 Jan-Mar;52(1):11-8.

    Nitric oxide-mediated pathogenesis during nicotine and alcohol consumption.

    Cooper RG, Magwere T.

    Source

    Division of Physiology, Faculty of Health, Birmingham City University, 701 Baker Building, Franchise Street, Perry Barr, Birmingham B42 2SU, U.K. rgcooperuk@yahoo.com

    Abstract

    Nitric oxide (NO) is formed by different cell types in response to a variety of physiological and patho-physiological stimuli. The intake of nicotine and/or alcohol has patho-physiological effects on organ function, and the progression of alcohol-/tobacco-related diseases seem to be directly influenced by NO-mediated mechanisms. Nicotine has an adverse influence on blood vessel functionality, repair and maintenance. Chronic nicotine exposure augments atherosclerosis by enhancing the production of proinflammatory cytokines by macrophages which then activate atherogenic NF-kB target genes in aortic lesions. Alcohol produces NO which speeds up the apoptosis of neutrophils. Alcohol sensitizes the liver to endotoxemic shock. Nitrosative stress and increased basal levels of NO contribute to tumour growth. The progression of disease seems to be directed via a definite NO-mediated mechanism. This review gives an insight into how intake of tobacco and alcohol may affect quality of life.

    PMID:
    18831348
    [PubMed - indexed for MEDLINE]

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