1Department of Biochemistry, Government Medical College, Nagpur, India
2Department of Biochemistry, Chalmeda Anandarao Institute of Medical Sciences,karimnagar, India
3Department of Microbiology, Prathima Institute of Medical Sciences, Karimnagar, India
American Journal of Biomedical Research.
2014,
Vol. 2 No. 1, 7-10
DOI: 10.12691/ajbr-2-1-2
Copyright © 2014 Science and Education PublishingCite this paper: Neelesh Deshpande, Sabitha Kandi, Manohar Muddeshwar, K V Ramana. Effect of Alcohol Consumption and Oxidative Stress and Its Role in DNA Damage.
American Journal of Biomedical Research. 2014; 2(1):7-10. doi: 10.12691/ajbr-2-1-2.
Correspondence to: K V Ramana, Department of Microbiology, Prathima Institute of Medical Sciences, Karimnagar, India. Email:
ramana_20021@rediffmail.comAbstract
Oxidative stress has been increasingly implicated in different stages of liver cirrhosis and has been found responsible for DNA damage. Alcohol consumption and oxidative stress have been linked with DNA damage and progression of disease, leading to the hypothesis that chronic alcoholism causes DNA damage. The study was aimed at evaluating the relation between alcohol consumption and relative oxidative damage in different stages of liver cirrhosis. The study included two groups based on severity of cirrhosis of liver; categorized as compensated and decompensated liver cirrhotic patients based on child Pugh criteria. All decompensated cirrhotic patients in the study group had significantly higher MDA levels (P < 0.001) associated with DNA Damage (P > 0.01) than those with compensated cirrhotic patients and control group who were not suffering from liver cirrhosis. These results highlighted a significant higher degree of DNA damage in decompensated cirrhotic patients associated with oxidative stress as shown from greater average DNA migration in decompensated cirrhotic patients than in the compensated cirrhotic patients with low level of oxidative stress. Thus these results suggest that increase in MDA levels may be associated with pathogenesis and progression of liver cirrhosis.
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