Objectives: It is well established that long-term alcohol consumption leads to liver cirrhosis and other related disorders. Sufficient work has been done on biochemical markers of liver damage and antioxidant status of chronic alcoholics in general population. In the current study chronic alcoholics from a community called Koraga are analysed for the same parameters in a view to assess the extent of liver damage as compared to healthy controls and other alcoholics. Methods: Serum and urine samples from Koraga alcoholics (n=28), general alcoholics (n=30) and healthy controls (n=31) were analysed for liver function parameters and antioxidant markers. Liver function parameters were determined by automated analyzer. Markers of antioxidant status were estimated spectrophotometrically. The data was analysed using SPSS version 16.0. Results: There was significant increase in serum AST, serum ALT, serum GST and urine GST in both general and Koraga alcoholics when compared to healthy controls (p<0.0001). Serum ALT, serum GST and urine GST activity was significantly higher in general alcoholics when compared to Koraga alcoholics (p<0.001). Serum and urine total thiol levels were significantly lower in general alcoholics when compared to healthy controls and Koraga alcoholics (p<0.0001). We have observed no difference in total thiols level between healthy controls and Koraga alcoholics, in fact, there was significant increase in urine total thiols level in Koraga alcoholics compared to healthy controls (p<0.001). On Pearson’s correlation serum AST, serum ALT correlated positively with serum and urine GST (p<0.0001) and negatively with serum total thiols (p<0.0001). Serum GST correlated negatively with serum total thiols (p<0.0001). Conclusion: Results of our study possibly indicate that the extent of alcohol induced liver damage in Koraga subjects is comparatively lower than general alcoholics, even though the alcohol consumption is found to be higher in them. There may be some mechanism that is rendering them resistant to alcoholic liver damage which needs to be explored through further studies at molecular level
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