INTRODUCTIONAdenosine deaminase also known as adenosine aminohydrolase involved in purine metabolism. Its primary function is development and maintenance of immune system. 1 It has two isoenzymes ADA1 and ADA2 which is encoded by different genes.2 In humans ADA1 is called as single-chain Zn binding protein and it is found in lymphocytes and macrophages.Physiological role of ADA2 was not clearly known and it might be produced by monocytes in negligible quantities.3,4 The activity of ADA2 was drastically increased in patient's plasma of liver diseases like chronic hepatitis and cirrhosis and also in diseases like AIDS, Tuberculosis, Diabetes mellitus, adult T-cell leukemia and acute lymphoblastic leukemia. 5-8Cigarette smoke has various toxic substances and it promotes oxidative damage and also initiates platelet aggregation. 9Number of cigarette smoked per day is directly related to cardiovascular morbidity and mortality. Nicotine a major component of cigarette smoke leads to the production of free radicals and increases the oxidative stress. It stimulates lipolysis thus increasing the flux of free fatty acids to liver and re-esterification of free fatty acid in the liver leads to the enhanced VLDL secretion, thus explaining the atherogenic effect of smoking. 10ABSTRACT Background: Adenosine deaminase also known as adenosine aminohydrolase involved in purine metabolism. Its primary function is development and maintenance of immune system. The main objective of the study was to estimate adenosine deaminase (ADA) enzyme and find its correlation with lipoprotein(a) and insulin resistance among smokers and healthy non-smokers. Methods: Fifty smokers and fifty healthy non-smokers were selected based on WHO definition. ADA, lipid profile and glucose was estimated on a fully automated analyser by IFCC approved methods and lipoprotein(a) was done by latex enhanced immune-turbidimetric assay method respectively. Results: After appropriate screening ADA activity and insulin was significantly elevated among smokers when compared with healthy non-smokers. A positive correlation was found between pack size of cigarette and ADA activity and also with Lp(a) respectively. In addition, there was no correlation between serum lipid profile and ADA activity. Conclusions: Adenosine deaminase activity was increased in patients in response to nicotine which is the key component of cigarette smoke. These findings indicate that nicotine and carbon monoxide can alter lipoprotein synthesis and also modify LDL to oxidized form which can lead to ischemic heart disease.
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