A modified smoking machine has been constructed in our lab and used for monitoring the effects of cigarette smoke on albino rats.  Long-term administration of cigarette smoke lowers the activity of antioxidant enzymes and NADPH generating enzyme in liver, lung and kidney. In comparison with control animals the cigarette smoke exposure caused a significant decrease in catalase specific activity compared with control by 23, 18 and 50% in liver, kidney and lung tissues respectively. However, during the recovery period this enzyme activity retained almost normal levels by 97, 99 and 95% respectively. Similarly, smoking caused a significant reduction in glutathione peroxidase (GPx) specific activity compared to control by 16, 13 and 35% in liver, kidney and lung tissues, respectively. After the recovery period glutathione peroxidase (GPx) activities in liver, kidney and lung retained almost normal levels 97, 99 and 96% respectively. Also, smoke exposure caused a significant reduction in G6PD specific activities compared to control by 29, 18 and 38% in liver, kidney and lung tissues respectively. However, during the recovery period, the enzyme activity retained almost normal levels in liver, kidney and lung by 98, 97 and 96 % respectively. Long-term administration of cigarette smoke impairs the enzymatic antioxidant defence system in liver, lung and kidney. These alterations may be one of the responsible factors for cigarette smoke induced inflammation in these organs. Cigarette smoke causes severe histological effects especially in lung alveoli. It induces apoptosis only in lung alveoli. Smoking has more severe inhibitory and damaging effects on lung due to the differential load of metabolites of cigarette smoke in correlation with the alterations in enzymes activities. Present study demonstrated an induction of inflammatory changes in tissues due to the effect of chronic smoking exposure on rats. These changes involved an interstitial inflammation comprised of lymphocytes and plasma cells in lung, portal tract inflammation in liver and mesangial cell proliferation in kidney corpuscles. All these inflammatory changes almost diminished in tissues after the recovery period from smoking effects, indicating reversible effects of smoking on tissues and enzymes of the rat.