FREE-RADICAL PRODUCTION IN NICOTINE TREATED PANCREATIC TISSUE

The ability of nicotine to induce oxidative stress in the pancreatic t issue of rats was investigated. Homogenized pancreatic tissue of Sprag ue-Dawley rats was incubated with nicotine in a dose of 200 ng/mg prot ein/ml for 15, 30, 45, and 60 min or was incubated for 30 min with nic otine in a dose of 50, 100, 200, 400, and 800 ng/mg protein/ml. Pancre atic tissue was also incubated with 200 ng/mg protein/ml nicotine with or without the scavengers superoxide dismutase (SOD), catalase, SOD catalase, inactivated SOD, inactivated catalase, or albumin. Incubati on with 0.9% NaCl served as control. There was a positive correlation between the duration of nicotine incubation and chemiluminescence (r = 0.6) or lipid peroxidation (r = 0.71) and also between the nicotine d ose and chemiluminescence (r = 0.54) or lipid peroxidation (r = 0.66). Thirty minutes incubation of pancreatic tissue with nicotine in a dos e of 200 ng/mg protein/ml increased chemiluminescence 5 fold and lipid peroxidation 2.5 fold. This response was dampened by SOD or catalase and abolished by SOD + catalase. Inactivated enzymes or albumin had no scavenging effect. These results demonstrate that nicotine causes oxi dative stress to the pancreatic tissue rats.