[Effect of tobacco smoke on lipids peroxidation and liver function in streptozotocin diabetic rats--preliminary study].

Diabetes is considered a group of diseases with chronic hyperglycemia caused by various organ disorders, failure or damage as a common feature. Hyperglycemia exerts toxic effect on endothelium, promotes oxidative stress, inhibits bioavailability of nitrogen monoxide (NO) and leads to formation of advanced glycation end products. Moreover, hyperglycemia induces production of reactive oxygen specimens (ROS) through several distinct mechanisms, such as: glucose autoxydation activation of polyol (sorbitol-aldose reductase) pathway, non-enzymatic glycation and neutrophil granulocyte's stimulation. These changes lead to uncontrolled oxidation and peroxidation of lipids, nucleic acids, certain enzymes and most of all--oxidative protein damage (OPD) in many tissues. The aim of this study was to evaluate influence of exposure to tobacco smoke on lipid peroxidation and liver function in experimentally induced diabetes. The research showed that the protein level in blood serum did not change neither in case of induced diabetes nor after tobacco smoke exposure. However a statistically significant increase of lipid peroxidation was observed in rats with pharmacologically induced diabetes. In animals exposed to tobacco smoke only lipid peroxidation increasing trend was demonstrated, while in animals with induced diabetes and exposed to tobacco smoke a statistically significant decrease of lipid peroxidation was noticed. In the adopted experimental model basically no alterations of hepatic aminotranspherases were observed, with exception of AIAT in the group of diabetic animals compared to rats in the control group. Results of the study do not explicitly explain the influence of tobacco smoking in experimentally induced diabetes on lipid peroxidation and liver functions.