Résumé
Background: Cigarette smoking, a major cardiovascular risk factor, has been shown to be associated with impaired endothelium- dependent vasodilatation [EDV]. Nitric Oxide [NO] being a primary vasodilator produced by endothelial cells, its production is probably affected by cigarette smoking. Cigarette smoke contains superoxide anions and a great number of other reactive oxygen species [ROS], the accumulation of which brings about oxidative damage of endothelial cells. A free radical catalyzed isomers of arachidonic acid [8-epi- PGF2infinity] is a potent vasoconstrictor and serves as a marker of oxidative stress
Objective: To evaluate the level of serum [NO] and urinary 8-epi- PGF2infinity in mild, moderate, and heavy smokers and to correlate their levels with urinary cotinine which is considered a sensitive markers of exposure to nicotine of tobacco smoke
Subjects: 20 heavy smokers, 20 moderate smokers, 20 mild smokers, and 20 controls were the material of the present study
Results: The present study revealed significant increase in urinary 8-epi- PGF2infinity in smokers compared to control subjects. Also significant increase was found in urinary 8-epi- PGF2infinity in heavy compared with moderate smokers. However, there was a significant decrease in serum [NO] in the same two groups as compared to controls. Positive correlation for urinary 8-epi- PGF2infinity and negative correlation for serum [NO] as compared to urinary cotinine were detected. It may be concluded that concentration of 8-epi- PGF2infinity and cotinine in the urine as well as NO in the sera of smokers might give more accurate information about ROS which play an important role in the pathogenesis of many diseases affecting the physiological functions of body systems
Résumé
Background: Kidney irradiation clearly leads to a progressive reduction in function associated with concomitant glomerulosclerosis and/or tubulointerstitial fibrosis. Administration of Angiotensin-converting enzyme [ACE] inhibitor markedly abrogates the severity of radiation nephropathy and can prevent the functional changes that occur after irradiation
Objective: The present study was designed to test the efficacy of converting enzyme inhibition [enalapril] and its possible mechanistic basis in preventing functional changes in irradiated rats
Method: Prior to irradiation, rats were randomized to groups receiving enalapril or no treatment, in addition to a control group of non-irradiated, non-treated rats. Enalapril was administered intraperitoneally [0.1 mg/kg body weight/day], 4 weeks before and 12 weeks after irradiation. Both groups were exposed to a single dose of 7Gy gamma radiation
Results: Irradiation induced significant elevations in the levels of blood urea nitrogen, serum creatinine, and serum activities of lactate dehydrogenase [LDH]; creatine kinase [CK]; alanine amino transferase [ALT]; and aspartate amino transferase [AST] compare to control values, indicative of renal, cardiac, and hepatic injury. Also there was an increase in the serum levels of triglycerides, total cholesterol, and LDL-cholesterol. On the contrary, HDL-cholesterol level was decreases. The heart, kidney and liver antioxidant enzymes including total glutathione peroxidase. [total-GPX], glutathione reductase [OR], and superoxide dismutase [SOD] activities were inhibited, while malondialdehyde [MDA] level in these organs was elevated, indicative of increased lipid peroxidation. These data confirm the role of oxidative stress in radiation injury. It can be concluded that enalapril treatment of rats prior to irradiation was able to diminish the functional changes that occur after irradiation as evidenced by a beneficial decrease in all parameters determined in the sera of these rats, with an increase in the level of HDL-cholesterol and an amelioration of inhibition of antioxidant enzymes activities in the organs of these rats