Introduction: The rapid and recent rise in the pandemic of cardiovascular disease implies that the environment plays a significant role. Numerous biological systems, such as the cardiovascular, blood-forming organs, liver, and kidneys, can be affected by gasoline and smoking. Because filling station employees, repair service workers, gasoline truck drivers, and refinery workers are all at a greater risk of being exposed to gasoline fumes. Even though gasoline and smoking have been investigated for so many years, few studies have looked into the effects of gasoline exposure combined with smoking on a variety of physiological mechanisms. As a result, we propose that combining gasoline exposure with smoking is a risk factor for cardiovascular diseases and impaired hepatic function. Methods: The study included 95 male adult volunteers who worked with gasoline and were exposed to different fuel derivatives as study group and age and sex-matched seemingly healthy non-exposed people as the controls. Questionnaire interviews were used to collect socio-demographic data and a standard technique was used to collect the blood samples. The levels of cholesterol, HDL4, LDL-C, triglyceride, and VLDL were measured, as well as for liver enzymes ALP, AST, ALT, indirect bilirubin, direct bilirubin, and total bilirubin were measured. Results: Our data suggest that smoking with gasoline exposure causes an increase in total and bad cholesterol levels, as well as a significant shift concerning the control group in lipid profile and liver enzymes. the exposed group had higher levels of ALP, and AST and significantly increased. In the nonsmoker exposed group D-bilirubin decreased in comparison to the control and exposed smoker group. Conclusion: This research concluded that the liver enzymes (ALP, AST, ALT) were higher among workers who smoke and are exposed to gasoline than in control subjects, similarly, the bad cholesterol also increase. Therefore, people who smoke and are handled with gasoline are at a higher risk of having heart and hepatic diseases.

ABSTRACT:Nitric oxide (NO) is produced from virtually all cell types composing the cardiovascular tissue and regulates vascular function through fine regulation of excitation-contraction coupling. Endogenous metabolites play a major role in coronary autoregulation. Therefore, the aim of the present study is to investigate the contribution of Glyceryl trinitrate (GTN) and Adenosine 5-triphosphate (ATP) mediated relaxation in rat aortic smooth muscle in intact and endothelium denuded endothelium rings precontracted with Phenylephrine (PE). The thoracic aorta was isolated, cut into rings, and mounted in organ-bath chambers and isometric tension was recorded using PowerLab Data Acquisition System (Model ML 870). The results showed that GTN as NO donor produced dose-dependent relaxation in intact aortic rings precontracted with PE (1 µM) that disinhibited in the presence of Glibenclamide (GLIB), while GLIB attenuate the response induced by ATP in intact aortic rings. L-nitroarginine methylester (L-NAME) an antagonist for nitric oxide synthases (NOS), not abolish the response induced by GTN (Emax 55.28% ± 0.18). Caffeine, ATP receptors antagonist, were partially inhibit the relaxation induced by ATP (vasodilation rate decreased by about 20.57 %). In endothelium denuded aortic rings, vasorelaxation induced by ATP were significantly attenuated , while GTN significantly increased relaxation by removing endothelium. These results suggested that (1) ATP-dependent potassium channel did not involve in GTN inducing vasorelaxation while K ATP and A 2B receptors have a role in ATP mediated vasorelation (2) ATP partially dependent on endothelium in contrast to NO donors that independent to endothelium.