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SMOKING JEOPARDIZED MITOCHONDRIAL FUNCTION VITIATING LIPID PROFILE.

Smoking has increasingly reported as deleterious behavior associated with serious problems, ranging from mood changes to cancer. The basic and common landmark associated with these disorders is derangement of mitochondrial quasi-equilibrium. This study aimed to identify the role of smoking in modulation of lipid profile in the view of mitochondrial dysfunctionality. To do so, smokers were recruited, serum lipid profile, serum pyruvate, and serum lactate were determined to confirm the link between serum lipid profile and smoking induced lactate to pyruvate ratio. The recruited subjects were sub-classified into three groups; G1 includes smokers for up to 5 years, G2 includes smokers for 5-10 years, and G3 includes smokers for more than 10 years alongside the control non-smokers group. The results confirmed that lactate to pyruvate has significantly (p<0.05) increased in smoker groups (G1, G2, G3) compared to control group and smoking has significantly increased LDL and TG with no effects on cholesterol or HDL levels in G1 group alongside minimal or no changes associated with G2 or G3 compared to control group. In conclusion, smoking impacted lipid profile in smokers during initial stages of smoking, however, the effect started to be tolerated with continuous smoking after 5 years with obscure mechanism. Nonetheless, pyruvate/lactate modulation due to restoration of mitochondrial quasi-equilibrium might be the cause. Cigarette cessation campaign should be advocated to ensure smoking-free society.

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