Once absorbed through lung tissues, smog-soluble substances are readily distributable throughout organ system reaching approximately all cells perturbing the subcellular events at mitochondrial level. The present study aimed to detect the deleterious impact of smog-containing materials on mitochondrial and thereby serum pyruvate/lactate levels coincidentally with liver proper functionality. To do so, chronic smokers were recruited and sub-classified into groups based on chronicity of smoking; control (never smoked), G1=smokers for up to 5 years, G2=smokers for up to 10 years, and  G3=smokers for up to 15 years. Serum samples were collected and stored for later on analysis. Results have confirmed that serum pyruvate/lactate and liver enzymes modulated reciprocally with smoking compared to control. The results also confirmed that liver enzymes were strongly modulated, GOT elevated while GPT reduced in a way reciprocal to chronicity, while ALP elevated in first few years of smoking in G1 group compared to other groups or control group. Serum albumin was significantly elevated in studied groups compared to control group with no changes appeared in total plasma protein and the bilirubin levels were higher in G2 group compared to G1 or G3 or control groups. Serum lactate and to certain extent serum pyruvate were also significantly perturbed showing higher levels in smokers compared to control or junior smokers. In conclusion, mitochondrial subcellular machinery are strongly affected following smoking indicated by serum pyruvate/lactate measurement and this in turn strongly affect liver functionality as an important organ involved in pyruvate-lactate demarcation and pertaining to the liver functionality indicated by bilirubin and total plasma protein or albumin measurements.

Keywords: smoking; liver enzymes; lactate; pyruvate; mitochondria