a comparison of toxicity mechanisms of cigarette smoke on isolated mitochondria obtained from rat liver and skin

previous studies demonstrated that cse induces oxidative stress and its consequences on isolated mitochondria obtained from lung, heart and brain which may provide insight into the role of cse in human health and disease. the present study was carried out to further characterize and compare toxic effect of cse extract on isolated mitochondria obtained from either a directly contacting tissue (i.e. skin) and a vital visceral tissue (i.e. liver). we obtained rat liver and skin mitochondria by differential ultracentrifugation and incubated the isolated mitochondria with different concentrations (1, 10 and 100%) of standardized cigarette smoke extract (cse). our results were similar to our previous study which discovered cse toxicity mechanisms on isolated mitochondria obtained from lung, heart and brain with minor changes. cse induced significant rise in ros formation, lipid peroxidation and mitochondrial membrane potential collapse and mitochondrial swelling on isolated mitochondria obtained from both liver and skin. cse induced decrease in atp concentration on isolated mitochondria obtained from both liver and skin did not include cse lowest concentration (1%). our findings showed that cse-induced toxicity in liver and skin is due to disruptive effect on mitochondrial respiratory chain which can leads to cytochrome c release and apoptosis signaling.