Tissue-specific mitochondrial toxicity of cigarette smoke concentrate: consequence to oxidative phosphorylation.

Cigarette smoke exposure is a well-known risk factor for developing numerous chronic health conditions, including pulmonary disease and cardiometabolic disorders. However, the cellular mechanisms mediating the toxicity of cigarette smoke in extrapulmonary tissues are still poorly understood. Therefore, the purpose of this study was to characterize the acute dose-dependent toxicity of cigarette smoke on mitochondrial metabolism by determining the susceptibility and sensitivity of mitochondrial respiration from murine skeletal (gastrocnemius and soleus) and cardiac muscles, as well as the aorta to cigarette smoke concentrate (CSC).

Effects of cigarette smoke on in situ mitochondrial substrate oxidation of slow- and fast-twitch skeletal muscles.

Epidemiological and clinical evidence suggests that cigarette smoke exposure alters glucose and fatty acid metabolism, leading to greater susceptibility to metabolic disorders. However, the effects of cigarette smoke exposure on mitochondrial substrate oxidation in the skeletal muscle are still poorly understood. Accordingly, this study aimed to examine the acute effects of cigarette smoke on mitochondrial respiratory capacity, sensitivity, and concurrent utilization of palmitoylcarnitine (PC), a long-chain fatty acid, and pyruvate, a product of glycolysis, in permeabilized gastrocnemius and soleus muscle fibers exposed to an acute (1 h) dose (4 %) of cigarette smoke concentrate.