Cold exposure lowers energy expenditure at the cellular level.

Mitochondrial function is intimately involved in various metabolic processes and is therefore essential to maintain cell viability. Of particular importance is the fact that mitochondrial membrane potential (ΔΨm ) is coupled with oxidative phosphorylation to drive adenosine triphosphate (ATP) synthesis. We have examined the effects of cold temperature stress on ΔΨm and the role of cold temperature receptor expression on ΔΨm . Human bronchial endothelial cell line, BEAS-2B, and human embryonic kidney, HEK293, cell line were transfected with the gene for cold temperature responsive receptor protein TRPM8 or TRPA1, and exposed to cold temperature. ΔΨm was monitored using 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazoyl carbocyanine iodide derivative (JC-10), a ΔΨm probe. While cold temperatures significantly increased ΔΨm and mitochondrial ATP levels in cells transfected with temperature responsive receptor TRPM8 or TRPA1, no change was noted in wild-type cells. Moreover, the change in ΔΨm and ATP level was a dynamic process. ΔΨm was raised to peak levels within 10 min of cold exposure, followed by a return to baseline levels at 30 min. Our findings suggest that cold temperature exposure increased mitochondrial ΔΨm via a mechanism involving cold temperature receptors.