Research Progress on the Regulatory Effect of Nicotine on Mitochondria
TIAN Jianlu, WANG Hongjuan, CHEN Huan, HOU Hongwei*, HU Qingyuan*
Nicotine is the principal addictive component in tobacco, but also a toxic substance. As a semiautonomous organelle, mitochondria act significant roles in various biological functions, such as the process of cell growth, differentiation, apoptosis, energy supply and signal transduction. Mitochondria dysfunction will cause irreversible damage to cells and even the organism. Previous studies have shown that mitochondria are the potential target of nicotine. Nicotine can regulate mitochondria in a nicotinic acetylcholine receptors dependent or independent way. When the concentration gradient, exposure duration and target cells are different, the effects of nicotine on mitochondria are different. This review focuses on the effects of nicotine on mitochondrial gene expression, mitochondrial dynamics, mitochondrial respiratory chain, oxidative stress, calcium homeostasis and monoamine oxidase activity. The regulatory effects and mechanisms of nicotine on mitochondria are summarized from both positive and negative aspects; and it provides perspectives for the follow-up study of related mechanisms and control strategies of multiple biological effects of nicotine acting on mitochondria.
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