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Journal archive > 2011 > N 5 September-October


G. L. Gergalova, M. V. Skok

Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv;
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The effect of nicotine on the mouse liver mitochondria was studied by fluorescent flow cytometry. Mice consumed nicotine during 65 days; alternatively, nicotine was added to isolated mitochondria. Mitochondria of nicotine-treated mice had significantly lower basic levels of membrane potential and granularity as compared to those of the control group. Pre-incubation of the isolated mitochondria with nicotine prevented from dissipation of their membrane potential stimulated with 0.8 µM СаСl2 depending on the dose, and this effect was strengthened by the antagonist of ?7 nicotinic receptors (?7 nAChR) methyllicaconitine. Mitochondria of mice intravenously injected with the antibodies­ against ?7 nAChR demonstrated­ lower levels of membrane potential. Introduction of nicotine, choline, acetylcholine or synthetic ?7 nAChR agonist PNU 282987 into the incubation medium inhibited Ca2+ accumulation in mitochondria, although the doses of agonists were too low to activate the ?7 nAChR ion channel. It is concluded that nicotine consumption worsens the functional state of mitochondria by affecting their membrane potential and granularity, and this effect, at least in part, is mediated by ?7 nAChR desensitization.

Key words: isolated mitochondria, nicotine, ?7 nicotinic acetylcholine receptor, fluorescent flow cytometry, membrane potential, Ca2+.

The original article in Ukrainian is available for download in PDF format.

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