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Inflammation. 2014 Jun;37(3):785-92. doi: 10.1007/s10753-013-9797-6.

Nicotine mediates hypochlorous acid-induced nuclear protein damage in mammalian cells.

Author information

  • 1Division of Biochemistry and GTMR Unit, College of Clinical Pharmacy, Taif University, Al-Haweiah, Taif, 21974, Kingdom of Saudi Arabia, salama.3@buckeyemail.osu.edu.

Abstract

Activated neutrophils secrete hypochlorous acid (HOCl) into the extracellular space of inflamed tissues. Because of short diffusion distance in biological fluids, HOCl-damaging effect is restricted to the extracellular compartment. The current study aimed at investigating the ability of nicotine, a component of tobacco and electronic cigarettes, to mediate HOCl-induced intracellular damage. We report, for the first time, that HOCl reacts with nicotine to produce nicotine chloramine (Nic-Cl). Nic-Cl caused dose-dependent damage to proliferating cell nuclear antigen (PCNA), a nuclear protein, in cultured mammalian lung and kidney cells. Vitamin C, vitamin E analogue (Trolox), glutathione, and N-acetyl-L-cysteine inhibited the Nic-Cl-induced PCNA damage, implicating oxidation in PCNA damage. These findings point out the ability of nicotine to mediate HOCl-induced intracellular damage and suggest antioxidants as protective measures. The results also raise the possibility that Nic-Cl can be created in the inflamed tissues of tobacco and electronic cigarette smokers and may contribute to smoking-related diseases.

PMID:
24357417
[PubMed - in process]
PMCID:
PMC4035441
[Available on 2015/6/1]
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