Effects of peroxiredoxin 1 on nicotine induced apoptosis in mouse tongue

Local action of nicotine on oral mucosa contributes to the pathogenesis of precancerous and cancerous lesions. Nicotine participation in the mechanism of apoptosis in normal mucosa has not been established. Peroxiredoxin 1 (Prx1) is a cellular antioxidant that participates in regulating apoptosis. We investigated expression of Prx1 and proteins in apoptosis-related downstream signaling by mitogen-activated protein kinases (MAPKs) in nicotine-treated tongue tissues of wild-type and Prx1 knockout (Prx1^±) mice; we also investigated these processes in mouse embryonic fibroblast (MEF) cells in vitro. Nicotine increased the expression of Prx1 mRNA in tongue tissues in vivo. The rate of apoptosis was similar among the nicotine-treated mice, nicotine-treated + Prx1^± mice and untreated controls. The expression of p-JNK was greater in Prx1^± mice compared to control mice. In MEF cells, nicotine increased the expression of Prx1 and inhibited apoptosis and expression of p-p38 and p-JNK. Prx1 knockdown animals exhibited increased apoptotic rate and expression of p-p38 and p-JNK in MEFs. Nicotine-regulated apoptosis might occur via a Prx1-dependent pathway.