Exposure to cigarette smoke condensate has a differential effect on primary human melanocytes from light skin and dark skin.

Abstract

Smoking causes pigmentation changes and skin aging, according to epidemiological research. Nicotine affected melanogenesis and increased oxidative stress in primary human melanocytes from darkly pigmented (DP) and lightly pigmented (LP) skin. However, research on the effects of cigarette smoke condensate (CSC) on primary human melanocytes from light and dark pigmentations in an in vitro culture over long-term durations is lacking. Herein, CSC was tested on LP and DP melanocytes for 6 days. CSC suppressed tyrosinase activity and lightened LP and DP pellets, indicating melanin production suppression. However, CSC increased melanocyte dendricity in LP cells at 25, 50, and 100 µg/mL doses, indicating melanin export. In DP cells, CSC biphasically increased dendricity at 25 µg/mL and decreased it at 50 µg/mL. In CSC-free cultures, LP cells exhibit complete dendricity recovery at 25 µg/mL, partial recovery at 50 µg/mL, and further augmentation at 100 µg/mL. Dendricity in DP cells were recovered only at 25 µg/mL, not at 50 µg/mL. In LP cells, CSC increased ROS production and SA-β-gal staining, but in DP cells, ROS decreased and no senescence was seen. The data show that CSC concentration and melanocyte pigmentation affect melanocyte damage, oxidative stress, and senescence. Melanocytes from LP skin are more susceptible to CSC damage than DP skin.