PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes

Abstract

Recent growing evidence suggested that particulate matter 2.5 (PM2.5) has strong toxic effects on skin systems. However, the possible effects and the mechanisms of PM2.5 on vitiligo remain poorly understood. Therefore, the present study aimed to further investigate the effects and possible mechanisms of PM2.5 on vitiligo. Human keratinocytes (HaCaT cells) and human melanocytes (PIG1 cells and PIG3V cells) were exposed to PM2.5 (0-200 µg/ml) for 24 h. The cell viability of the three cell lines was measured by a Cell Counting Kit-8 assay. The secretions of stem cell factor (SCF) and basic fibroblast growth factor (bFGF) in HaCaT cells were evaluated by ELISA. The melanin contents, cellular tyrosinase activity, apoptosis, cell migration, malondialdehyde (MDA) contents, superoxide dismutase (SOD) levels, glutathione peroxidase (GSH-Px) levels and related protein expressions in PIG1 cells and PIG3V cells were evaluated by a NaOH assay, DOPA assay, Annexin V-FITC/Propidium Iodide staining, MDA assay, SOD assay, GSH-Px assay and western blotting, respectively. It was demonstrated that PM2.5 exposure inhibited cell viability of all three cell lines (HaCaT, PIG1 and PIG3V cells). PM2.5 exposure attenuated the secretions of SCF and bFGF in HaCaT cells. Moreover, PM2.5 exposure attenuated the activation of tyrosinase and melanogenesis, inhibited cell migration, and induced apoptosis and oxidative stress injury in PIG1 cells and PIG3V cells. In addition, PM2.5 exposure caused upregulated cytosolic cytochrome C and activated caspase-3 in PIG1 cells and PIG3V cells. Furthermore, PM2.5 exposure activated the nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 signaling pathway. The present results suggested that PM2.5 exposure could inhibit the secretions of SCF and bFGF in keratinocytes, and cause oxidative stress injury and melanin metabolic disorder in melanocytes. Therefore, PM2.5 could be a new risk factor for vitiligo. PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes

Effects of DNA Damage and Oxidative Stress in Human Bronchial Epithelial Cells Exposed to PM2.5 from Beijing, China, in Winter

“…We have measured ROS, oxidative stress markers (MDA and GSH), and HO-1 to show that PM 2.5 enhanced ROS generation and eliminated the homeostasis of oxidative stress, causing a severe oxidative tendency in cells. These findings are consistent with the report that PM 2.5 (0–200 µg/mL) from Shanghai induced oxidative stress in human keratinocytes and human melanocytes, which was manifested as an increase in MDA and HO-1 [ 28 ]. MDA is a product of lipid peroxidation, while GSH acts as a ROS scavenger, so it reflects the severity of the cells attacked by ROS.…”

Autophagy attenuates particulate matter 2.5-induced damage in HaCaT cells

“…Hence, the interaction between PM2.5 and the skin barrier makes the underlying mechanism of skin lesions an important consideration when evaluating the skin toxicity of PM2.5. Ambient PM2.5 exposure reduced the viability of keratinocytes (19) and activated inflammatory factors including IL-6 and TNF-α, and all of the above processes led to inflammation in skin tissue (20). Dong et al determined that oxidative stress is involved in the process of skin inflammatory and aggravates atopic dermatitis (21).…”

Lycium Barbarum polysaccharide protects HaCaT cells from PM2.5-induced apoptosis via inhibiting oxidative stress, ER stress and autophagy

“…With the seriousness of air pollution, our skin is more likely to be exposed to toxic substances in the air, especially PM2.5, which can cause skin aging, inflammation and even skin cancer [ 29–31 ]. It has been reported that exposure of HaCaT cells to PM2.5 can cause cellular oxidative damage, vitality reduction and apoptosis [ 7 , 8 , 32 ]. Therefore, it is urgent to seek effective drugs to prevent and treat skin damage and degeneration caused by PM2.5.…”