Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis

Abstract

The skin is the largest organ of the human body and the one mostly exposed to outdoor contaminants. To evaluate the biological mechanisms underlying skin damage caused by fine particulate matter (PM2.5), we analyzed the effects of PM2.5 on cultured human keratinocytes and the skin of experimental animals. PM2.5 was applied to human HaCaT keratinocytes at 50 µg/mL for 24 h and to mouse skin at 100 µg/mL for 7 days. The results indicate that PM2.5 induced oxidative stress by generating reactive oxygen species both in vitro and in vivo, which led to DNA damage, lipid peroxidation, and protein carbonylation. As a result, PM2.5 induced endoplasmic reticulum stress, mitochondrial swelling, and autophagy, and caused apoptosis in HaCaT cells and mouse skin tissue. The PM2.5-induced cell damage was attenuated by antioxidant N-acetyl cysteine, confirming that PM2.5 cellular toxicity was due to oxidative stress. These findings contribute to understanding of the pathophysiological mechanisms triggered in the skin by PM2.5, among which oxidative stress may play a major role.

Protective Effect of Diphlorethohydroxycarmalol Isolated from Ishige okamurae Against Particulate Matter-Induced Skin Damage by Regulation of NF-κB, AP-1, and MAPKs Signaling Pathways In Vitro in Human Dermal Fibroblasts

“…Skin is the largest organ of the human body, as well as the primary organ which is exposed to outdoor contaminants. Exposure to PM causes epithelium damage, and endothelial dysfunction has been reported previously [8,9,38]. PM induce skin damages or diseases mainly through stimulating inflammatory response and oxidative stress [5,39].…”

“…The results indicated that PM significantly stimulated the expression of pro-inflammatory cytokines through activating NF-κB pathway [39]. Piao et al evaluated the effect of PM on human keratinocytes, and the results indicated that PM significantly induced oxidative stress by production of ROS, which causes lipid peroxidation, DNA damage, and protein carbonylation [9].…”

“…In general, PM were produced by human activity, such as chemical production and fossil fuel combustion [1,2]. PM are related to various diseases, including inflammations such as skin inflammation and lung inflammation, kidney diseases such as chronic kidney disease and end-stage renal disease, metabolic syndromes such as diabetes and obesity, as well as skin aging such as wrinkle formation [3][4][5][6][7][8][9][10][11]. Skin is the largest organ in humans and the primary organ exposed to PM.…”

Biological evaluation of rare earth complexes bearing 1H‐imidazo[4,5‐f]‐1,10‐phenanthroline moiety as promising anticancer chemotherapeutics

“…Recently, the depolarization of the mitochondrial membrane has become the basic method for detecting the early stage of cell apoptosis . The membrane‐permeant dye JC‐1 is widely used in apoptosis studies to monitor the status of mitochondria where JC‐1 accumulates in a potential‐dependent manner as indicated by a fluorescence emission shift from green ( ca 529 nm) to red ( ca 590 nm).…”

Hematological effects of ultrafine carbon black on red blood cells and hemoglobin

“…PM 2.5 induces oxidative stress by generating reactive oxygen species (ROS), which leads to DNA damage and lipid peroxidation . Oxidative stress is a crucial mechanism of toxicity .…”