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Abstract
Background: Urban air pollution contributes to lung and cardiovascular system dysfunction, making it a major concern for human health. Its impact on skin integrity, associated with increased occurrence of atopic dermatitis, is now recognized, but its cellular mechanisms remain poorly understood. Objective: In the present study we aimed at establishing the impact of urban pollutant on mitochondrial dynamics and bioenergetics using the HaCaT cell model. We also sought to establish the protective effect of ECH-5195 (red Panax ginseng extract), standardized in ginsenosides, in reversing pollution-induced mitochondrial defects. Methods: Urban pollution exposure was mimicked by 1 h exposure of HaCaT cells with standardized atmospheric particulate matter containing PAHs, nitro-PAHs, PCB congeners, and chlorinated pesticides with a mean particulate diameter of 5.85 μm (SRM1648). Results: The presence of urban pollutant in the cultures increased the prevalence of hyperfission by 1.41-fold (p = 0.023) and fission by 1.35 fold (p = 0.006) in the reticular mitochondrial network. ECH-5195 reduced both pollution-induced hyperfission by 0.54-fold (p = 0.004) and fission by 0.68-fold (p = 0.0006) normalizing the mitochondrial reticular network. Pollution exposure was associated with a significant reduction of basal OCR and increased lactate production, pushing the cell to rely on glycolysis for ATP production. When ECH-5195 was used, OCR was significantly increased, and the glycolytic contribution to ATP production was reduced while both oxidative phosphorylation and mitochondrial respiration were increased demonstrating mitochondrial re-engagement in ATP production. Conclusions: Pollution exposure was disruptive for both the mitochondrial network dynamics and mitochondrial respiration. Ginsenosides in ECH-5195 efficiently protected both from pollution-induced defects.
Highlights
The 2019 review from the World Health Organization (WHO) states that exposure to ambient air pollution is responsible for 2.4 million deaths. 91% of the world’s population lives in places where air pollution exceeds WHO guideline limits, which places air pollution as the world’s largest single environmental health risk factor [1] [2]
A clear difference exists between unexposed HaCaT cells and HaCaT cells exposed with urban pollutants, in which fragmentation of the mitochondrial reticular network was observed
Our data demonstrate that ginsenosides in ECH-5195 normalized cell energy production and reduced mitochondrial fission and hyperfission in HaCaT cells exposed to urban pollutants
Summary
The 2019 review from the World Health Organization (WHO) states that exposure to ambient air pollution is responsible for 2.4 million deaths. 91% of the world’s population lives in places where air pollution exceeds WHO guideline limits, which places air pollution as the world’s largest single environmental health risk factor [1] [2]. Despite the prominent impact of ambient air pollution on cardiovascular diseases, stroke, chronic obstructive pulmonary disease and lung cancer, skin may be affected by environmental pollutants concentrating on its surface [3]. Few published epidemiological reports associate the impact of urban pollutant on human health and skin barrier function. Objective: In the present study we aimed at establishing the impact of urban pollutant on mitochondrial dynamics and bioenergetics using the HaCaT cell model. Results: The presence of urban pollutant in the cultures increased the prevalence of hyperfission by 1.41-fold (p = 0.023) and fission by 1.35 fold (p = 0.006) in the reticular mitochondrial network. ECH-5195 reduced both pollution-induced hyperfission by 0.54-fold (p = 0.004) and fission by 0.68-fold (p = 0.0006) normalizing the mitochondrial reticular network.
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