Abstract
The damaging effects of air pollution on the skin are becoming increasingly researched and the outcomes of this research are now a major influence in the selection and development of protective ingredients for skincare formulations. However, extensive research has not yet been conducted into the specific cellular defense systems that are being affected after exposure to such pollutants. Research investigating the affected systems is integral to the development of suitable interventions that are capable of augmenting the systems most impacted by air pollutant exposure. The following studies involved exposing primary human dermal fibroblasts to different concentrations of particulate matter and analyzing its effects on mitochondrial complex activity, nuclear factor erythroid 2‐related factor 2 localization using immunocytochemistry and protein expression of electron transport chain complex proteins, sirtuin‐1 (SIRT1), and peroxisome proliferator‐activated receptor gamma coactivator‐1α (PGC‐1α) using western blotting. Particulate matter‐induced alterations in both mitochondrial complex protein and activity, indicating oxidative stress, which was also complimented by increased expression of antioxidant proteins GSTP1/2 and SOD2. Particulate matter also seemed to modify expression of the proteins SIRT1 and PGC‐1α which are heavily involved in the regulation of mitochondrial biogenesis and energy metabolism. Given the reported results indicating that particulate matter induces damage through oxidative stress and has a profound effect on mitochondrial homeostasis, interventions involving targeted mitochondrial antioxidants may help to minimize the damaging downstream effects of pollutant‐induced oxidative stress originating from the mitochondria.
Highlights
The mitochondria are responsible for producing the energy serving molecule adenosine triphosphate (ATP) via the action of oxidative phosphorylation, a process involving both the electron transport chain (ETC) and chemiosmosis
Preparation of Particulate Matter SRM 1649b aka “urban dust particulate matter” (PM) was purchased from the National Institute of Standards and Technology (NIST), and a master stock prepared at a concentration of 50mg/ml in dimethyl sulfoxide (DMSO)
Dermal fibroblasts were exposed to PM for seven days before the cells were lysed and analysed for mitochondrial complex I (NDUFA9), II (SDHA), III (UCCR) and IV (COXVA) proteins using Western blotting (Figure 1A)
Summary
The mitochondria are responsible for producing the energy serving molecule adenosine triphosphate (ATP) via the action of oxidative phosphorylation, a process involving both the electron transport chain (ETC) and chemiosmosis. This molecule supplies the cell with the energy required to maintain normal cellular functions, this is substantiated by the fact that high energy demanding cells like hepatocytes have ~2500 mitochondria per cell, in contrast to only ~200 mitochondria per cell for low energy demanding cells such as dermal fibroblasts [1]. These pathways are responsible for inducing the transcription of both proinflammatory cytokines and matrix metalloproteinases (MMPs), and for this reason the roles extrinsic factors such as UV and air pollution play in premature skin ageing and inflammatory skin conditions are being investigated [6]
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