Abstract
Astaxanthin, a natural antioxidant carotenoid, is a nutrient with diverse health benefits, given that it decreases the risk of oxidative stress-related diseases. In the present study, we investigate the functional role of astaxanthin during autophagic cell death induced by the estrogenic endocrine-disrupting chemical bisphenol A (BPA) in normal human dermal fibroblasts (NHDF). BPA significantly induced apoptotic cell death and autophagy in NHDF. Autophagic cell death evoked by BPA was significantly restored upon a treatment with astaxanthin (10 μM) via the inhibition of intracellular reactive oxygen species (ROS) production. Astaxanthin inhibited the phosphorylation of extracellular signal-regulated kinases (ERK) stimulated by ROS production, but it did not influence the activation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) in BPA-treated NHDF. Astaxanthin abrogated the ERK-mediated activation of nuclear factor-kappa B (NF-κB), which is responsible for the mRNA expression of LC3-II, Beclin-1, Atg12, and Atg14 during apoptotic cell death induced by BPA. These results indicate that astaxanthin is a pharmacological and nutritional agent that blocks the skin fibroblastic autophagic cell death induced by BPA in human dermal fibroblasts.
Highlights
Bisphenol A (BPA), ubiquitously present in consumer products containing polycarbonate plastics and epoxy resins, has been utilized extensively in dentistry, food packaging, thermal printing papers, and lacquers [1]
To determine the functional role of astaxanthin in the dermal fibroblastic damage, normal human dermal fibroblasts (NHDF) was exposed to the BPA in the presence astaxanthin at various concentrations (0.1–10 μM)
RFU, relative fluorescence units. (B) NHDF was exposed to the BPA in the presence of astaxanthin
Summary
Bisphenol A (BPA), ubiquitously present in consumer products containing polycarbonate plastics and epoxy resins, has been utilized extensively in dentistry, food packaging, thermal printing papers, and lacquers [1]. While oral intake from contaminated food and drinks represents the predominant source of BPA exposure and given the well-known pathophysiological role of ingested BPA, the potential risk of BPA exposure via dermal contact and absorption in the skin is not well documented. Skin is the largest organ of human body consisting of three primary layers and diverse cell types [4], where dermal fibroblasts are an essential component, maintaining the structure of fibers by producing a collagen-rich extracellular matrix and playing an important role in the production of inflammatory mediators against chemical, microbial, viral, and fungal agents [5,6,7]. Given that approximately 46% of BPA is diffused through the skin [8], recent studies have suggested that BPA causes oxidative dermal damage and stimulates the expression of many pro-inflammatory mediators associated with human skin diseases [9]. The underlying pathophysiological mechanisms of BPA involved in oxidative dermal damage remain undescribed
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