Abstract

Infection by the severe acute respiratory syndrome (SARS) coronavirus-2 (SARS-CoV-2) is the causative agent of a new disease (COVID-19). The risk of severe COVID-19 is increased by certain underlying comorbidities, including asthma, cancer, cardiovascular disease, hypertension, diabetes, and obesity. Notably, exposure to hormonally active chemicals called endocrine-disrupting chemicals (EDCs) can promote such cardio-metabolic diseases, endocrine-related cancers, and immune system dysregulation and thus, may also be linked to higher risk of severe COVID-19. Bisphenol A (BPA) is among the most common EDCs and exerts its effects via receptors which are widely distributed in human tissues, including nuclear oestrogen receptors (ERα and ERβ), membrane-bound oestrogen receptor (G protein-coupled receptor 30; GPR30), and human nuclear receptor oestrogen-related receptor gamma. As such, this paper focuses on the potential role of BPA in promoting comorbidities associated with severe COVID-19, as well as on potential BPA-induced effects on key SARS-CoV-2 infection mediators, such as angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2). Interestingly, GPR30 appears to exhibit greater co-localisation with TMPRSS2 in key tissues like lung and prostate, suggesting that BPA exposure may impact on the local expression of these SARS-CoV-2 infection mediators. Overall, the potential role of BPA on the risk and severity of COVID-19 merits further investigation.

Highlights

  • Infection by the novel severe acute respiratory syndrome (SARS) coronavirus-2 (SARS-CoV-2) causes a severe new disease, i.e., COVID-19

  • Chronic respiratory diseases, cardiovascular disease (CVD), hypertension, diabetes, immunosuppression, and cancer are among the identified comorbidities which predispose individuals to severe COVID-19 [1]

  • In the present paper, we focus on the potential role of Bisphenol A (BPA) in promoting the development of comorbidities which increase the risk of severe COVID-19, as well as on potential BPA-induced effects on key molecular targets which mediate the infection by SARS-CoV-2

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Summary

Introduction

Infection by the novel severe acute respiratory syndrome (SARS) coronavirus-2 (SARS-CoV-2) causes a severe new disease, i.e., COVID-19. A computational systems biology approach revealed that a number of signalling pathways which are dysregulated by EDCs (e.g., Th17 and advanced glycation end-products (AGE)/receptor for AGE (RAGE), AGE/RAGE, pathways) might be related to the severity of COVID-19 [11]. As these detrimental effects of EDCs overlap with key risk factors for severe COVID-19, the hypothesis that exposure to EDCs may be linked to the severity of COVID-19 merits further investigation [12]. In the present paper, we focus on the potential role of BPA in promoting the development of comorbidities which increase the risk of severe COVID-19, as well as on potential BPA-induced effects on key molecular targets which mediate the infection by SARS-CoV-2

BPA and Cardiometabolic Diseases
BPA and Cancer
BPA and Modulation of Immune System Responses
BPA and Links to Pregnancy and Placentation Complications
BPA and Key Molecular Targets of SARS-CoV-2
BPA and Expression of TMPRSS2
BPA and Expression of ACE2 and Furin
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