Disrupting effects of the emerging contaminant octylmethoxycinnamate (OMC) on human umbilical artery relaxation

Cardiovascular diseases (CVD) represent the number one cause of death worldwide. The vascular endothelium may play a role in the pathophysiology of CVD diseases. Octylmethoxycinnamate (OMC) is a UV-B filter (CAS number: 5466-77-3) widely used worldwide in numerous personal care products, including sunscreens, daily creams, and makeup. This UV-B filter is considered an endocrine disruptor. Therefore, this investigation aimed to evaluate the direct effects of OMC in human umbilical arteries (HUAs) with endothelium and the possible mechanisms involved in the response. The results demonstrated that OMC exerts a rapid (non-genomic) and endothelium-dependent arterial relaxant effect on HUAs previously contracted with serotonin (5-HT) and Histamine (His). On the other hand, when HUAs were contracted with potassium chloride (KCl), the relaxing effect was only observed in HUAs without endothelium, and it appeared to be inhibited in HUAs with endothelium. Thus, the vasorelaxant effect of OMC depends on the endothelium and depends on the contractile agent used, suggesting that OMC may act through different signaling pathways. Furthermore, computational modulation studies, corroborated the binding of OMC to all the proteins under investigation (eNOS, COX-2, ET-1, and TxA2), with higher affinity for COX-2. In summary, the vascular effect of OMC may involve activating different pathways, i.e., acting through the NO pathway, COX pathway, or activating the endothelin-1 pathway.

Automated summary

Cardiovascular diseases (CVD) are the leading cause of death worldwide, and the vascular endothelium may play a role in their pathophysiology. Octylmethoxycinnamate (OMC), a commonly used UV-B filter, has been found to act as an endocrine disruptor. This study aimed to investigate the direct effects of OMC on human umbilical arteries (HUAs) with endothelium and the underlying mechanisms. The results showed that OMC had a rapid and endothelium-dependent arterial relaxant effect on HUAs contracted with serotonin and histamine. However, this effect was inhibited in HUAs contracted with potassium chloride and appeared to be dependent on the presence of endothelium. Computational modeling studies also revealed the binding of OMC to several proteins involved in vascular function. Overall, the vascular effect of OMC may involve activation of different pathways, including the NO pathway, COX pathway, or endothelin-1 pathway.