Vascular damage induced by plasticizers could also be mediated by oxidative stress on endothelial cells, as seen with the increasing level of reactive oxygen species (ROS) in EA.hy926 cells exposed to mono-2-ethylhexyl phthalate (MEHP), the main metabolite of DEHP. Moreover, DEHP contributed to inflammation by increasing the serum level of pro-inflammatory cytokines in ApoE −/ − mice and in human umbilical vein endothelial cells. DEHP was shown to induce vascular injury in orally exposed C57/BL6 mice through alterations in vascular tone. Īmong the few studies conducted on the circulatory system, bis-(2-ethylhexyl) phthalate (DEHP) is by far the most studied plasticizer, even though there is a diversity of plasticizers on the market. However, investigation on the toxicological effects of plasticizers on the cardiovascular system remain limited, particularly considering that various medical devices containing a high plasticizer content can expose the circulatory system. More recently, cardiovascular mortality was attributed to phthalate exposure. Lately, studies have reported the association between exposure to plasticizers and cardiovascular risk factors (e.g., high blood pressure, arrythmias, atherosclerosis). Many epidemiological and experimental studies have focused on evaluating their reproductive disorders. This is a matter of particular concern because human exposure to plasticizers has been related to adverse health effects. Human exposure can occur through multiple pathways of exposure, including oral, respiratory, dermal and parenteral routes. Thus, plasticizer leaching from products is at risk of exposure, although this is unintentional. Plasticizers can leach out during product use because they are not covalently bound. This study provides additional information on the adverse effects of plasticizers on endothelial cells. These results suggest that endothelial cells could go through a metabolic adaptation to face plasticizer-induced cellular stress, to effectively maintain their cellular processes.
Additionally, delayed effects were observed between the cellular and the mitochondrial parameters. Plasticizers induced a cytotoxicity by targeting mitochondrial respiration, depleting mitochondrial ATP production and increasing glycolytic metabolism.
Results showed cellular physiological perturbations induced with all the condition tested, excepted for DEHT. In this study, their cytotoxicity on HMEC-1 cells was evaluated on cell function (viability, cell counting, total glutathione and intracellular adenosines) and mitochondrial function (mitochondrial respiration). The aim of the study was to evaluate the in vitro toxicity on endothelial cells by considering the individual and the mixture effects of bis-(2-ethylhexyl) phthalate (DEHP), diisononyl phthalate (DINP) or bis-(2-ethylhexyl) terephthalate (DEHT). The vascular system carries plasticizers throughout the body and therefore can interact with the endothelium.
This is a matter of concern, as it may contribute to adverse health effects. Human are exposed through multiple pathways, from numerous sources, to multiple plasticizers. Plasticizers are chemicals in high demand, used in a wide range of commercial products.
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