Effect of bisphenol A on stress-induced premature senescence



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Plastics are used for a wide variety of commercial applications all over the world, but recently a number of health risks have been linked to plastics and plastic products. For example, bisphenol A (BPA) is a plasticizer used in the production of plastics such as storage containers, plastic bottles, adhesives, and many other everyday objects. BPA-containing plastics are subject to degradation, resulting in the ingestion of BPA from many different sources. BPA has been shown to cause negative side-effects once ingested due to its ability to act as an estrogen mimic, along with being implicated in the formation of cancers and the metabolic syndrome. BPA has also been linked to inducing oxidative stress, which can lead to damaged DNA, promote tumorigenesis, and can cause cell death in extreme cases. On the other hand, little is known about the effect of BPA on cellular senescence, a state of irreversible cell cycle arrest and a recognized barrier to cancer progression. Because of its pro-oxidizing role, it was hypothesized that BPA could increase the likelihood of cells becoming senescent. To test this, cells were exposed to a variety of experimental conditions for varying lengths of time; they were then stained for β-galactosidase, a widely used biomarker of senescence, and interleukin-6, a pro-inflammatory cytokine linked to senescence. It was found that, although BPA may not have a direct effect on senescence induction in a dose dependent manner, dimethyl sulfoxide (DMSO), the vehicle used to dissolve BPA in this experiment, could have an effect on senescence induction at very low doses.



Stress-induced premature senescence, Bisphenol A, β-galactosidase, Interleukin-6, Senescence-associated secretory profile