الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Environmental toxins as endocrine-disrupting chemicals (EDCs) are known recently to cause metabolic problems related to insulin resistance and T2DM. Bisphenol-A (BPA), which is one of the EDCs and structurally is simulator to endogenous estrogens, has been involved in the etiology of several diseases including type 2 diabetes mellitus (T2DM).
Bisphenol-A (BPA) found its usage in plastic industry, used in the manufacture of epoxy resins, and is commonly applied in daily consumer products. Chlorinated BPA derivatives are created when BPA from these goods combines with chlorinated tap water. Oral consumption is the main way that people are exposed to BPA. BPA may be an additional risk factor to take into account in the emergence of insulin resistance and T2DM, according to numerous recent studies that have highlighted this possibility.
Increasing evidence suggests that the reactive oxygen species (ROS) induction by BPA is the most important causing factor of its toxicity. Moreover, as a result of BPA exposure, oxidative stress is stimulated, and this starts the aging process. Malondialdehyde (MDA), a marker of lipid peroxidation, has been commonly believed as a possible biomarker for oxidative stress, and numerous findings show its rise in BPA-exposed organisms.
It was assumed that BPA could enhance the risk of cells being senescent because of its pro-oxidizing function. Cellular senescence, an unavoidable cell cycle stop, is a known impediment to the spread of cancer. Senescent cells may influence the function of pancreatic β cells, accelerate tissue damage through the senescence-associated secretory phenotype (SASP), and enhance and propagate a number of tissue abnormalities. The identification of senescent cells is dependent on high level of lysosomal β-galactosidase activity, which is a protein in humans encoded by the galactosidase beta 1 (GLB1) gene.
Senescent cells stop dividing but continue to function metabolically and secrete cytokines and chemokines through the SASP phenomenon in a complex pro-inflammatory response. Tumor necrosis factor alpha (TNF-α) is one of these cytokines that promotes insulin resistance and induce inflammation in the pathogenesis of T2DM.
This study aims to analyze the ambient exposure to BPA by evaluating its blood level along with the relative expression level of GLB1, TNF-α mRNAs, and serum MDA. It also seeks to establish the relationship between these markers and the glycemic control of Egyptian patients with T2DM.