Abstract
BackgroundExposure to glyoxal, the smallest dialdehyde, is associated with several diseases; humans are routinely exposed to glyoxal because of its ubiquitous presence in foods and the environment. The aim of this study was to examine the damage caused by glyoxal in human aortic endothelial cells.MethodsCell survival assays and quantitative fluorescence assays were performed to measure DNA damage; oxidative stress was detected by colorimetric assays and quantitative fluorescence, and the mitogen-activated protein kinase pathways were assessed using western blotting.ResultsExposure to glyoxal was found to be linked to abnormal glutathione activity, the collapse of mitochondrial membrane potential, and the activation of mitogen-activated protein kinase pathways. However, DNA damage and thioredoxin oxidation were not induced by dialdehydes.ConclusionsIntracellular glutathione, members of the mitogen-activated protein kinase pathways, and the mitochondrial membrane potential are all critical targets of glyoxal. These findings provide novel insights into the molecular mechanisms perturbed by glyoxal, and may facilitate the development of new therapeutics and diagnostic markers for cardiovascular diseases.
Highlights
Glyoxal (GX), the smallest dialdehyde, is the most widely used retarding agent in the synthesis of chemicals, such as novel bio-adhesives for wood [1,2,3], and is found in the environment [4]
Trx1, phospho extracellular signal regulated kinase (P-ERK), phospho c-Jun N-terminal kinase (P-JNK), and phospho p38 kinase (P-P38) antibodies were purchased from Abcam (Cambridge, UK), and enhanced chemiluminescence (ECL) western blotting substrate was obtained from Biosharp (Hefei, China)
DNA repair is not important in attenuating GX toxicity interstrand crosslinks (ICLs) are amongst the most serious types of DNA damage induced by aldehydes, the accumulation of which results in growth arrest and cell death; the FANC pathway is capable of rescuing lCL-stalled replication forks while maintaining the genetic stability of the daughter cells to ensure survival [24, 25]
Summary
Glyoxal (GX), the smallest dialdehyde, is the most widely used retarding agent in the synthesis of chemicals, such as novel bio-adhesives for wood [1,2,3], and is found in the environment [4]. Xie et al BMC Cardiovascular Disorders (2021) 21:603 the progression of several degenerative conditions, such as Alzheimer’s disease and diabetes mellitus, in which increased serotonin release from the cells stimulate serotonin-mediated intestinal motility [7]. Erythrocytes take up exogenous GX and convert it primarily to glycolate, and approximately 1% of this is converted to oxalate This pathway of oxalate formation may be enhanced in diabetes and other diseases associated with increased oxidative stress [12]. Thioredoxin-1 (Trx1) mainly acts by cleaving the disulfide bonds of oxidized proteins, affecting intracellular scavenging of oxidative stress. This action relies on cell survival, cell growth, and gene transcription [17]. The aim of this study was to examine the damage caused by glyoxal in human aortic endothelial cells
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