The Effect Of Ochratoxin A On Cytotoxicity And Glucose Metabolism In Human Esophageal Epithelium Het-1a Cells

Ochratoxin A (OTA) is a widespread mycotoxin worldwide that causes major health risks. The esophageal epithelium is unavoidably exposed to food contaminated OTA after ingestion. Yet, few studies have involved in the putative effects of OTA on the cytotoxicity and glucose metabolism responses on esophageal epithelial cells. In this in vitro study, we aimed to investigate the effects of OTA on esophageal epithelial cell intracellular apoptosis, oxidative stress, DNA damage, mitochondrial function and glucose metabolism. Human esophageal epithelial Het-1A cells were exposed to 2.5, 5 or 10 mu M OTA for 24 h. The results showed that OTA decreased cell viability and concomitantly increased apoptosis-related indices, reactive oxygen species generation, oxidative DNA damage, mitochondrial dysfunction and mitochondrial apoptotic pathway activation. In addition, OTA switched the glucose metabolism of Het-1A cells from oxidative phosphorylation towards glycolysis by decreasing the expression of tricarboxylic acid cycle-associated enzymes such as a-ketoglutarate dehydrogenase and isocitrate dehydrogenase 1 and by increasing pyruvate dehydrogenase kinase 1 expression. The data indicated that cell apoptosis, oxidative damage, mitochondrial dysfunction and glucose metabolism perturbation might play pivotal roles in the mechanism of OTA-induced esophageal toxicity.