Selenium and mitochondrial integrity in the pancreas of the chick.
The activity of selenium-dependent glutathione peroxidase (SeGSH-Px) in the pancreas was found to decline in response to Se depletion in the chick at approximately the same time as the appearance of histopathological changes in the acinar cells of the pancreas, indicative of the onset of nutritional pancreatic atrophy. Oral administration of 10 micrograms of Se as Na2SeO3 to Se-deficient chicks increased SeGSH-Px activity in liver and plasma within 12 hours but not in pancreas until 36 hours. Histological signs of regeneration were not observed within 48 hours of Se repletion; however, acinar nuclei were significantly larger within 12 hours of Se repletion. The apparent rates of synthesis of DNA, RNA, and protein in liver, and of DNA in pancreas, were not affected by Se deficiency. The apparent rates of synthesis of pancreatic RNA and protein were depressed in Se-deficient chicks and were increased within 24 and 36 hours, respectively, upon Se repletion. Electron microscopic observation of pancreatic acinar cells from Se-deficient chicks revealed disruption of inner and outer mitochondrial membranes. However, no impairment was noted in rate of oxygen uptake, respiratory control index, or ADP:oxygen ratio of pancreatic mitochondria due to Se deficiency. The mitochondrial protein yield of the Se-deficient chick pancreases was 27% less than that of Se-adequate chicks. These data suggest that a decreased number of functional acinar mitochondria may result in nutritional pancreatic atrophy in the Se-deficient chick.
D000818:Animals; D001284:Atrophy; D002645:Chickens / Q000378:metabolism*; D004247:DNA / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D008297:Male; D008928:Mitochondria / Q000378:metabolism*; D010179:Pancreas / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D012643:Selenium / Q000502:physiology*
D004247:DNA; D005979:Glutathione Peroxidase; D012643:Selenium