Selenium and Mitochondrial Integrity in the Pancreas of the Chick

Abstract

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.

Mineral and vitamin deficiencies can accelerate the mitochondrial decay of aging

“…Selenium is also an essential element and component of the mitochondrial protein, glutathione peroxidase (Levander et al, 1974). Several reports have shown that selenium deficiency causes defects in mitochondrial structure, integrity, and electron transport chain function (Whitacre and Combs, 1983;Sokolove et al, 1993;Rani and Lalitha, 1996). The loss of antioxidant capacity of the mitochondria due to reduced glutathione peroxidase activity is the likely etiology.…”

Dietary selenium influences pancreatic tissue levels of selenoprotein W in chickens

“…However, the pancreas of chickens is a major target organ of Se deficiency [16,17]. Thompson and Scott (1970) reported that diets extremely deficient in Se produced severe pancreatic degeneration in chicks [18].…”

Disruption of Endoplasmic Reticulum Is the Primary Ultrastructural Lesion of the Pancreas in the Selenium-Deficient Chick

“…On the basis of these findings, they suggested that the primary metabolic lesion in severe Se deficiency may be the loss of mitochondrial integrity due to diminished antioxidant protection via SeGSHpx in the cytosol and mitochondria1 matrix space. Whitacre and Combs (7) supported their hypothesis with limited observations of pancreatic acinar ultrastructure using transmission electron microscopy which they interpreted as showing both loss of ER and mitochondria1 disruption in affected cells.…”

“…Noguchi et al (6) found that atrophied pancreases from Se-deficient chicks contained reduced amounts of zymogen. In subsequent work, the respiratory function of mitochondria isolated from Se-deficient chicks with early-stage pancreatic atrophy (i.e., without fibrosis) was found to be normal (3,7); however, the yield of mitochondria from Se-deficient pancreases was only 72% of that of Se-adequate controls (7). Whitacre and Combs (7) found that early-stage Se-deficiency involved marked reductions in the synthesis of RNA and protein in the pancreas (but not in the liver).…”

“…In subsequent work, the respiratory function of mitochondria isolated from Se-deficient chicks with early-stage pancreatic atrophy (i.e., without fibrosis) was found to be normal (3,7); however, the yield of mitochondria from Se-deficient pancreases was only 72% of that of Se-adequate controls (7). Whitacre and Combs (7) found that early-stage Se-deficiency involved marked reductions in the synthesis of RNA and protein in the pancreas (but not in the liver). On the basis of these findings, they suggested that the primary metabolic lesion in severe Se deficiency may be the loss of mitochondrial integrity due to diminished antioxidant protection via SeGSHpx in the cytosol and mitochondria1 matrix space.…”