Effects of selenium status and supplementary seleno-chemical sources on mouse T-cell mitogenesis

Ueno, Hitoshi; Hasegawa, Gohki; Ido, Ryoko; Okuno, Tomofumi; Nakamuro, Katsuhiko

doi:10.1016/j.jtemb.2007.10.002

Cited by 21 publications

(15 citation statements)

References 43 publications

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“…Poultry diets lacking Se result in slow growth and development, reduced egg production, decreased hatchability, pancreatic degeneration, nutritional muscular dystrophy, and necrotic lesions in the liver, muscle, and heart [27][28][29][30]. Excess dietary Se induces decreased relative weight, lesions, and apoptosis of chicken bursa of Fabricius [31]. Both excess and deficiency of Se supply lead to impaired growth.…”

Section: Discussionmentioning

confidence: 99%

Selenium Regulates Gene Expression of Selenoprotein W in Chicken Gastrointestinal Tract

Gao

Xing

et al. 2011

Biol Trace Elem Res

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Selenoprotein W (SelW) is an existing form of selenium (Se). Se influences the levels of SelW in mammals. However, little is known about the pattern of SelW expression in the gastrointestinal tract tissue of bird. The present paper describes the effects of different dietary levels of Se on the SelW mRNA expression in the gastrointestinal tract tissue of chicken. The expression levels of SelW mRNA and the Se contents in the gastrointestinal tract tissues (glandular stomach, gizzard, duodenum, small intestine, and rectum) were determined on days 15, 25, 35, 45, and 55, respectively. The results showed that the Se contents and the SelW mRNA expression were significantly higher (p < 0.05) in the high-Se group, and the Se contents and SelW mRNA expression in the low-Se group were significantly lower (p < 0.05) than in the controls. The Se contents were the highest in the duodenum and the lowest in the rectum, while the SelW mRNA expression was the highest in the gizzard and the lowest in the rectum. In addition, the SelW mRNA levels in the gastrointestinal tract tissue were found to increase in a time-dependent manner with increasing feeding time. Furthermore, the expression of the SelW mRNA in the gastrointestinal tract tissues of chickens was found to correlate with the dietary Se concentrations, but not with the tissue Se contents.

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Section: Discussionmentioning

confidence: 99%

Selenium Regulates Gene Expression of Selenoprotein W in Chicken Gastrointestinal Tract

Gao

Xing

et al. 2011

Biol Trace Elem Res

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“…This is also supported by reports of Se contents in various tissues of mice largely declining by continuous ingestion of Se-deficient diet for more than 4 weeks. 37,38) The Se contents in all the tissues of DL and DH groups largely increased compared with that of DC group (Fig. 1B, 1D and 1F).…”

Section: Discussionmentioning

confidence: 86%

Effect of Sodium Selenite Supplementation on Glucose Intolerance and Pancreatic Oxidative Stress in Type 2 Diabetic Mice under Different Selenium Status

Shimizu

Ueno

Okuno

et al. 2009

JOURNAL OF HEALTH SCIENCE

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The objective of this study was to investigate the effect of various selenium (Se) status on glucose intolerance and pancreatic oxidative stress or the defense systems in Nagoya-Shibata-Yasuda (NSY) mice as the animal model for type 2 diabetes mellitus. To let the mice become Se-insufficient to Se-sufficient conditions, the NSY mice were given normal or Se-deficient diet with 0-7.0 mg/l Na 2 SeO 3 -containing drinking water for 6, 8 or 12 weeks. In NSY mice ingested normal diet, levels of blood glucose and plasma insulin after intraperitoneal glucose tolerance test (IPGTT) were not significantly affected by Na 2 SeO 3 -supplementation. In Se-deficient diet-treatment groups, however, the supplementation resulted in the decrease of blood glucose and the increase of plasma insulin after IPGTT. Although glutathione peroxidase (GPX) 1 activity in pancreas of the NSY mice ingested Se-deficient diet was augmented by Na 2 SeO 3 -supplementation, pancreatic glutathione was depressed by the supplementation, accompanying by the increase of 2-thiobarbituric acid-reactive substances. These results indicated that although the supplemented Na 2 SeO 3 may not protect against oxidative stress in the pancreas of NSY mice under Se-insufficient condition, the Se compound improved glucose intolerance of the mice.

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“…Dietary Se is involved in immunoregulation, such as preventing excessive responses and chronic inflammation [11,12]. Deficiency in dietary Se induces decreased relative weight, lesions, and apoptosis of the chicken's bursa of Fabricius [22]. It has been reported that Se deficiency inhibits the growth of immune organs and decreases immune function, causing many inflammatory diseases [23].…”

Section: Discussionmentioning

confidence: 99%

Selenium Deficiency-Induced Inflammation and Increased Expression of Regulating Inflammatory Cytokines in the Chicken Gastrointestinal Tract

Gao

Zhang

Xing

et al. 2016

Biol Trace Elem Res

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Selenium (Se), a nutritionally essential trace element, plays an important role in various aspects of health for a wide range of species, including birds. Se deficiency inhibits the growth of immune organs and decreases immune function, leading to many inflammatory diseases. The present study determined the effects and mechanism of dietary Se deficiency on gastrointestinal tract tissue inflammation. The histopathological changes showed that Se deficiency induced inflammatory lesions in the gastrointestinal tract tissues (glandular stomach, gizzard, duodenum, small intestine, and rectum). The expression levels of PTGE (prostagland E synthase), COX-2 (cyclooxygenase-2), TNF-α (tumor necrosis factor α), and NF-κB (nuclear transfer factor κB) in the gastrointestinal tract tissues (glandular stomach, gizzard, duodenum, small intestine, and rectum) were determined by qPCR on days 15, 25, 35, 45, and 55, respectively. The results showed that Se deficiency induced high expression levels of PTGE, COX-2, TNF-α, and NF-κB in the gastrointestinal tract tissues. The effects were more obvious in the duodenum and small intestine than those in the glandular stomach, gizzard, and rectum. In addition, the expression levels of these proteins in the gastrointestinal tract tissue increased in a time-dependent manner with Se deficiency feeding time. Furthermore, Se deficiency induced the production of pro-inflammatory factors, thus aggravating inflammatory lesions in the gastrointestinal tract. The effect of Se deficiency on inflammation and other gastrointestinal tract diseases should be further studied.

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Effects of selenium status and supplementary seleno-chemical sources on mouse T-cell mitogenesis

Cited by 21 publications

References 43 publications

Selenium Regulates Gene Expression of Selenoprotein W in Chicken Gastrointestinal Tract

Selenium Regulates Gene Expression of Selenoprotein W in Chicken Gastrointestinal Tract

Effect of Sodium Selenite Supplementation on Glucose Intolerance and Pancreatic Oxidative Stress in Type 2 Diabetic Mice under Different Selenium Status

Selenium Deficiency-Induced Inflammation and Increased Expression of Regulating Inflammatory Cytokines in the Chicken Gastrointestinal Tract

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