An in vivo and in vitro study of selenium deficiency and infection in rats

Boyne, R.; Arthur, John R.; Wilson, Anand Babu

doi:10.1016/0021-9975(86)90033-2

Cited by 25 publications

(7 citation statements)

References 9 publications

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“…Thus, a relatively narrow range of selenium concentrations must be maintained for optimal function of the immune system. 2,3,7,12,13,16,21,25,27,29,30,32 This study and results of a field investigation failed to clarify the association between subclinical selenium toxicosis and abortion/perinatal mortality. However, data from a limited number of animals suggest that current values indicative of perinatal selenium toxicosis (Ն3 ppm) may underestimate the resistance of animals to chronic selenium toxicosis and that marked elevations in hepatic selenium concentration (Ͼ9 ppm) may be clinically relevant.…”

Section: Discussionmentioning

confidence: 76%

The Effect of Subclinical Selenium Toxicosis on Pregnant Beef Cattle

et al. 1998

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Abstract. A field investigation conducted by the South Dakota Animal Disease Research and DiagnosticLaboratory suggested that subclinical selenium toxicosis in pregnant cows may have contributed to an outbreak of aborted/stillborn calves in a high-selenium region of South Dakota. This study was undertaken to evaluate the relationship between abortion and subclinical selenium toxicosis in the dam and to assess the effects of subclinical selenium toxicosis on the bovine immune system. Fifteen pregnant cows were fed diets containing 0.25 (control), 6.0, and 12.0 ppm selenium beginning at 80-110 days gestation. Although selenium toxicosis has been reported to cause abortion, this study failed to reproduce abortions. A single cow in the 12-ppm selenium treatment group gave birth to a weak calf, which subsequently died. This calf had myocardial lesions consistent with those described for selenium toxicosis and had hepatic selenium levels of 9.68 ppm (wet weight). Elevated dietary selenium resulted in the depression of several leukocyte function parameters in pregnant cows. A statistically significant depression in forced antibody response was identified in both selenium-supplemented groups. A significantly diminished mitogenic response to concanavalin A and pokeweed mitogen was also observed in the 12-ppm selenium group. Although a similar pattern of depression was also observed with phytohemagglutinin, differences were not significant. These findings indicate that even in the absence of clinical alkali disease, elevated selenium levels may adversely affect both pregnancy outcome and the bovine immune system.

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Section: Discussionmentioning

confidence: 76%

The Effect of Subclinical Selenium Toxicosis on Pregnant Beef Cattle

et al. 1998

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“…2B) Sec and Selenoprotein GPx1-On the basis of studies in selenium-deficient animals, it was expected that Trsp deletion in myelomonocytic cells might interfere with the phagocytic function of neutrophils and macrophages (34) and the biosynthesis of leukotriene B 4 by macrophages (35). We found that Trsp fl/del mice carrying the LysM-Cre gene (thereby presumably null mutants in myelomonocytic lineages) displayed no obvious phenotypic abnormalities under pathogen-free conditions.…”

Section: Deletion Of Trsp In Peritoneal Macrophages and Effect On Trnamentioning

confidence: 79%

Deletion of the Selenocysteine tRNA Gene in Macrophages and Liver Results in Compensatory Gene Induction of Cytoprotective Enzymes by Nrf2

Suzuki

Kelly

Motohashi

et al. 2008

Journal of Biological Chemistry

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The selenocysteine tRNA (tRNA Sec ) molecule is the sight of synthesis for the amino acid selenocysteine and the adaptor for its translational insertion into selenoprotein enzymes, the majority of which contribute to cellular redox homeostasis. To examine the consequences of selenoprotein depletion on the oxidative environment of the cell, we generated a conditional knock-out mouse for the tRNA Sec gene (Trsp). Deletion of Trsp in either macrophages or liver elevated oxidative stress and activated the transcriptional induction of cytoprotective antioxidant and detoxification enzyme genes, including glutathione S-transferase P1 and NAD(P)H:quinone oxidoreductase 1, and other well known target genes of the transcription factor Nrf2 (NF-E2-related factor 2). Simultaneous disruption of Trsp and Nrf2 severely compromised the cytoprotective response. Double knock-out macrophages displayed reduced viability, elevated oxidative stress, and increased susceptible to hydrogen peroxide treatment compared with deletion of either gene alone. Mice carrying a liver-specific deletion of Trsp on an Nrf2-null background experienced hepatocellular apoptosis and displayed a severely reduced survival rate compared with loss of Trsp alone. Our results thus demonstrate that reduced selenoprotein activity is counterbalanced by an Nrf2-mediated cytoprotective response, which is essential for maintaining cellular redox homeostasis and viability.

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“…Selenium (Se) deficiency has important pathological sequelae in both animals and in man. Animals deficient in the trace nutrient may exhibit poor growth, impaired neutrophil function and increased susceptibility to infection [1][2][3]. In the presence of concurrent vitamin E deficiency, animals may develop liver necrosis or myopathy [4,5].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of hepatic deiodination of thyroxine is caused by selenium deficiency in rats

Beckett

Beddows

Morrice

et al. 1987

Biochemical Journal

166

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Selenium (Se) deficiency produced up to a 14-fold decrease in hepatic tri-iodothyronine (T3) production from thyroxine (T4) in vitro. The T3 production rate could not be restored by the addition of a variety of cofactors, nor by the addition of control homogenate. The impairment in hepatic T3 production observed in Se deficiency was reflected in the concentrations of thyroid hormones circulating in plasma, T4 being increased approx. 40% and T3 being decreased by 30%. However, the fall in plasma T3 concentrations was smaller than might be expected in view of the marked decreased in T3 production. Se deficiency had no measurable effect on plasma reverse-tri-iodothyronine concentrations. The data suggest that Se deficiency produces an inhibition of both 5- and 5'-deiodination, consistent with the widely held view that these reactions are catalysed by the same enzyme complex. The mechanism of inhibition appears not be mediated by changes in thiol levels, but a direct role of Se in the activity of the deiodinase complex cannot be excluded.

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An in vivo and in vitro study of selenium deficiency and infection in rats

Cited by 25 publications

References 9 publications

The Effect of Subclinical Selenium Toxicosis on Pregnant Beef Cattle

The Effect of Subclinical Selenium Toxicosis on Pregnant Beef Cattle

Deletion of the Selenocysteine tRNA Gene in Macrophages and Liver Results in Compensatory Gene Induction of Cytoprotective Enzymes by Nrf2

Inhibition of hepatic deiodination of thyroxine is caused by selenium deficiency in rats

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