Comparative Metabolism and Biochemistry of Selenium and Sulfur

Shamberger, Raymond J.

doi:10.1007/978-1-4684-4313-4_4

Cited by 7 publications

(5 citation statements)

References 150 publications

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“…Metabolism of sulfur and selenium has much in common. When selenium is available in excess, it incorporates in amino acids and/or proteins replacing sulfur (16). Several cells such as the mammotrophs and the somatotrophs include sulfur-containing proteins in their secretory granules (17,18).…”

Section: Discussionmentioning

confidence: 99%

Evidence that Selenium Induces Growth Retardation through Reduced Growth Hormone and Somatomedin C Production*

1987

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Growth retardation has long been known to be a major characteristic in selenium-intoxicated animals. As selenium is known to accumulate in the anterior pituitary, especially in the secretory granules of the somatotroph, we have investigated the GH secretion after GH-releasing factor 40 stimulation and the somatomedin C secretion in young male rats exposed to 15 mg sodium selenite/liter drinking water. The immediate output to 900 +/- 120 ng/ml GH in control animals was reduced to 200 +/- 69.4 ng/ml in selenium-treated animals. The somatomedin C level was reduced from 720 +/- 16 ng/ml in control to 119 +/- 17 ng/ml in selenium-treated animals. Both differences were highly significant. These findings suggest that growth retardation in selenium-treated rats could be mediated by reduced GH and somatomedin C production.

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Section: Discussionmentioning

confidence: 99%

Evidence that Selenium Induces Growth Retardation through Reduced Growth Hormone and Somatomedin C Production*

1987

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“…1982;Kiffney & Knight 1990). Selenium toxicity can be explained in a number of ways, for example the immediate inhibition of photosynthesis (Shrift 1967), blockage of biosynthesis of chlorophyll (Kiffney & Knight 1990), substitution of sulfur during the synthesis of cystine and methionine with the formation of dysfunctional and even hazardous polypeptides (Stadtman 1979;Shamberger 1983) or by interference with phosphorus uptake (Moede et at. 1980).…”

Section: Discussionmentioning

confidence: 99%

Effect of selenium on the growth of some selected green and blue‐green algae

Abdelhamid

Skulberg

1995

Lakes & Reservoirs

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An algal assay procedure using microplate technique was carried out to assess the effect of selenium on the growth of some green and blue-green algae. Sodium selenite pentahydrate (NaSeOs.5 HzO) and selendioxide (Sez04) were tested as selenium. The test algae were Selenastrum capricornutum, Scenedesmus obliquus, Chlorella sp., Monoraphidium convolutum, Monoraphidium contortum, Monoraphidium griffithii, Anabaena flos-aquae, Microcystis aeruginosa, and Oscillatoria agardhii. The blue-green algae are toxin-producing strains. Cell number and in vivo chlorophyll fluorescence were the growth parameters of green and blue-green algae respectively. Doseresponse curves quantify the selenium toxicity in terms of EGO. The lowest selenium concentrations giving no detectable growth (EC , , , ) were visually inspected. The test algae showed distinctly different responses to various selenium treatments. Selenium at concentrations < 0.1 mg L-1 stimulates, to varying degrees, the growth of all the green algae with one exception: S. capricornutum was dramatically inhibited at all treatments. 0. agardhii, A. flos-aquae and M. aeruginosa showed marginal growth stimulation up to O.lmg Se L-1, 1.0mg Se L-1 and 3.2 mg Se L-1 respectively. In terms of EGO, the compound selendioxide was more toxic to greens than sodium selenite. The reverse was indicated for the blue-greens. In general, the ECso presented a wide range (0.08-7.2 mg Se L-I), with the lowest values reported for S. obliquus and the highest for M. aeruginosa. All the test algae, except S. obliquus, maintained observable growths at higher selenium levels (ECIOO > 1.0 < 100 mg Se L-I).

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“…It is, however, interesting that selenium apparently also induces an inde¬ pendent inhibition of the SMC production, as the animals in the two selenium-treated groups had very low plasma levels irrespective of hGH treat¬ ment. A possible explanation is an attempted incorporation of selenium instead of sulphur in either SMC or the enzymes responsible for its production, as the metabolisms of selenium and sulphur have much in common (Shamberger 1983b). Another possibility is an oxidation of sulphur groups in these proteins, as selenium is known to exert such a process.…”

Section: Histologymentioning

confidence: 98%

Growth hormone restores normal growth in selenium-treated rats without increase in circulating somatomedin C

Thorlacius‐Ussing

Flyvbjerg²,

Kd³

et al. 1988

Acta Endocrinologica

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Selenium intake (5.0 ppm) induces growth retardation, accumulation of selenium in somatotrophs, lack of growth hormone response to GHRH and an 80 per cent reduction in serum somatomedin C in infant rats. In addition, it induces a slight reduction in serum albumin and occasionally slight central liver necrosis. In order to determine the role of insufficient growth hormone production, the influence of exogenous growth hormone was studied during selenium intake in groups of rats during 25 to 46 days of age (post-weaning). A dosage of human growth hormone (100 \ g=m\ g twice daily) was chosen, this being sufficient to restore normal growth rate and normal serum somatomedin C in hypophysectomized rats of similar age. The weight gain in selenium-treated (3.3 ppm) rats was 46.0 \m=+-\11.7 g (sd)/21 days, whereas in selenium rats given growth hormone it was 66.6 \m=+-\8.9 g (P = 0.01), which was similar to the gain in control rats 72.3 \m=+-\6.9 g. The latter two were less than the weight gain in control rats given growth hormone: 91.5 \m=+-\11.5 g (P = 0.01 and P < 0.01). Serum somatomedin C in untreated rats was 151 \m=+-\66(SD) \g=m\g/l (25 days) increasing to 532 \m=+-\ 91 \ g=m\ g/ l (34 days) and 482 \ m=+-\64 \g=m\g/l(46 days). It did not increase above these levels in control rats given growth hormone. In selenium-treated rats, no increase occurred during growth hormone administration 138 \m=+-\148 \ g=m\ g/ l (34 days) and 185 \m=+-\84 \g=m\g/l(46 days) (P < 0.001 and P < 0.001 vs untreated controls). Furthermore, there was no reduction in serum protein or albumin and no liver necrosis in these selenium-treated rats. As exogenous administration of growth hormone normalizes weight gain, the results indicate that growth retardation is at least partly due to insufficient growth hormone production. The increased growth rate in seleniumtreated and control rats given growth hormone appears to be independent or circulating somatomedin C. This may be a direct effect of growth hormone or, more likely, may be caused by GH stimulation of peripheral (paracrine) formation of growth factors, possibly somatomedin C.

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Comparative Metabolism and Biochemistry of Selenium and Sulfur

Cited by 7 publications

References 150 publications

Evidence that Selenium Induces Growth Retardation through Reduced Growth Hormone and Somatomedin C Production*

Evidence that Selenium Induces Growth Retardation through Reduced Growth Hormone and Somatomedin C Production*

Effect of selenium on the growth of some selected green and blue‐green algae

Growth hormone restores normal growth in selenium-treated rats without increase in circulating somatomedin C

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