A New Toxicant Occurring Naturally in Certain Samples of Plant Foodstuffs

Franke, Kurt W.; Tully, W. C.

doi:10.3382/ps.0140273

Cited by 49 publications

(7 citation statements)

References 17 publications

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“…A similar damaging effect was reported by Franke and Tully (1935) and Franke et al (1936) in chickens and by Carlson et al (1951) in turkeys. Se alone to the diet reduced hatchability and also caused a high percentage of deformed embryos compared to the control (Tables 4, 5 and 6).…”

Section: Fertility and Hatchabilitysupporting

confidence: 86%

A Mutual Protective Effect of Mercury and Selenium in Japanese Quail

1977

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Dietary interactions between methylmercury (Ch3Hg) and sodium selenite (Na2SeO3) were studied in Japanese quail. Addition of 0.35-6 p.p.m. Se to diets containing toxic levels of Hg (5-30 p.p.m. Hg) reduced the toxicity of methylmercury and increased the survival of Japanese quail. The survival increased with increasing levels of Se in the diet. Selenium as 6 p.p.m. did not cause any mortality in males and caused only relatively low mortality in females. However, 12 p.p.m. Se depressed the survival of quail, especially females. No consistent effect of Hg, Se or both was observed on body weight or feed consumption. High levels of Hg reduced egg production, fertility and hatchability, and the addition of Se lessened these effects of Hg. Selenium in the diet alone (6 or 12 p.p.m.) generally produced lower hatchability and a high percentage of deformed embryos, and 12 p.p.m. Se also depressed egg production. Addition of 5-15 p.p.m. Hg to such Se diets overcame these effects and reduced the percentage of abnormal embryos more than 50%. Analysis of tissues for total Hg showed that Hg was distributed in a pattern typical for alkyl mercurials. Hg levels in Se-protected birds equaled or exceeded the levels in those fed Hg without Se. Se levels in tissues were generally elevated by feeding Hg, especially in brain. Extremely high brain Hg levels, up to 58 p.p.m., were observed in birds fed 15 p.p.m. Hg plus 6 p.p.m. Se for 20 weeks prior to sacrifice. The levels of Se in the brain of these birds was elevated (4 p.p.m.), but not equimolar to Hg.

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Section: Fertility and Hatchabilitysupporting

confidence: 86%

A Mutual Protective Effect of Mercury and Selenium in Japanese Quail

1977

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“…Historically, reproductive problems have been associated with excess selenium since the 1930s when chickens that consumed grain grown on seleniferous soil had poor hatching success and embryos exhibited multiple malformations of the extremities (Franke and Tully, 1935). However, until recently there has been virtually no documenta- tion on the effects of excess selenium intake by natural populations of wild aquatic birds.…”

Section: Introductionmentioning

confidence: 99%

Embryotoxic and teratogenic effects of selenium in the diet of mallards

Hoffman¹,

Heinz²

1988

Journal of Toxicology and Environmental Health

116

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Mallards (Anas platyrhynchos) were fed a control diet, diets containing 1, 5, 10, or 25 ppm Se as sodium selenite, or a diet containing 10 ppm Se as seleno-DL-methionine in the first of two experiments. Selenium at 10 ppm as selenomethionine or 25 ppm as sodium selenite caused a 40-44% decrease in the total number of eggs that hatched compared to controls. Selenium at 25 ppm (sodium selenite) resulted in a 19% decrease in mean embryonic weight at 18 d of incubation, accompanied by a 6% decrease in crown-rump length. Ten parts per million Se as selenomethionine was more teratogenic than sodium selenite at 25 ppm. Selenomethionine (10 ppm Se) resulted in an incidence of 13.1% malformations that were often multiple, whereas sodium selenite (10 and 25 ppm Se) resulted in 3.6 and 4.2% malformations. The teratogenicity of selenomethionine was confirmed in a second experiment in which mallards received 1, 2, 4, 8, or 16 ppm Se as selenomethionine, resulting in 0.9, 0.5, 1.4, 6.8, and 67.9% malformations, respectively. These malformations included hydrocephaly, microphthalmia, lower bill defects, and foot defects with ectrodactyly. Both forms of selenium increased the incidence of edema and stunted embryonic growth. Selenomethionine (10 ppm Se) resulted in a significant increase of approximately 40% in plasma glutathione peroxidase activity and a 70% increase in sorbitol dehydrogenase activity (indicative of hepatotoxicity) in hatchlings. Sodium selenite (25 ppm Se) resulted in fourfold elevation in plasma uric acid concentration, indicative of renal alteration. Selenomethionine accumulated much better in eggs than did sodium selenite. These findings indicate that selenomethionine is considerably more teratogenic and generally more embryotoxic than sodium selenite, probably due to higher uptake of selenomethionine.

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“…The toxic effects of selenium were first described in South Dakota (USA), where chickens (Gallus domesticus) were observed to have poor reproductive success as a result of chick teratogenesis and mortality when fed grains from specific sources [1]. Subsequent studies identified elevated selenium content in the grains as the cause of the observed effects [2].…”

Section: Introductionmentioning

confidence: 99%

Analysis of Field and Laboratory Data to Derive Selenium Toxicity Thresholds for Birds

Adams¹,

Brix²,

Edwards³

et al. 2003

Environ Toxicol Chem

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In this paper, we critically evaluate the statistical approaches and datasets previously used to derive chronic egg selenium thresholds for mallard ducks (laboratory data) and black-necked stilts (field data). These effect concentration thresholds of 3%, 10% (EC10), or 20% have been used by regulatory agencies to set avian protection criteria and site remediation goals, thus the need for careful assessment of the data. The present review indicates that the stilt field dataset used to establish a frequently cited chronic avian egg selenium threshold of 6 mg/kg dry weight lacks statistical robustness (r2 = 0.19-0.28 based on generalized linear models), suggesting that stilt embryo sensitivity to selenium is highly variable or that factors other than selenium are principally responsible for the increase in effects observed at the lower range of this dataset. Hockey stick regressions used with the stilt field dataset improve the statistical relationship (r2 = 0.90-0.97) but result in considerably higher egg selenium thresholds (EC10 = 21-31 mg/kg dry wt). Laboratory-derived (for mallards) and field-derived (for stilts) teratogenicity EC10 values are quite similar (16-24 mg/kg dry wt). Laboratory data regarding mallard egg inviability and duckling mortality data provide the most sensitive and statistically robust chronic threshold (EC10) with logit, probit, and hockey stick regressions fitted to laboratory data, resulting in mean egg selenium EC10 values of 12 to 15 mg/kg dry weight (r2 = 0.75-0.90).

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A New Toxicant Occurring Naturally in Certain Samples of Plant Foodstuffs

Cited by 49 publications

References 17 publications

A Mutual Protective Effect of Mercury and Selenium in Japanese Quail

A Mutual Protective Effect of Mercury and Selenium in Japanese Quail

Embryotoxic and teratogenic effects of selenium in the diet of mallards

Analysis of Field and Laboratory Data to Derive Selenium Toxicity Thresholds for Birds

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