Dietary Selenium and Arsenic Additions to Diets for Chickens Over a Life Cycle

Thapar, Nirwan Tilak; Guenthner, E.; Carlson, C. W.; Olson, O. E.

doi:10.3382/ps.0481988

Cited by 27 publications

(8 citation statements)

References 7 publications

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“…Studies with sodium selenite in the diet also demonstrated reduced hatchability in chickens receiving 5-8 ppm Se (Thapar et al, 1969;Arnold et al, 1972;Ort and Latshaw, 1978) and in Japanese quail {Coturnix japonica) with 6-12 ppm (El-Begearmi et al, 1977). However, in the above studies, selenium as sodium selenite did not appear to be highly teratogenic in the diet of chickens.…”

Section: Introductionmentioning

confidence: 60%

“…Multiple malformations of the extremities have been reported in chickens following dietary exposure of 5-15 ppm Se from naturally occurring seleniferous grains containing Se probably as selenomethionine (Poley et al, 1937;Poley and Moxon, 1938). Studies that examined the effects of sodium selenite in the diet of chickens revealed embryotoxicity and poor hatching success without a high level of teratogenicity (Thapar et al, 1969;Arnold et al, 1972;Ort and Latshaw, 1978). However, egg injections of sodium selenite were reported to cause malformations similar to those caused by selenomethionine (summarized by Olson, 1986), which also included thinning of the ventricular walls of the heart (Khan and Gilani, 1980), as well as gastroschisis (Sukra et al, 1976).…”

Section: Discussionmentioning

confidence: 97%

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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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Section: Introductionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 97%

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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“…Se failed to improve production. Earlier studies reported by Thapar et al (1969) did not show increases in egg production due to addition of selenium to either a practical or a purified diet given over a life cycle. The lack of an effect could have been due to the fact that the purified diet used in these experiments contained an average of 0.08 p.p.m.…”

Section: Results From Experiments Ib Presented Inmentioning

confidence: 89%

“…Selenium analyses of diets and egg samples were performed according to the method of Olson (1969). Egg samples were prepared by homogenizing the liquid contents of all eggs pooled within a replicate.…”

Section: Methodsmentioning

confidence: 99%

The Effect of Selenium in the Hen’s Diet on Egg Production, Hatchability, Performance of Progeny and Selenium Concentration in Eggs

Cantor

Scott

1974

Poultry Science

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Studies were conducted on the effects of supplemental selenium upon the performance of S.C.W.L. hens raised from hatching on selenium-low, semipurified diets (0.02 p.p.m. Se) containing adequate vitamin E. In hens continued on a Se-low laying diet, supplements of 0.015 p.p.m. Se and 0.030 p.p.m. Se as NajSeOj significantly increased egg production and hatchability. The Se concentration in the eggs was approximately equal to the dietary Se level throughout a 13 week period. When fed a selenium-low chick starter diet, offspring of the hens receiving 0.030 p.p.m. Se showed improved growth, but no protection against exudative diathesis and no improvement in hepatic glutathione peroxidase activity.When selenium-depleted hens were fed a low selenium (0.027 p.p.m.) practical diet, supplementation of 0.1 p.p.m. Se as selenomethionine significantly increased egg production. Hatchability of fertile eggs from the unsupplemented group fell to 42% after 6 weeks, while the values for the hens receiving either selenite or selenomethionine (0.1 p.p.m. Se) remained at approximately 90%. By 20 weeks, the hens receiving 0.1 p.p.m. Seas Na 2 Se0 3 showed improved egg production as compared to those on the basal diet, and hatchability fell below 10% for the unsupplemented group but remained at 90% for the group receiving Se. The concentration of Se in eggs from hens fed the basal diet alone and supplemented with 0.1 p.p.m. as selenite and selenomethionine was 0.026, 0.121 and 0.124 p.p.m., respectively, after 3 weeks. After 15 weeks eggs from hens fed the basal diet alone and supplemented with 0.1 p.p.m. Se as selenite contained 0.035 and 0.138 p.p.m. Se, respectively. Both supplements of NajSeOj and selenomethionine delayed the onset of symptoms of exudative diathesis. The results indicate a nutritional requirement for selenium for normal hatchability, egg production and performance of progeny.

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“…Later, studies with human malignant melanoma cells demonstrated that arsenite-induced apoptosis is prevented by selenite [32]. A Human cells As-induced apoptosis is prevented by Se [32] A Mice As prevents carcinogenic effect of Se [30] A Rats As prevents carcinogenic effect of Se [31] A Rats As protects against the toxicity of Se (growth, mortality rate, pathological condition of the liver) [20,33,186] A Rats As induces mucosal glutathione synthesis, explaining its protective effect against Se [187] A Dogs As antagonizes Se-induced subnormal growth and restricted food intake [35] A Cattle As protects against Se toxicity [36] A Hogs As protects against Se toxicity [ Se prolongs the half-lives of Hg-exposed animals [190] A Rats Se changes the subcellular Hg distribution [191] S Oysters High levels of Se increase Hg toxicity [192] SeO 3 2− /MeHg + A Chickens Se changes the subcellular and pattern distribution of Hg [193] A Medaka fish Se protects against Hg-induced histopathological changes [151] SeO 2 /Hg 2+ A Chicks Se toxicity is decreased by Hg [194] SeO 4 2− /MeHg + A Mice Se protects against Hg-induced neurotoxicity [63] Protective effects of arsenic in rats [19,20,23,33,34], dogs [35], cattle [36], mice [37], hogs [38], steers [39], mallards [40] and poultry [41][42][43] have been observed/proposed. Several studies apparently suggest that the same interaction can occur in humans [44][45][46]…”

Section: Arsenic and Seleniummentioning

confidence: 99%

Biological responses related to agonistic, antagonistic and synergistic interactions of chemical species

et al. 2012

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The fact that the essential or toxic character of elements is species specific has encouraged the development of analytical strategies for chemical speciation over the last twenty years; indeed, there are now a great number of them that provide very good performance. However, biological systems are exposed to a complex environment in which species of elements can interact in a synergistic/antagonistic fashion. Thus, the metabolism of trace elements cannot be considered in isolation. On the other hand, biological systems are dynamic, so it is necessary to study the trafficking of species of elements between organs, tissues or cell compartments in order to decipher the biochemical processes of the interactions in which they are involved. Although the application of liquid chromatography-inductively coupled plasma-based "metallomics" methods in combination with organic mass spectrometry can provide much-needed insight, new analytical strategies are required to really understand the role of species of elements in biological systems and the mechanisms of their interactions. In the present paper, the interactions of the most widely studied elements in this context (Se, Hg and As) are discussed, as well as other important interactions between different elements.

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Dietary Selenium and Arsenic Additions to Diets for Chickens Over a Life Cycle

Cited by 27 publications

References 7 publications

Embryotoxic and teratogenic effects of selenium in the diet of mallards

Embryotoxic and teratogenic effects of selenium in the diet of mallards

The Effect of Selenium in the Hen’s Diet on Egg Production, Hatchability, Performance of Progeny and Selenium Concentration in Eggs

Biological responses related to agonistic, antagonistic and synergistic interactions of chemical species

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