Growth of Steers on Seleniferous Range

Moxon, A. L.; Rhian, Morris; Anderson, H. D.; Olson, O. E.

doi:10.2527/jas1944.33299x

Cited by 36 publications

(11 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…34,35,38,39,60 The distinctive histological changes that developed in hooves, particularly in stratum medium, may account for the dystrophic digital lesions in selenosis. These lesions were accompanied by mild to marked hyperplasia and parakeratosis in laminar epithelium and, to a lesser extent, in coronary epidermis and loss of the normal abrupt transition between stratum spinosum and stratum comeum.…”

Section: Discussionmentioning

confidence: 99%

“…3,11, [33][34][35]39 The Na-ly circulated popular accounts of naturally induced seltional Academy of Sciences estimated the chronic, di-enosis describe heavy losses in livestock and native etary no-effect level at 4 ppm. 50 Remarkably, although ruminants in the American West and draw heavily on alkali disease ("the alkali," "bob tail disease") was these early clinicopathological studies.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Pathology of Experimentally Induced Chronic Selenosis (Alkali Disease) in Yearling Cattle

O’Toole¹,

Raisbeck²

1995

J VET Diagn Invest

View full text Add to dashboard Cite

Abstract. Prolonged oral exposure of cattle to elevated dietary selenium (Se) in forage and seleniferous plants in seleniferous areas of the western United States is associated historically with 2 clinical syndromes: alkali disease and "blind staggers." The potential for Se-induced disease in cattle and other species is considerable in areas with seleniferous shales, Se-accumulating plants, arid climates, and alkaline soils. These 2 Se-associated conditions were defined in the 1930s and 1940s, and the nosology of blind staggers is questionable. Seventeen yearling steers fed 0.15, 0.28, and 0.8 mg Se/kg body weight as selenomethionine or selenite for 120 days were euthanized and examined postmortem. Significant lesions were confined to 4 steers in the medium-and highdose selenomethionine group and to 1 steer in the high-dose selenite group. Grossly, dystrophic hoof lesions developed in 2 steers, 1 of which had extensive separation of horn from lamellar and coronary epidermis and also lost hair from the tail switch. Histologically, tubules in the stratum medium of hooves from these 5 steers were replaced by islands of parakeratotic cellular debris, separated by more normal hoof matrix. Two of the 5 steers also had hyperplasia, acanthosis, parakeratosis, and disorganized germinal epithelium of varying severity in hoof epithelium, particularly at the tips of epidermal lamellae. These changes may distinguish the hoof lesions of chronic selenosis from those of chronic laminitis in cattle, in which dermal (chorial) changes predominate. In skin from the distal part of the tail of the animal that lost its switch, most follicles were atrophic and devoid of hairshafts and displayed dyskeratosis and mild superficial follicular keratosis. No significant lesions developed in tissues other than integument. Autometallographic staining for catalytic Se bonds in various tissues, including skin, liver, and kidney, revealed no positive staining of hair shafts; the correlation between stain intensity and dose group was poor. These findings indicate that dietary exposure for 4 months to 0.28 and 0.8 mg Se/kg in the form of selenomethionine and to 0.8 mg Se/kg in the form of sodium selenite reproduces in some cattle mild (subclinical) to severe (clinical) forms of alkali disease. No significant neurological, renal, or hepatic lesions developed, supporting the contention that blind staggers is caused by factors other than excessive dietary selenium.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Pathology of Experimentally Induced Chronic Selenosis (Alkali Disease) in Yearling Cattle

O’Toole¹,

Raisbeck²

1995

J VET Diagn Invest

View full text Add to dashboard Cite

show abstract

“…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

View full text Add to dashboard Cite

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.

show abstract

“…Toxicity alleviation was observed in all trials even though gains were not always stimulated. Moxon et (1944) had previously observed that steers consuming hay with up to 5.6 ppm selenium and pastures up to 13.0 ppm selenium gained more rapidly and had fewer incidences of selenium poisoning when allowed access to a salt mixture containing 25 ppm ar senic as sodium arsenite.…”

Section: Factors Influencing Poisoning and Chronic Selenosismentioning

confidence: 99%

Selenium and sulfur nutrition of beef cattle

Shively

View full text Add to dashboard Cite

Growth of Steers on Seleniferous Range

Cited by 36 publications

References 4 publications

Pathology of Experimentally Induced Chronic Selenosis (Alkali Disease) in Yearling Cattle

Pathology of Experimentally Induced Chronic Selenosis (Alkali Disease) in Yearling Cattle

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

Selenium and sulfur nutrition of beef cattle

Contact Info

Product

Resources

About