Association of sulfate-water and blood thiamine concentration in beef cattle: Field studies

Olkowski, A. A.; Christensen, David A.; Rousseaux, Colin G.

doi:10.4141/cjas91-097

Cited by 18 publications

(11 citation statements)

References 21 publications

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“…Increased thiamine destroying activity [74] and reduced thiamine synthesis [74,75] in rumen-like conditions due to increased dietary sulfate were demonstrated in vitro. These studies suggest that excess dietary S may have detrimental effects on the host's thiamine status and are consistent with observations that feedlot cattle exposed to excess dietary S have reduced blood thiamine level [34,76]. The importance of thiamine in the pathogenesis of S-induced PEM is further evidenced by the findings that thiamine supplementation reduced the incidence of PEM in lambs fed high dietary S [12].…”

Section: Possible Role Of Sulfur-thiamine Interaction In the Developmsupporting

confidence: 88%

A review of polioencephalomalacia in ruminants: is the development of malacic lesions associated with excess sulfur intake independent of thiamine deficiency?

Amat

Olkowski²,

Atila³

et al. 2013

Vet Med Anim Sci

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Polioencephalomalacia (PEM), also known as cerebrocortical necrosis, is an important neurologic disease that affects ruminants. Thiamine deficiency and sulfur (S) toxicity have been well recognized as major etiological factors. The mechanism of thiamine deficiency associated PEM has been well elucidated. However, the role of S in PEM pathogenesis remains unclear, although the relationship between S toxicity and PEM has been established for 3 decades. The development of S-induced malacic lesions is believed to be independent of thiamine deficiency, since blood thiamine levels in affected individuals remain in the range of normal animals. However, cattle affected by S-induced PEM frequently respond to thiamine treatment in early disease stages. Thiamine supplementation is reported to reduce the incidence and severity of S-induced PEM. This suggests a possible metabolic relationship between excess S intake and thiamine in the development of malacic lesions. Such an association is further supported by recent studies reporting that high dietary S may increase the metabolic demand for thiamine pyrophosphate (TPP), a critical cofactor in several metabolic pathways. Systemic failure to synthesize metabolically requisite levels of TPP in the brain may be an important precursor in the pathogenesis of S-induced PEM. There is increasing evidence of the importance of thiamine in the pathogenesis of S-induced PEM. Thus, understanding the potential role of S-thiamine interaction in the development of malacic lesions is important step to determine the mechanism of S-induced PEM. The objective of this article is to provide an overview of thiamine deficiency and S toxicity associated PEM, and to discuss the potential role of S-thiamine interaction in the pathogenesis of S-induced PEM in ruminants.

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Section: Possible Role Of Sulfur-thiamine Interaction In the Developmsupporting

confidence: 88%

A review of polioencephalomalacia in ruminants: is the development of malacic lesions associated with excess sulfur intake independent of thiamine deficiency?

Amat

Olkowski²,

Atila³

et al. 2013

Vet Med Anim Sci

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“…High dietary S can reduce the bioavailability of Se in ruminants (Spears 2003). Adverse effects of dietary S on Se availability and absorption were detected in several studies (Whanger et al 1969;White and Somers 1977;Pope et al 1979). Three-way interactions between Cu, Se and S have also been identified (Van Ryssen et al 1998).…”

Section: Serum Mineral Statusmentioning

confidence: 94%

“…High dietary S, therefore, often results in Cu deficiency in ruminants (Hill 1969;Gooneratne et al 1989). Excess S intake may also reduce ruminal magnesium (Mg) absorption (Ferreira et al 1966;Martens and Blume 1986;Richter et al 2012), decrease selenium (Se) bioavailability (Spears 2003;Pope et al 1979;Ivancic Jr. and Weiss 2001), or interfere with zinc (Zn) status in ruminants (Cammack et al 2010;Gooneratne et al 2011).…”

mentioning

confidence: 99%

“…SulfurÁmineral interactions may be involved in the pathogenesis of PEM lesions in the brain. Three-way interactions between S, Cu and thiamine have been postulated to be involved in the development of malacic lesions (Olkowski et al 1991;Gooneratne et al 2011). A depressed thiamine pyrophosphate (TPP), a metabolically important form of thiamine, was detected in the brain of S-induced PEM affected cattle (Amat et al 2013).…”

mentioning

confidence: 99%

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Evaluation of mineral status in high dietary sulfur exposed or sulfur-induced polioencephalomalacia affected beef cattle

et al. 2014

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Amat, S., McKinnon, J. J., Penner, G. B., Simko, E. and Hendrick, S. 2014. Evaluation of mineral status in high dietary sulfur exposed or sulfur-induced polioencephalomalacia affected beef cattle. Can. J. Anim. Sci. 94: 139–149. We examined the mineral status in beef heifers fed high S containing diets with differing forage-to-concentrate ratio (F:C), and in S-induced polioencephalomalacia (PEM) affected feedlot steers. A metabolism trial was conducted as a randomized complete block design using a 2×2 factorial treatment arrangement with main effects of dietary S and F:C using 16 ruminally cannulated heifers. The F:C was modified by altering the proportion of barley silage (4 vs. 51% dry matter), whereas, the S content was modified by using differing sources of wheat dried distillers’ grains with solubles (WDDGS) to achieve low and high S diets (LS=0.30 vs. HS=0.67%). Minerals including Cu, Co, Fe, Mg, Mn, Mo, Se and Zn were determined from rumen fluid, blood, brain tissue and urine. Urinary mineral excretion was also assed. During the course of the metabolic trial, an outbreak of S-induced PEM in a commercial feedlot was documented and brain minerals of these PEM steers (n=4) were contrasted with the experimental heifers fed HS diet. There were no interactions between dietary S concentration and F:C (P>0.05). Heifers fed HS diet had reduced (P<0.05) mineral intakes (except for Mo), ruminal Co, Fe and Mn, and serum Mg and Fe relative to those fed LS diet. Heifers fed low F:C diet had reduced (P<0.05) Cu, Fe, Mo and Se intakes, greater (P<0.05) ruminal Cu, Fe, Mn and Zn, and reduced (P<0.05) serum Cu and Se, and greater (P<0.05) serum Mg than heifers fed high F:C diet. Brain minerals were not affected (P>0.05) by F:C or dietary S. However, the PEM brains had reduced Cu (P=0.058), Fe (P=0.003) and Mo (P<0.001) relative to normal brains. Dietary S and F:C did alter the mineral status of the heifers, but no deficiencies or PEM were induced.

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“…However, the PEM disorder may be the result of ingesting excess S rather than Se (Beke and Hironaka 1991;Gooneratne et al 1989;Gould et al 1991;Hamlen et al 1993;James eta!. 1994;Olkowski et al 1991;Raisbeck, 1982;Sager et al 1990). …”

Section: Introductionmentioning

confidence: 99%

Absorption of Excess Selenium and Sulfur by Plants and Animals

Mayland¹

1995

ASMR

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High concentrations of selenium (Se) and sulfur (S) often occur in over-burden soils and underlying shales associated with western coal mining areas. Knowing the ·role of Se and S in the soil-plant-animal system is important for proper management of mine spoil reclamation. This paper will discuss recent findings about Se and S forms in soil, their absorption and accumulation by plants, and their subsequent toxicity to grazing animals. Selenium absorbed by the accumulating plants is generally metabolized to non-protein forms, while that absorbed by the non-accumulating plants occurs predominantly as selenomethionine. Selenomethionine is readily absorbed by animals. In animals, both acute and chronic forms of selenosis are known. Death occurs when a large dose of highly-available Se is ingested. One chronic form includes symptoms of inappetence, hair loss, hardening and extension of nails and hooves, reduced weight gains, and poor reproductive performance. Beath and Rosenfield identified "blind staggers" as another form of selenosis, but this disorder; more appropriately called polioencephalomalcia (PEM), occurred only in ruminants. However; the historical association of selenosis to blind staggers has been questioned. Recent experimental evidence has shown that PEM is likely caused by excess SO,. Cases of this disorder have been documented in the USA and Canada when ruminants have high S intake from herbage and/or drinking water. Western mine reclamation decisions should consider the potential for not only excess Se, but also excess SO 4 in water, soil, and plants.Additional

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Association of sulfate-water and blood thiamine concentration in beef cattle: Field studies

Cited by 18 publications

References 21 publications

A review of polioencephalomalacia in ruminants: is the development of malacic lesions associated with excess sulfur intake independent of thiamine deficiency?

A review of polioencephalomalacia in ruminants: is the development of malacic lesions associated with excess sulfur intake independent of thiamine deficiency?

Evaluation of mineral status in high dietary sulfur exposed or sulfur-induced polioencephalomalacia affected beef cattle

Absorption of Excess Selenium and Sulfur by Plants and Animals

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