Sulfur

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Sulfur is an essential nutrient (micro-mineral). It is a nonmetallic element that is essential for life. In most animals it represents about 0.25% of the body weight. However, sulfur is normally present as part of larger compounds, and the requirement for pure sulfur has not been determined for most species. In recent years, sulfur toxicity has become more common because of its high concentration in many byproduct feeds. The use of these feeds in ruminant diets is increasing, which in turn may increase the trace mineral requirement. The purpose of this article is to review our current understanding of sulfur nutrition and to look at how sulfur level in the diet may influence the copper requirement.

Essential Functions

Compounds containing sulfur play a variety of essential functions in the body. They act as structural entities (collagen), as catalysts (enzymes), as oxygen carriers (hemoglobin), as hormones (insulin), and as vitamins (thiamine and biotin). Sulfur is present in four amino acids: methionine, cystine, cysteine and taurine. The secondary structure of many proteins is determined by the cross linkage or folding due to covalent disulfide bonds between amino acids.

Sulfur is the element that gives many key compounds their unique functional properties. For example, acetate is linked to coenzyme A by a thioester linkage to form acetyl coenzyme A. This compound is required for the formation of key metabolic intermediates such as citrate, acetoacetate and malonate. The sulfur in thiamine allows it to serve as a molecule which transfers carbonyl groups. Thiamine plays a key role in the formation of pentose sugars which are required for ribonucleic acids synthesis and photosynthesis. Biotin, another sulfur-containing B vitamin, acts a carrier for carbon dioxide in carboxylation reactions.

Inorganic vs. Organic Sulfur

Despite the fact that sulfur is a key mineral in many compounds essential for life, dietary inorganic sulfur is not necessary for the health of most animals. Pigs and poultry can do quite well with only organic sulfur (sulfur amino acids, thiamine, biotin, etc.) sources in their diets. The total absence of inorganic sulfur from the diet may increase the sulfur-amino acid requirement, which suggest that sulfur from the amino acids is used to synthesize other organic compounds containing sulfur.

In contrast, ruminants may respond to inorganic sulfur supplementation, especially if the diet is high in nonprotein nitrogen. Block et al., (1951) showed that ruminal microorganism are capable of synthesizing all organic sulfur containing compounds essential for life from inorganic sulfur. When urea or other nonprotein nitrogen sources are fed, the diet may become deficient in sulfur. Goodrich et. al., (1978) reported that the nitrogen to sulfur ratio in rumen microbial protein averages 14.5:1. The common recommendation for the nitrogen:sulfur ratio is 10:1 in diets containing high levels of urea.

Sulfur Source

The source of sulfur can influence its bioavailability. Goodrich et. al,. (1978) gave the following rankings from the most available to the least available: L-methionine> calcium sulfate >ammonium sulfate> sodium sulfate>molasses sulfur>sodium sulfide>lignin sulfonate>elemental sulfur. The recommend concentration of sulfur in beef cattle diets is 0.15% (NRC, 1996). However, this assumes the sulfur source is highly bioavailable.

The type of forage in the diet may also influence sulfur requirement. For example, Archer and Wheeler, (1978) showed that increasing the sulfur concentration from 0.08% to 0.12% in cattle grazing sorghum sudangrass increased weight gains by 12%. Sulfur requirements may be higher for cattle grazing sorghum sudangrass because sulfur is required in the detoxification of the cyanogenic glucosides found in most sorghum forages. Sulfur bioavailability varies with the type of forage; fescue has a lower sulfur availability than other grasses. Cattle consuming fescue hay will often respond with improved intake and fiber digestion following sulfur supplementation. Forages usually contain between 0.1-0.3% sulfur, except for corn silage which is often lower. The following list shows common feedstuffs and their sulfur concentrations:

Sulfur Concentrations of Feedstuffs

Feed

Sulfur (% of DM)

Feed

Sulfur (% of DM)

Alfalfa hay

0.30

Corn steep liquor

0.70

Barley malt sprouts

0.85

Corn gluten meal

0.90

Beet pulp, dehydrated

0.22

Molasses, beet

0.60

Beet pulp w/ molasses

0.42

Molasses, cane

0.47

Blood meal

0.80

Sorghum grain

0.14

Brewers grains

0.40

Sorghum silage

0.10

Canola meal

1.17

Soybean meal

0.46

Corn, dent

0.14

Sunflower meal

0.33

Corn silage

0.12

Turnip root

0.43

Corn distiller grains

0.44

Wheat midds

0.22

Corn gluten feed

0.47

Whey, dehydrated

1.12

As one analyzes this list of feeds, corn, sorghum grain, and their silages are the only feeds that are below the sulfur requirement. For example, a common diet of 40% corn, 40% corn gluten feed, 10% corn silage, 5% beet molasses and 5% minerals and vitamins would contain approximately 0.30% sulfur. Although this is well below the 0.40% sulfur estimated to be the maximum tolerable concentrations (NRC, 1980), it is high enough for producers to consider if problems arise.

For example, Zinn et al., (1997) reported that when ammonium sulfate was used to produce diets containing 0.15, 0.20 and 0.25% sulfur (DM basis), feedlot performance was reduced with the higher sulfur concentration. The diets were based on steam-flaked corn and fed to heifers weighing 845 pounds initially. Increasing dietary sulfur above 0.20%, caused a strong trend (P <.10) for decreased gains, feed intake and gain per unit of feed intake. The excess sulfur also caused a reduction (P <.05) in the ribeye area which is an important factor determining the yield grade of the carcass. Sulfur intake from the drinking water was not reported.

PEM

Another problem that can occur when high dietary sulfur leads to the production of excess sulfides in the rumen is polioencephalomalacia, or PEM (Gould et al., 1991; Lowe et al., 1996). The most defining sign of PEM is the necrosis of the cerebrocortical region of the brain. Animals with PEM will often press their head against a wall or post. In some instances they become "star gazers," where they stand with their head back over their shoulders looking up at the sky. If not treated with thiamine, most animals with PEM will die within 48 hours.

A thiamine deficiency has been considered the most common cause of PEM in ruminants. However, recent research suggests that sulfur may play a key role in many instances of PEM. PEM has often been seen in animals that have had access to plants containing high amounts of thiaminase such as bracken fern (Merck, 1991). Thiamine is a B vitamin that plays a key role in the tri-carboxcylic acid cycle and pentose shunt. When thiamine is deficient, key tissues that require large amounts of thiamine, such as the brain and heart, are the first to show lesions.

In ruminants, a rapid change from an all forage to high-concentrate diet can cause PEM. This results from a shift in the bacterial populations in the rumen which can produce thiaminase. The thiaminase breaks down thiamine producing an analog which inhibits the thiamine-dependent reactions of glycolysis and the tri-carboxcylic acid cycle (Brent and Bartley, 1984).

The exact interaction between dietary sulfur, thiaminase production, and PEM is not understood. Kung et al. (1998) postulated that sulfates in the feed or water are converted to hydrogen sulfide in the rumen. When the hydrogen sulfide is eructated with the other rumen gases, it is inhaled and can damage lung and brain tissues. Several researchers (Oliveria et al., 1996; Brent and Bartley, 1994 and Olkowski, et al., 1992) have suggested that high sulfide levels could cause the brain lesions associated with PEM.

Kung et al., (1998) summarized six different reports in the literature where high sulfur intakes were associated with PEM. In these studies thiamine status was within normal ranges and giving thiamine did not prevent the signs in all cases. In these cases sulfur intakes from feed and water would have ranged from 0.40 to over 0.80% of the diet dry matter.

Drinking Water

Sulfates in the water can be a major source of sulfur intake. For example, in one of the cases cited by Kung et al., (1998), sulfates in the drinking water ranged from 2,200 to 2,800 ppm. When the water sulfur intake was expressed as a percent of the dry matter consumed, it averaged 0.67%. Digesti and Weeth (1976) proposed that the maximum safe concentration of sulfates in drinking water for cattle was 2,500 ppm. Water sulfate concentrations as high as 5,000 ppm have been reported (Veenhuizen et al., 1992).

Accurately estimating water intake in these situations can also be a challenge. Water meters can be used for confined livestock to estimate the average intake, but with grazing animals drinking from ponds or streams, one can only estimate the intake. Usually water consumption will be 3-5 times the dry matter intake. Dry matter intake for grazing beef cattle and sheep will normally be between 1.5 and 2.5% of their body weight. Lactating dairy cows may consume over 3.5% of their body weight when grazing high quality forage. Although this is not a precise means of measuring water sulfur intake, it does allow one to estimate the relative contributions of the feed and water.

Excess Sulfur

Excess sulfur can also impair animal performance by reducing the availability of other minerals. For example, hydrogen sulfide in the rumen binds with molybdenum to form thiomolybdates. Thiomolybdates bind with copper in the rumen to form an insoluble complex. Some thiomolybdates are absorbed and impair the metabolism of copper in the body. For example, Gooneratne et al. (1989) reported that certain thiomolybdates cause copper to be bound to blood albumins which renders the copper unavailable for biochemical reactions in the body. Price et al., (1987) showed that tri- and tetrathiomolybdates were the sulfur-molybdenum complexes responsible for reducing copper absorption, while the di- and trithiomolybdates had the greatest effect on copper metabolism in the body.

Sulfur also reduces copper absorption by the formation of insoluble copper sulfide in the rumen, independent of the formation of thiomolybdates. Rumen protozoa degrade sulfur amino acids to sulfide which binds to copper to form an insoluble complex. Smart et al., (1986) reported that decreasing the sulfate concentration of drinking water from 500 to 42 ppm, improved the copper status of cattle. These same researchers reported that the 10 ppm copper recommended by the Beef NRC (1996) was not adequate when cattle drank high-sulfur water, which resulted in a total dietary sulfur intake of 0.35%.

Copper Supplement

The optimum level of copper supplementation required to combat high sulfur intakes has not been determined. The maximum tolerable level of copper for cattle has been estimated at 100 ppm (NRC 1980). Although this level is being fed in diets that are high in sulfur, certain breeds of dairy cattle such as the Jersey and Guernsey are susceptible to copper toxicity at concentrations below 100 ppm.

In these situations, the source of copper is also important. Although copper sulfate is a common copper source, it would not be recommended if the diet is already high in sulfur. Copper oxide would not contribute to the sulfur problem, but because of its poor availability is not recommended. Copper carbonate is probably the best copper source for this situation. It has a bioavailability similar to copper sulfate, with out increasing sulfur intake.

Salt and Trace Mineral Mix

Copper deficiency is one of the most common nutritional problems seen in cattle today. As the price of high-sulfur byproduct feeds continues to fall relative to other feeds, they will be used at increasing levels in cattle diets. As nutrition professionals we need to be aware of the potential problems and adjust the copper level in the diet accordingly. Properly fortifying the salt and trace mineral mix with highly available copper sources should be the first step in achieving a well balanced diet.

Literature Cited

Archer, K.A., and J.L. Wheeler, 1978. Response of cattle grazing sorghum to salt-sulfur supplements. Aust. J. Exp. Agric. Anim. Husb. 18:741.

Block, R.J., J.A. Stekol, and J.K. Loosli. 1951. Synthesis of sulfur amino acids from inorganic sulfate by ruminants. II. Synthesis of cystine and methionine from sodium sulfate by the goat and the macroorganisms of the rumen of the ewe. Arch. Biochem. Biophys. 33:353.

Brent, B.E. and E.E. Bartley. 1984. Thiamin and niacin in the rumen. J. Anim. Sci. 59:813.

Digesti, R.D. and Weeth. 1976. A defensible maximum for inorganic sulfate in drinking water of cattle. J. Anim. Sci. 42:1498.

Goodrich, R.D., T.S. Kahlon, D.E. Pamp, and D.P. Cooper. 1978. Sulfur in ruminant Nutrition. Des Moines: National Feed Ingredient Association.

Gooneratne, S.R., A.A. Olkowski and D.A. Christensen. 1989. Sulfur-induced polioencephalomalacia in sheep: some biochemical changes. Can. J. Vet. Res. 53:462.

Gould, D.H., M.M. McAllister, J.C. Savage, and D.W. Hamar. 1991. High sulfide concentrations in rumen fluid associated with nutritionally induced polioencephalomalacia. J. Vet. Res. 52:1164.

Kung, L. Jr., J.P. Bracht, A.O. Hession, and J.Y. Tavares. 1998. High-sulfate induced PEM in cattle examined. Feedstuffs Nov. 16, 1998. p. 12.

Lowe, J.C., P.R. Scott, f. Howie, M. Lewis, J. Fitzsimons and J.A. Spence. 1996. Sulphur-induced polioencephalomalacia in lambs. Vet. Rec. 138:327.

Merck Veterinary Manual. 1991. Whitehouse Station, New Jersey. Merck and Co. Inc. 614-616.

NRC, 1980. Mineral Tolerance of Domestic Animals. National Academy Press. Washington, D.C.

NRC, 1996. Nutrient requirements of beef cattle. 7th Revised Edition. National Academy Press. Washington, D.C.

Oliveira, de L.A., C Jean-Balin, V.D. Corso, V. Benard, A. Durix and S. Komisarczuk-Bony. 1996. Effect of high sulfur diet on rumen microbial activity and rumen thiamine status in sheep receiving a semi-synthetic, thiamine-free diet. Reprod. Nutr. Dev. 36:31.

Olkowski, A.A., S.R. Gooneratne, C.G. Foussaux and D.A. Christensen. 1992. Role of thiamine status in sulfur induced polioencephalomalacia in sheep. Res. in Vet. Sci. 52:78.

Price, J., A.M. Will, G. Paschaleris, and J.K. Chesters. 1987. Identification of thiomolybdates in digesta and plasma for sheep administration of 99Mo-labelled compounds in the rumen. Br. J. Nutr. 58:127.

Smart, M.E., R. Cohen, D.A. Christensen, and C.M.Williams. 1986. The effects of sulfate removal from the drinking water on plasma and liver copper and zinc concentrations of beef cows and their calves. Can. J. Anim. Sci. 66:669.

Veenhuizen, M.F. and G.C. Shurson. 1992. Effects of sulfate in drinking water for livestock. JAVMA 201:487.

Zinn, R.A., E. Alvarez, M. Mendez, M. Montano, E. Ramirez and Y. Shen. 1997. Influence of Dietary sulfur level on growth performance and digestive function in feedlot cattle. J. Anim. Sci. 75:1723.

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