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Effects of Excess Dietary Sulfur on Mitochondrial Complex IV Activity in Beef Steers

Wednesday, March 15, 2017
Grand Ballroom Foyer (Century Link Center)
J. Hawley , Department of Animal Science, Division of Agriculture, University of Arkansas, Fayetteville, AR
E. B. Kegley , Department of Animal Science, Division of Agriculture, University of Arkansas, Fayetteville, AR
D. L. Galloway , Department of Animal Science, Division of Agriculture, University of Arkansas, Fayetteville, AR
W. G. Bottje , Department of Poultry Science, Division of Agriculture, University of Arkansas, Fayetteville, AR
In ruminants, the ingestion of large amounts of dietary S can lead to acute S toxicosis. Sulfide is readily absorbed through the rumen wall into the bloodstream, and once absorbed sulfide is thought to be involved in the competitive inhibition of mitochondrial complex IV, resulting in a shutdown of the mitochondrial electron transport chain and cellular ATP generation. Therefore, to test the effects of excess dietary S on mitochondrial complex IV activity in beef steers, 20 steers (initial BW = 283 ± 7.2 kg; 13 ± 0.6 mo of age) of predominantly Angus breeding were stratified by initial BW and assigned randomly to 1 of 6 pens (3 to 4 steers/pen). Pens were assigned randomly to 1) no additional S (~ 0.15% S) or 2) high S (0.40% S; from Na2SO4). Steers grazed fall mixed-grass pastures and were offered corn and soybean meal supplements for a 114-d growing phase. When the average BW of the steers reached 373 ± 0.2 kg, steers were stratified within dietary treatment by BW and assigned randomly to 16 dry-lot pens (1 to 2 steers/pen; 8 pens/dietary treatment). Steers remained on the same dietary treatments, and received corn and soybean meal concentrate diets for a 123-d finishing phase. Steers were slaughtered at an average BW of 565 ± 38.4 kg. Liver and LM samples were collected immediately postmortem and snap-frozen. Mitochondrial protein yield and complex IV activity obtained from liver and LM mitochondrial preparations were measured spectrophotometrically. Liver mitochondrial protein yield was 2.41 times greater (P < 0.0001) when compared to the LM mitochondrial protein yield. There was no effect (P ≥ 0.66) of dietary S on the extractable yield of mitochondrial protein per gram of liver or LM. Liver and LM mitochondrial complex IV activities were not (P ≥ 0.38) influenced by dietary S. These results suggest that feeding beef steers 0.40% S in the total diet DM is insufficient to cause measureable mitochondrial complex IV activity inhibition. Understanding the role of mitochondrial complex IV activity inhibition in ruminants ingesting large amounts of dietary S will aid in understanding the cellular basis of S toxicosis.