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Adipic acid is only partially catabolized when it is fed to animals, and a portion of it is excreted in urine. The excreted portion may lower urinary pH and, as a result, ammonia emission. The present study tested this hypothesis. In Exp. 1, nursery pigs (n = 14) were fed (for a period of 7 d) either a standard nursery diet or the same diet supplemented with 1% adipic acid to assess effects on urinary pH (collected on d 5 or 6) and in vitro ammonia emission from the collected urine samples that were mixed with control feces. In Exp. 2, grower pigs housed 10 each in one of two chambers were fed a control diet or the same diet supplemented with 1% adipic acid. Ventilated air was quantified and analyzed for ammonia using Fourier transform infrared spectroscopy to determine the effects of feeding 1% adipic acid on ammonia emission. The results from Exp. 1 showed that adipic acid strongly reduced urinary pH (from 7.7 to 5.5, P [is less than] 0.05). In vitro ammonia emission from these urine samples was significantly reduced at all the time points evaluated (1, 3, 18, and 46 h with reductions of 94, 93, 70, and 39%, respectively, P [is less than] 0.05). Experiment 2 showed that adipic acid supplementation reduced ammonia emission by 25% (P [is less than] 0.05), which corresponded to the predicted reduction in ammonia emission based on the reduction in manure pH observed. In conclusion, feeding adipic acid lowers urinary pH and reduces ammonia emission. The reduction in ammonia emission, though, does not correspond to the reduction in urinary pH but corresponds to the reduction in fecal pH as a result of mixing the urine and feces, in which feces act as a strong buffer. Key Words: Adipic Acid, Ammonia, pH, Pigs, Urine

Adipic acid, upon catabolism, results in intermediates that bear a structural similarity to lysine degradation products. The objectives of this research were to determine whether adipic acid affects lysine concentrations in plasma and to evaluate whether adipic acid improves the efficiency of lysine utilization in pigs. In Exp. 1, nursery pigs (n = 14) were fed (for a period of 7 d) either a standard nursery diet or the same diet supplemented with 1% adipic acid to assess effects on plasma amino acid concentrations (plasma collected on d 7). In Exp. 2, nursery pigs (n = 56) were fed (for a period of 15 d) either a control diet or the same diet but deficient in either lysine, threonine, or tryptophan with or without supplemental adipic acid to assess the effects of adipic acid on the efficiency of amino acid utilization. The results from Exp. 1 showed that adipic acid increased plasma lysine (by 18%) but not [Alpha]-amino adipic acid, an intermediate in lysine degradation. Experiment 2 demonstrated that adipic acid did not increase the efficiency of utilization of lysine, threonine, or tryptophan. The lack of effects on [Alpha]-amino adipic acid in Exp. 1 and the lack of a positive effect on the efficiency of utilization of lysine, threonine, and tryptophan suggest that adipic acid does not inhibit the mitochondrial uptake of lysine and(or) its degradation in the mitochondrion. It is concluded that feeding adipic acid increases plasma lysine but does not improve the efficiency of lysine utilization. Key Words: Adipic Acid, Lysine, Pigs

Vitamin E is important for animal production because of its effects on health and product quality, but the amount and form required remains controversial. Our objective was to quantify the absolute bioavailability of oral all-rac-α-tocopheryl acetate (α-TAc) in swine (22 ± 1 kg and 8 wk old, fitted with jugular catheters) adapted to a diet supplemented with 75 mg/kg all-rac-α-TAc; 75 mg/kg was chosen because this level represents the nonweighted average inclusion level in piglet diets across Western key swine-producing countries. For this, a 350-g test meal (6% fat) was supplied at time 0 containing 75 mg deuterated (D9) all-rac-α-TAc to 9 animals, and 8 animals received an intravenous (i.v.) dose containing deuterated (D6) RRR-α-tocopherol (α-T) at one-eighth the oral dose and a test meal without supplemental vitamin E. Plasma samples (12 to 13 per animal) were obtained at incremental intervals over 75 h for analysis of deuterated α-T using liquid chromatography--tandem mass spectrometry. Surprisingly, the i.v. dose rapidly disappeared from plasma and then reappeared. The half-life for this first peak was only 1.7 ± 0.3 min. The second peak had an appearance rate (Ka) of 0.10 ± 0.06 d-1 and a half-life of 5.9 ± 1.2 h. Oral dosing resulted, after a lag of 56 min, in a Ka of 0.91 ± 0.21 d-1 and a half-life of 2.6 ± 0.8 h. The bioavailability for oral α-TAc was 12.5%, whereas the area under the curve was only 5.4%. This low bioavailability, small area under the curve, and short half-life are likely because of various factors, that is, the use of only 6% fat in the diet, the use of the acetate ester and all-rac, and the high dose relative to requirements. In conclusion, i.v. dosed vitamin E shows both a rapid and a very slow pool, whereas orally dosed vitamin E shows a single slow pool. The oral material has a very short half-live (44% of i.v. or 2.6 h), low bioavailability (12.5%), and a very small area under the curve (5.4%), bringing into question the efficacy of typical doses of vitamin E in swine diets for alleviating oxidative stress. [ABSTRACT FROM AUTHOR]