Two experiments with finishing pigs were conducted to evaluate the effects of fluctuating dietary CP levels and ractopamine on performance and carcass traits. In Exp. 1, a total of 408 finishing pigs (mixed sex) were assigned to 1 of 4 protein regimens. Average initial and final BW were 89 and 123 kg, respectively. Pigs on treatments 1 to 4 were fed 16, 11, 16, and 13% CP from wk 0 to 2, respectively. From wk 2 to 5, the pigs on regimens 1 to 4 were then fed 15, 18.33, 18, and 20% CP, respectively, with regimens 3 and 4 also containing supplemental ractopamine (9.9 mg/kg) from wk 2 to 5. Overall (wk 0 to 5), BW gain, G:F, loin depth, percentage of lean, and dressing percentage were improved (P < 0.05) in pigs on regimens 3 and 4 compared with those on regimens 1 and 2. No statistically significant overall (wk 0 to 5) protein sequence regimen differences occurred between the standard regimens (1 and 3) and the low-high CP regimens (2 and 4). Experiment 2 involved 172 finishing pigs (mixed sex) in 2 protein regimens. Average initial and final BW were 91 and 136 kg, respectively. The diets consisted of 1) a control (16% CP from d 0 to 14, 18% CP + 4.95 mg of ractopamine/kg from d 14 to 24, and 18% CP + 9.9 mg of ractopamine/kg from d 24 to 35; 2) a low-high CP regimen (12.5% CP from d 0 to 14, 20.33% CP + 4.95 mg of ractopamine/kg from d 14 to 24, and 20.33% CP + 9.9 mg of ractopamine/kg from d 24 to 35. From d 0 to 14, pigs fed the low CP diet (12.5% CP) had reduced (P < 0.05) BW gain and G:F compared with those fed the control diet (16% CP). In contrast, from d 14 to 35, pigs on the low-high regimen had improved (P < 0.08) BW gain and G:F compared with pigs on the control regimen. Despite the wide dietary CP fluctuations for pigs in Exp. 2, performance and carcass traits were similar for both regimens over the 35-d test period. These data indicate that pigs fed deficient levels of CP and Lys for 14 d, followed by increased levels of CP and Lys during a subsequent 21-d period can recover and achieve growth performance and carcass merit equal to that achieved with a conventional protein feeding regimen.

Two chick experiments were conducted to compare the growth-promoting efficacy as well as the toxicity of a new source of L-tryptophan and L-lysine, Tryptosine(R) (16.1% tryptophan, 56.3% lysine). A corn-feather meal-soybean meal basal diet was made singly deficient in either lysine or tryptophan, and graded doses of lysine or tryptophan from either Tryptosine(R) or feed-grade sources of lysine and tryptophan were Supplemented. Linear (P < .01) weight gain responses occurred, and responses to lysine or tryptophan in Tryptosine(R) were similar to those obtained with equal doses of lysine or tryptophan provided by feed-grade sources of L-lysine HCl or L-tryptophan. The toxicity trial involved additions of 1, 2, or 4% lysine with .29, .58, or 1.16% tryptophan to a lysine- and tryptophan-adequate corn-soybean meal diet. Both amino acids were provided as either Tryptosine or as feed-grade sources of lysine and tryptophan. Weight gain and feed intake were reduced in a linear fashion (P < .01) as levels of the two excess amino acids increased. The decreases caused by Tryptosine were similar to those caused by equivalent levels of excess feed-grade lysine and tryptophan.

Four chick bioassays were conducted to evaluate the threonine (Thr) replacement value of l-homoserine (HS). Growth rate was increased (P < 0.05) by dietary addition of 800 mg l-HS/kg diet to a purified diet severely deficient in Thr or by the addition of 800 or 1000 mg of l-HS/kg diet to a corn-peanut meal diet distinctly deficient in Thr. The addition of an isomolar level of alpha-ketobutyrate, a catabolic product of both Thr and HS, did not elicit a response. Standard-curve methodology predicted a Thr replacement value of 38 +/- 9% for HS. Interactions (P < 0.01) were observed in assays 2 and 4 between dietary Thr adequacy and 800 or 1000 mg l-HS/kg supplementation. Thus, HS improved growth performance when added to a Thr-deficient diet (0.46 g Thr/100 g diet), but it decreased growth performance when added to the same diet containing surfeit Thr (0.80 g Thr/100 g diet). The results indicate that low levels of HS elicit a growth response in young chicks fed Thr-deficient diets.

Three experiments with weanling American Shorthair kit tens fed a purified L-amino acid diet (4700 kcal metabolizable energy/kg diet) were conducted to determine the methionine and cystine require ments and to also estimate the portion of the total sulfur amino acid re quirement that could be furnished by cystine. All diets were fortified with both taurine and inorganic sulfate. Both rate and efficiency of weight gain responded linearly to graded increments of dietary L-methionine (in the presence of excess cystine), a plateau being reached at about 0.45%. At this level of methionine, cats grow maximally when fed 0.457o L-cystine. Thus, 50% of the sulfur amino acid need of the cat can be furnished by cystine. A third experiment was carried out to establish whether cystine is a dispensable or an indispensable amino acid for feline growth. Cats grew just as well when fed their sulfur amino acids in the form of methionine alone ( 1.0% of the diet ) as when fed an isosulfurous level of a methionine- cystine combination (0.457o methionine + 45% cystine). Hence, similar to findings with other mammalian species, cystine is a dispensable amino acid for cat growth, but it can contribute significantly to the total sulfur amino acid requirement and thereby spare dietary methionine. J. Nutr. 108: 291-295, 1978.

Current knowledge in nutrition is based largely on the use of appropriate animal models together with defined diets. Numerous examples are cited where animal models have been used to solve nutrient x nutrient interactions, to evaluate bioavailability of nutrients and nutrient precursors, and to test for nutrient tolerances and toxicities. Advantages, disadvantages, and idiosyncrasies of various animal species are discussed.

Five 9- or 12-d chick growth bioassays were done in batteries using 2 Met-deficient diets: a purified AA-based diet containing (by analysis, as-fed) 20.3% CP, 0.12% Met, and 0.05% cyst(e)ine; and an AA-fortified corn-peanut meal diet containing (by analysis, as-fed) 19.0% CP, 0.22% Met, and 0.23% cyst(e) ine. Feed-grade DL-Met (dl-M; 99%) was compared with feed-grade DL-OH-Met, Ca (OH-M; 84%). When the purified diet was modified to contain 0.12% Met and 0.20% or greater cyst(e)ine, slope-ratio assays involving graded dosing of DL-M (0, 404, 808, and 1,212 mg of DL-M/kg) or isosulfurous levels of OH-M resulted in linear (P < 0.01) BW gain and G:F responses. Multiple linear regression analysis (BW gain vs. supplemental sulfur intake, R(2) = 0.98) resulted in a mean bioefficacy estimate of 78.1% for OH-M vs. DL-M (equivalent to 65.6% on a supplemental compound basis). In assay 3, the purified diet was modified to be equally deficient in Met and cyst(e)ine [i.e., 0.12% Met, 0.12% cyst(e)ine]. When this diet was supplemented with either 404 mg of DL-M/kg or 476 mg of OH-M/kg, BW gain and G:F responded (P < 0.01) markedly to either compound, and differences between DL-M and OH-M were not significant (P > 0.10). Assays 4 and 5 used the corn-peanut meal basal diet containing 0.22% total Met and 0.23% total cyst(e)ine. In both assays, addition of either 465 mg of DL-M/kg or 554 mg of OH-M/kg resulted in increased (P < 0.01) BW gain and G:F, regardless of dietary cyst(e)ine concentration. In the absence of excess cyst(e)ine, BW gain responses to DL-M and OH-M were similar, but when 0.10% excess cyst(e)ine was provided as L-cystine or feather meal, DL-M responses tended to exceed those of OH-M. Moreover, this small excess of dietary cyst(e)ine, regardless of source, depressed (P < 0.01) feed intake and BW gain when added to the basal diet. Overall, these results suggest that excess dietary cyst(e)ine, when included in Met-deficient diets, has the potential to be both anorexigenic and pernicious to OH-M utilization.

The ideal protein concept has allowed progress in defining requirements as well as the limiting order of amino acids in corn, soybean meal, and a corn-soybean meal mixture for growth of young chicks. Recent evidence suggests that glycine (or serine) is a key limiting amino acid in reduced protein [23% crude protein (CP) reduced to 16% CP] corn-soybean meal diets for broiler chicks. Research with sulfur amino acids has revealed that small excesses of cysteine are growth depressing in chicks fed methionine-deficient diets. Moreover, high ratios of cysteine:methionine impair utilization of the hydroxy analog of methionine, but not of methionine itself. A high level of dietary l-cysteine (2.5% or higher) is lethal for young chicks, but a similar level of dl-methionine, l-cystine or N-acetyl-l-cysteine causes no mortality. A supplemental dietary level of 3.0% l-cysteine (7x requirement) causes acute metabolic acidosis that is characterized by a striking increase in plasma sulfate and decrease in plasma bicarbonate. S-Methylmethionine, an analog of S-adenosylmethionine, has been shown to have choline-sparing activity, but it only spares methionine when diets are deficient in choline and(or) betaine. Creatine, or its precursor guanidinoacetic acid, can spare dietary arginine in chicks.

A 72-h time-course study was conducted to elucidate the physiological mechanism underlying cysteine (Cys) toxicity in chicks beginning at 8-d posthatch. Biochemical markers quantified in plasma and liver samples collected from chicks receiving 30 g/kg excess dietary Cys were compared with baseline measurements from chicks receiving an unsupplemented corn-soybean meal diet over a 72-h feeding period. Concomitant with chick mortality were indices of acute metabolic acidosis, including a rapid increase (P < 0.001) in anion gap that resulted from a reduction (P < 0.001) in plasma HCO(3)(-) of approximately 40% and a 2.8-fold increase (P < 0.001) in plasma sulfate in chicks receiving excess Cys. Additionally, provision of 30 g/kg excess Cys resulted in a 1.5-fold increase (P < 0.05) in hepatic oxidized glutathione compared with the 0-h control time-point. Excess dietary Cys did not affect plasma free Met, but plasma free Cys increased (P < 0.05) from 89 to 107 mumol/L at 12 h and remained elevated through 36 h. Strikingly, ingestion of 30 g/kg excess Cys caused more than a doubling (P < 0.001) of plasma free cystine, the oxidized form of Cys, beginning 12 h after initiating the study, and it remained elevated throughout the 72-h feeding period. Taken together, these data suggest that ingestion of 30 g/kg excess l-Cys causes both acute metabolic acidosis and oxidative stress in young chicks when fed a nutritionally adequate, corn-soybean meal diet.

The focus of the 6th workshop is on lysine, arginine, and related amino acids. Functions, metabolic pathways, clinical uses, and upper tolerance intakes are emphasized in the articles that follow. Lysine is arguably the most deficient amino acid in the food supply of countries where poverty exists, and since the discovery of the nitric oxide synthase pathway, arginine has come into prominence clinically because of the role of nitric oxide in cardiovascular physiology and pathophysiology.

Three bioassays were conducted to elucidate the effects of dietary cystine on the efficacy of L-Met and DL-Met fed to chicks. In assay 1, a purified diet markedly deficient in Met (0.12%) and cyst(e)ine (0.05%) was used to compare the relative effectiveness of L-Met and DL-Met in the presence of graded levels of dietary cystine. Addition of 0.05% Met improved (P < 0.01) weight gain when added to diets with 0 or 0.07% added L-cystine, but weight gain decreased linearly (P < 0.01) with greater cystine supplementation up to 0.35%, regardless of Met supplementation. There were no differences in growth performance due to supplementation of L-Met vs. DL-Met. In assay 2, a corn-soybean meal-peanut meal diet (0.25% Met and 0.25% cyst(e)ine) was supplemented with 0, 0.025, 0.05, or 0.075% L-Met plus 0 or 0.2% added L-cystine. Supplemental Met improved (P < 0.01) growth performance, but weight gain and feed intake were depressed (P < 0.01) by cystine supplementation. Whereas 0.2% added L-cystine depressed feed intake 6.9%, weight gain was reduced only 3.6%. Thus, cystine supplementation actually improved (P < 0.01) gain:feed. In assay 3, the corn-soybean meal-peanut meal diet was supplemented with 0 or 0.03% L-Met or DL-Met in the absence or presence of 0.2% added L-cystine. Again, Met supplementation improved (P < 0.01) growth performance, whereas supplemental cystine reduced (P < 0.05) weight gain and feed intake, but increased (P < 0.01) gain:feed. From these bioassays, it may be concluded that there is no evidence to suggest differences in effectiveness between L-Met and DL-Met in purified or practical-type low-protein diets of varying sulfur amino acid (SAA) content fed to chicks from 8 to 20 d of age. However, supplemental cystine has a negative impact on voluntary feed intake when supplemented in diets markedly deficient in SAA. This effect is evident with minimal SAA intake and when greater than 50% of SAA intake is provided by cyst(e)ine, rather than Met.

Relative bioefficacy and toxicity of Met precursor compounds were investigated in young chicks. The effectiveness of DL-Met and 2-keto-4-(methylthio)butyric acid (Keto-Met) to serve as L-Met precursors was quantified using Met-deficient diets of differing composition. Efficacy was based on slope-ratio and standard-curve methodology. Using L-Met as a standard Met source added to a purified diet, DL-Met and Keto-Met were assigned relative bioefficacy values of 98.5 and 92.5%, respectively, based on weight gain. Relative bioefficacy values of 98.5 and 89.3% were assigned to DL-Met and Keto-Met, respectively, when chicks were fed a Met-deficient, corn-soybean meal-peanut meal diet. Thus, both DL-Met and Keto-Met are effective Met precursor compounds in chicks. Additionally, growth-depressing effects of L-Met, DL-Met, and Keto-Met were compared using a nutritionally adequate corn-soybean meal diet supplemented with 15 or 30 g/kg of each compound. Similar reductions in weight gain, food intake, and gain:food ratio were observed for each compound. Subjective spleen color scores, indicative of splenic hemosiderosis, increased linearly (P , 0.01) with increasing intakes of each compound, suggesting a similarity in overall toxicity among these compounds. Because conversion of Keto-Met to L-Met in vivo merely requires transamination, Keto-Met may prove to be a useful supplement not only in food animal production, but also as a component of enteral and parenteral formulas for humans suffering from renal insufficiency. J. Nutr. 137: 1868–1873, 2007.

Relative bioavailability and toxicity of N-acetyl-l-Cys (NAC) were evaluated in 9-d chick growth assays. The bioavailability of NAC relative to Cys was determined by feeding young chicks a highly purified crystalline AA diet singly deficient in Cys. Bio-availability estimates were obtained using standard slope-ratio methodology. N-Acetyl-l-cysteine was shown to be as effective as Cys in supporting chick growth, and was assigned a relative bioavailability value of 100%. To assess toxicity, a nutritionally adequate corn-soybean meal diet was supplemented with graded concentrations of NAC (isomolar to 10, 20, 30, or 40 g/kg of Cys, as-fed). When NAC supplied 10 or 20 g/kg of Cys, chick growth performance was unaffected, but NAC supplying 30 or 40 g/kg of Cys reduced (P < 0.05) BW gain by 13 and 34%, respectively, relative to the unsupplemented control diet. Only plasma-free NAC was substantially increased (P < 0.05) because of excess dietary NAC; plasma-free Cys was unaltered. We concluded that dietary NAC is efficacious in supplying Cys in support of chick growth, and only large excesses of NAC are growth depressing. Hence, the human clinical benefits of oral NAC likely result from its ability to deliver Cys safely and effectively to the portal circulation.

Relative bioefficacy and toxicity of Met precursor compounds were investigated in young chicks. The effectiveness of DL-Met and 2-keto-4-(methylthio)butyric acid (Keto-Met) to serve as L-Met precursors was quantified using Met-deficient diets of differing composition. Efficacy was based on slope-ratio and standard-curve methodology. Using L-Met as a standard Met source added to a purified diet, DL-Met and Keto-Met were assigned relative bioefficacy values of 98.5 and 92.5%, respectively, based on weight gain. Relative bioefficacy values of 98.5 and 89.3% were assigned to DL-Met and Keto-Met, respectively, when chicks were fed a Met-deficient, corn-soybean meal-peanut meal diet. Thus, both DL-Met and Keto-Met are effective Met precursor compounds in chicks. Additionally, growth-depressing effects of L-Met, DL-Met, and Keto-Met were compared using a nutritionally adequate corn-soybean meal diet supplemented with 15 or 30 g/kg of each compound. Similar reductions in weight gain, food intake, and gain:food ratio were observed for each compound. Subjective spleen color scores, indicative of splenic hemosiderosis, increased linearly (P < 0.01) with increasing intakes of each compound, suggesting a similarity in overall toxicity among these compounds. Because conversion of Keto-Met to L-Met in vivo merely requires transamination, Keto-Met may prove to be a useful supplement not only in food animal production, but also as a component of enteral and parenteral formulas for humans suffering from renal insufficiency.

Four experiments (Exp.) were conducted with Cobb 500 chicks to evaluate variations in the estimated digestible sulfur amino acid (DSAA) requirement of broilers due to rearing environment, sex, or growth performance during the starter period (7 to 19 d), and live performance response and carcass yield characteristics during the grower period (21 to 42 d). In the first 3 experiments conducted during the starter period, chicks were allocated to battery or floor pens, and in the fourth experiment birds were reared in floor pens. For Exp. 1, 2, and 3 a sulfur amino acid deficient corn-soybean meal-corn gluten meal basal diet and for the grower experiment a corn-soybean meal-peanut meal basal diet was formulated to be isocaloric and isonitrogenous within experiment. Graded levels of DSAA ranged from 0.54 to 0.94% in Exp. 1, 0.53 to 1.03% in Exp. 2, 0.49 to 0.89% in Exp. 3, and 0.43 to 0.83% in Exp. 4. True digestibility of the diets was determined using the precision-fed rooster assay. The DSAA requirements were estimated using 1-slope broken-line methodology. During the starter period, the average DSAA requirement of males and females was similar when based on the gain to feed ratio (G:F; 0.71 and 0.71%, respectively) and BW gain (BWG; 0.67 and 0.67%, respectively). In Exp. 3 involving battery and floor pens, males and females had similar DSAA requirement estimates, but the DSAA requirement based on maximal G:F (0.68%) was higher than the maximal BWG requirement (0.61%). In the grower period, the estimated DSAA requirement for males based on G:F was higher than that based on BWG, but the BWG and G:F requirements were similar for females. The DSAA requirement estimates were similar for males and females based on BWG (0.55%), but the DSAA requirement based on G:F was higher for males than females. The DSAA requirement for maximum breast meat yield was similar for males (0.55%) and females (0.56%), and the requirement for maximal breast meat yield was similar to that for maximal BWG. The DSAA requirements were similar based on sex, rearing environment, or both; however, there was a difference in the estimated DSAA requirements between growth and carcass responses.

Feeding high leucine levels (2.0 and 3.0% total dietary leucine) to finishing pigs (73 to 127 kg liveweight) increased the intra muscular fat content of the longissimus muscle in pigs fed diets with low lysine levels (0.5% total dietary lysine) but not in animals fed high lysine levels (0.7 %). Key words: Lysine, leucine, growth performance, carcass and meat quality

The ability of betaine to serve as a methyl donor in chicks was assessed in 3 bioassays using a choline-free purified diet that contained adequate methionine (Met). In assay 1, choline and betaine were each supplemented at 300 mg/kg in a 2 x 2 factorial arrangement of diets. Supplemental choline improved (P < 0.05) growth performance over the 9-d growth period, whereas betaine alone had no effect. In assay 2, graded supplements of choline produced a linear increase (P < 0.05) in growth performance criteria over a 9-d growth period. Additionally, hepatic betaine-homocysteine (Hcy) methyltransferase (BHMT) activity decreased linearly (P < 0.05), whereas plasma total Hcy remained unchanged. Addition of 260 or 600 mg/kg betaine to the choline-free basal diet did not affect growth performance or BHMT activity, but 600 mg/kg betaine reduced (P < 0.05) plasma total Hcy. Assay 3 was designed to quantify the ability of betaine to spare choline. Minimal supplemental choline requirements of 20.8 +/- 1.50 mg/d (722 mg/kg diet) and 10.5 +/- 1.03 mg/d (412 mg/kg diet) were estimated in the absence and presence of 1000 mg/kg supplemental betaine, respectively. Based on these estimates, 50% of the dietary choline requirement must be supplied as choline per se, but the remaining 50% can be replaced by betaine. Collectively, these data suggest betaine and Met have minimal choline-sparing activity in chicks fed purified diets devoid of preformed choline. However, addition of betaine to diets containing minimal choline allows a marked reduction in the total dietary choline requirement.

The behavioural response to infection is well organized and may enhance disease resistance and facilitate recovery, but the behaviour of pigs with an acute respiratory infection has not been assessed. Therefore, the purpose of this study was to evaluate behaviour of pigs inoculated with Mycoplasma hyopneumoniae (Mh) and porcine reproductive and respiratory syndrome virus (PRRSV). Sixty-four pigs were subjected to one of four treatment combinations (2 × 2 factorial) of Mh (inoculated at 4 weeks of age) and PRRSV (inoculated at 6 weeks of age). The four treatments were (1) control, (2) inoculation with Mh, (3) inoculation with PRRSV, and (4) inoculation with both Mh and PRRSV. One-half of the pigs from each treatment were killed 7 days after PRRSV inoculation for purposes unrelated to this study and hence were not used for behavioural analysis. Pigs that were included were video recorded during the 18 h light phase for 13 days beginning the day of PRRSV inoculation. Food intake and time spent feeding, active (standing, including walking, sitting, or feeding) and lying were determined. When pigs were lying a determination was made as to whether they were lying ventrally or laterally, and in contact with a penmate. Body temperature was measured 7 and 14 days after PRRSV inoculation. After inoculation with PRRSV, there was no significant main effect of Mh or interaction between Mh and PRRSV for food intake, body temperature, or any behaviour measured. Thus, the four treatments were pooled to form two treatments designated PRRSV negative (control and Mh; PRRSV−) and PRRSV positive (PRRSV and Mh with PRRSV; PRRSV+) and analyzed. Each day after PRRSV inoculation, PRRSV+ pigs spent less time (P = 0.005) feeding compared to PRRSV− pigs, and the decrease in feeding time was associated with a decrease in food intake (P < 0.001). PRRSV+ pigs decreased (P < 0.001) activity after inoculation with PRRSV compared to PRRSV− pigs and the amount of time spent lying was greater (P < 0.001) in PRRSV+ pigs compared to PRRSV− pigs. Furthermore, PRRSV+ pigs spent more of their total lying time in a ventral position (P = 0.06) and in contact with a penmate (P < 0.001) compared to PRRSV− pigs. Body temperature was increased (P < 0.001) in PRRSV+ pigs 7 days after PRRSV inoculation. Since sickness behaviour and fever are adaptive responses to infection, these data indicate that pigs with an acute PRRSV infection evoke a behavioural strategy that may support recovery.

Catabolism of Trp and Lys produces α-ketoadipic acid as an intermediary metabolite. An alternate pathway of Trp turnover leads to NAD synthesis. We hypothesized that excess Lys might improve the conversion of Trp to niacin by causing a buildup of α-ketoadipic acid, thereby endproduct inhibiting the main Trp catabolic pathway and resulting in more niacin synthesis from Trp. Six bioassays were carried out in which 12 to 20 chicks were fed each experimental diet from d 8 to d 20 or 21 posthatching. The basal diet (4 mg/kg of bioavailable niacin) used for all assays was a semipurified corn gluten meal diet fortified with crystalline amino acids to 22.5% CP and 0.96% true digestible Lys. Assay 1 through 3 established the requirements for digestible Trp (0.16%) and bioavailable niacin (19.5 mg/kg) and showed that 0.96% digestible Lys was adequate for chick growth in the presence of adequate Trp and niacin. The fourth assay was done to determine the effect of 1% Lys (1.25% food-gradel-Lys·HCl) on niacin utilization. Excess Lys improved (P < 0.01) weight gain of niacin-deficient chicks. The fifth assay showed that 1% excess food-grade Lys improved weight gain in niacin-deficient (4 mg/kg) chicks but depressed weight gain in niacin-adequate (24 mg/kg) chicks (niacin × Lys interaction,P < 0.01). In assay 6, chicks fed 6 mg/kg of niacin gained faster (P < 0.01) than control chicks, but neither quinolinic acid (100 mg/kg) nor picolinic acid (4,200 mg/kg) elicited a response. These results suggest that excess Lys leads to an accumulation of α-ketoadipic acid, which causes endproduct inhibition of the main Trp catabolic pathway to CO2, therefore increasing flux of 2-amino-3-carboxymuconate semialdehyde to NAD.

Chick bioassays were conducted to compare the relative effects of L-methionine (Met), L-cysteine (Cys), L-cystine (CysCys), and N-acetyl L-cysteine (NAC) provided at 2-, 4-, 7-, or 9-times the dietary requirement on plasma free sulfur amino acid (SAA) concentrations as quantified by HPLC procedures. Excess dietary Met was shown to increase (P < 0.01) plasma Met by 57-fold, while oxidized glutathione was increased 2.5-fold (P < 0.01). Plasma Cys was not changed by an excess of any dietary SAA, and plasma CysCys was increased (P < 0.01) only by excess Cys or CysCys. Plasma cystathionine was increased (P < 0.05) 2-fold when the first increment of excess Met, Cys, CysCys, or NAC was fed, but did not increase further at higher levels of SAA addition. NAC could not be detected in the plasma of chicks consuming excess Met, Cys, or CysCys, but plasma NAC increased quadratically (P < 0.05) when excess NAC was supplemented to provide excess Cys. Additionally, the capacity of NAC to provide Cys in vivo was investigated using a diet made singly deficient in Cys. Standard slope-ratio methodology suggested that NAC supported chick growth equivalent to L-Cys in a 9-d growth assay. Thus, it was concluded that oral NAC is 100% efficacious in supplying Cys to the chick. Collectively, these data suggest that tight regulation of plasma SAA occurs in the chick. Additionally, it was concluded that dietary NAC was a safe and efficacious source of Cys.