Requirement, Bioefficacy, And Toxicity Of Methionine In Peking Ducks

Three trials were conducted in our study. On the basis of the research in methionine requirement ofgrowing Peking ducks, the bioefficacy of methionine hydroxy analogue relative to methionine wasevaluated at nontoxic or toxic supplemental levels and the toxicity mechanism of methionine and itshydroxy analogue were discussed from the points of regulation of feed intake, oxidative damage, andDNA methylation. Our objective was to provide an experimental support for accurate and safe use ofmethionine sources in meat duck production.Trial 1 was conducted to study the effect of methionine on growth performance and carcass quality ofgrowing ducks. In this trial, optimal supplementation of methionine caused a significant increase inweight gain and breast meat yield and a significant decrease in abdominal fat (P＜0.05). Moreover, asdietary methionine level increased, the weight gain and breast meat yield increased and then decreaedand these quadratic responses were significant (P＜0.05). Therefore, according to the quadratic model,the optimal methionine requirements for maximum weight gain or breast meat yield were all 0.38%.Trial 2 was carried out to determine the bioefficacy of methionine hydroxyl analogue free acid (DL-HMB-FA) relative to DL-Met (DLM) in Peking ducks. In this trial, supplementation of DLM and DL-HMB-FA could cause a significant increase in 7-21or 7-42 day weight gain of Peking ducks and asignificant decrease in 7-42 day feed/gain of birds (P＜0.05). No significant effects of DLM and DL-HMB-FA on breast meat, leg meat, skin fat, and abdominal fat were observed (P＞0.05). According tothe slope-ratio method with nonlinear model on the equimolar basis, the bioefficacies of DL-HMB-FArelative to DLM for 7-21 and 7-42 day Peking ducks were 78% and 67%, respectively when weight gainwere used as criterion and the values were 66% and 44%, respectively when feed/gain were used ascriterion.Trial 3 was conducted to determine the toxicity and its mechanism of DL-HMB-FA and DLM inPeking ducks. In this trial, excess DLM and DL-HMB-FA reduced weight gain, feed intake, and breastmeat yield significantly(P＜0.05) but excess DLM was more growth depressing than equimolar DL-HMB-FA. According to the intake of methionine sources, the tolerable upper limit of dietary methioninefor Peking ducks from 3 to 6 weeks of age was 2.86g/bird per day (1.41g/kg body weight per day) andbirds were more tolerable to excess DL-HMB-FA than DLM on the equimolar basis. In addition,according to the slopet-ratio method with linear model, at toxic supplemental level, the bioefficacy ofDL-HMB-FA relative to DLM was 50% on the equimolar basis when feed intake was used as criterion.In terms of hormonal regulation of feed intake, excess DLM and DL-HMB-FA did not affected plasmaleptin and insulin of ducks significantly (P＞0.05) but 2% DLM supplementation in diets elevated plasmaneuropeptide Y significantly (P＜0.05). In terms of toxic damage, supplementation of 2% DLM and2.26% DL-HMB-FA in diets elevated plasma alanine aminotransferase, aspartate aminotransferase, andlactate dehydrogenase significantly (P＜0.05), which indicated the liver damage cause by excessmethionine and its hydroxyl analogue. Supplementation of 2% DLM or 2.26% DL-HMB-FA in dietscaused a significant increase in plasma maleic dialdehyde and a significant decrease in superoxide dismutase and glutathione peroxidase in liver (P＜0.05), which suggeated that the toxicity of methionineand its hydroxy analogue was related to oxidative damage. Moreover, digestion of blood genomic DNAby methylation-sensitive restriction endonucleases showed that 2% DLM and 2.26% DL-HMB-FAsupplementation caused DNA hypermethylation.In conclusion, optimal supplementation of methionine in diets could improve growth performanceand carcass quality of Peking ducks but excess methionine or its hydroxy analogue reduced duck growthand methionine was more toxic than its hydroxy analogue. According to the slope-ratio method, thebioefficacy of methionine hydroxyl analogue was lower than methionine for ducks whether at nontoxicor toxic supplemental level. On the other hand, excess methionine and its hydroxy analogue could causeliver damage and oxidative damage and genomic DNA hypermethylation may be the toxicity mechanismof methionine and its hydroxy analogue.