Supplementation of amylase or amylase + xylanase improves performance and metabolism of broilers fed with diets containing newly harvested maize.

How supplementation with amylase or amylase + xylanase in newly harvested maize-based diets affects broiler nutrient metabolism and performance is unclear. Thus, this study evaluated whether the supplementation of amylase (CN) or amylase + xylanase (CAX) improves performance and metabolism of broilers fed with newly harvested maize-based diets during a 6-week production. The results showed that the body weight gain of broilers fed with CA or CAX diet was higher than that with the control (CN) diet at 1-21 d of age; however, an opposite trend was observed for feed/gain (p < 0.05). Furthermore, 150, 64 and 35 different metabolites were found between CA/CN, CAX/CN and CAX/CA, respectively. Overall, amylase supplementation improved broiler growth performance at 1-21 d of age, and the positive effects of amylase on nutrient utilization were mostly related to nicotinate, retinol and glutathione metabolism improvement. Moreover, CAX diet increased apparent metabolizable energy and growth performance of broilers at 22-42 d of age, and the difference might be related to sphingolipid, porphyrin and chlorophyll metabolism regulation. The findings prove amylase + xylanase supplementation is an effective method to improve the nutritional value of newly harvested maize for broilers.

A quantitative proteomic analyses of primary myocardial cell injury induced by heat stress in chicken embryo.

In this study, the model of heat stress was constructed in primary chick embryonic myocardial cells at 42 °C for 4 h. Proteome analysis using DIA identified 245 differentially expressed proteins (DEPs) (Q-value <0.05, fold change >1.5), of which 63 proteins were up-regulated and 182 proteins were down-regulated. Many were related to metabolism, oxidative stress, oxidative phosphorylation and apoptosis. Gene Ontology (GO) analysis showed that many DEPs under heat stress were involved in regulating metabolites and energy, cellular respiration, catalytic activity and stimulation. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that DEPs were enriched in metabolic pathways, oxidative phosphorylation, citrate cycle (TCA cycle), cardiac muscle contraction, and carbon metabolism. The results could help understanding of the effect of heat stress on myocardial cells and even the heart and possible action mechanism at the protein level.

Quantitative Proteomics Reveals Manganese Alleviates Heat Stress of Broiler Myocardial Cells via Regulating Nucleic Acid Metabolism.

Heat stress threatens severely cardiac function by caused myocardial injury in poultry. Our previous study has showed that manganese (Mn) has a beneficial effect on heat-stress resistance of broiler. Therefore, we tried to confirm the alleviation mechanism through proteomic analysis after heat stress exposure to primary broiler myocardial cells pretreated with Mn. The experiment was divided into four groups: CON group (37 °C, cells without any treatment), HS group (43 °C, cells treatment with heat stress for 4 h), HS+MnCl2 group (cells treated with 20 µM MnCl2 before heat stress), and HS+Mn-AA group (cells treated with 20 µM Mn compound amino acid complex before heat stress). Proteome analysis using DIA identified 300 differentially expressed proteins (DEPs) between CON group and HS group; 93 and 121 DEPs were identified in inorganic manganese treatment group and organic manganese treatment group, respectively; in addition, there were 53 DEPs identified between inorganic and organic manganese group. Gene Ontology (GO) analysis showed that DEPs were mainly involved in binding, catalytic activity, response to stimulus, and metabolic process. DEPs of manganese pretreatment involved in a variety of biological regulatory pathways, and significantly influenced protein processing and repair in endoplasmic reticulum, apoptosis, and DNA replication and repair. These all seem to imply that manganese may help to resist cell damage induced by heat stress by regulating key node proteins. These findings contribute to a better understanding of the effects of manganese on overall protein changes during heat-stress and the possible mechanisms, as well as how to better use manganese to protect heart function in high temperature.

Effects of Dietary Supplementation with Iron in Breeding Pigeons on the Blood Iron Status, Tissue Iron Content, and Full Expression of Iron-Containing Enzymes of Squabs.

This study was aimed at investigating the effects of diet iron levels on the blood iron status, tissue iron content, mRNA levels, and the activity of iron-containing enzymes in different tissues of squabs. A total of 120 pairs of healthy Silver Feather King parental pigeons with similar average body weight and egg production were randomly divided into 5 groups with 8 replicates and 3 pairs of pigeons per replicate. The five groups of breeding pigeons were fed an iron-unsupplemented basal diet and basal diet supplemented with 75, 150, 300, and 600 mg iron/kg, respectively. The diets were fed in the form of granular feed based on corn, soybean meal, wheat, and sorghum. A broken line model was used for regression analysis. The results showed that plasma iron (PI), serum ferritin, iron contents in crop milk and liver, liver catalase (CAT) activity, and heart succinate dehydrogenase (SDH) activity were affected by iron levels (P < 0.05). And PI, serum ferritin, iron content in crop milk, and heart SDH activity increased quadratically (P < 0.05), but the iron content and CAT activity in the liver decreased quadratically (P < 0.005) as dietary iron level increased. According to the broken-line model of serum ferritin fitting (P < 0.002), the optimal dietary iron level of breeding pigeons was estimated to be 193 mg/kg. In conclusion, serum ferritin is a sensitive index to evaluate the iron requirement of the breeding pigeon with two squabs, and the recommended iron supplemental level is 193 mg/kg.

Dietary zinc supplementation in breeding pigeons improves the carcass traits of squabs through regulating antioxidant capacity and myogenic regulatory factor expression.

The purpose of this experiment was to explore the effects of zinc supplementation in breeding pigeons diet on carcass traits, meat quality, antioxidant capacity and mRNA expressions of myogenic regulatory factors of squabs. A total of 120 healthy White King pigeons were randomly assigned to 5 treatments, each involving 8 replicates. The experiment lasted for 46 d (18-d incubation period of eggs and 28-d growth period of squabs). The 5 groups were 0, 30, 60, 90, and 120 mg/kg zinc addition. Results showed that the 28-d body weight, breast muscle yield, zinc content in crop milk and myogenic factor 6 (MyF6) abundance of breast muscle were linearly increased (P < 0.050), but the abdominal fat yield linearly decreased (P = 0.040) with increasing dietary zinc supplementation. Both the linear (P < 0.050) and quadratic responses (P < 0.001) were observed in copper zinc superoxide dismutase (Cu-Zn SOD), total antioxidant capacity (T-AOC) and malondialdehyde (MDA) contents in liver and breast muscle. The 28-d body weight was increased by 90 mg/kg zinc supplementation (P < 0.05), and there is no significant difference between 90 and 120 mg/kg zinc addition. The breast muscle yield, Cu-Zn SOD and T-AOC contents in breast muscle and liver, zinc contents in crop milk and breast muscle, MyF6 mRNA expression in breast muscle were higher (P < 0.05) in the group supplemented with 120 mg/kg zinc than the control. The abdominal fat yield was numerically lowest, and MDA contents in breast muscle and liver were significantly lowest in the group fed 120 mg/kg zinc (P < 0.05). However, the meat quality traits were not affected (P > 0.05) by zinc supplementation, except for shear force. It should be stated dietary zinc supplementation at the level of 120 mg/kg for breeding pigeons increased body weight and breast muscle yield of squabs, which may be associated with the up-regulating MyF6 mRNA expression and antioxidant capacity in liver and breast muscle.

Protective Effect of Manganese on Apoptosis and Mitochondrial Function of Heat-Stressed Primary Chick Embryonic Myocardial Cells.

Heat stress, as a kind of oxidative stress, induces cell apoptosis. Apoptosis is a form of programmed cell death, and mitochondria play an important role in apoptosis. Manganese (Mn) has an antioxidant capacity by enhancing the activity of manganese superoxide dismutase (MnSOD). To investigate the potential effect of Mn on heat stress-induced apoptosis and mitochondrial function, we examined crucial related factors in the context of heat stress using primary chick embryonic myocardial cells pretreated with Mn for 24 h. The results showed that Mn restored the heat stress-induced decrease in cell viability and reduced the activities of caspase-3 (P < 0.05). The repression of the Δψm and intracellular ATP content caused by heat stress was reversed dramatically in the Mn pretreatment group (P < 0.05). Additionally, Mn inhibited heat stress-induced mitochondrial fission, as shown by decreased mitochondrial fission-related protein dynamin-related protein 1 (Drp1) expression and increased mitochondrial fusion-related protein optic atrophy 1 (Opa1) and mitofusin 1 (Mfn1) (P < 0.05) in primary chick embryonic myocardial cells. It was concluded that Mn attenuates the mitochondrial-mediated apoptosis pathway and sustains mitochondrial structure and function under heat stress in primary chick embryonic myocardial cells.

Manganese Mitigates Heat Stress-Induced Apoptosis by Alleviating Endoplasmic Reticulum Stress and Activating the NRF2/SOD2 Pathway in Primary Chick Embryonic Myocardial Cells.

Heat stress leads to oxidative stress and induces apoptosis in various cells. Endoplasmic reticulum (ER) stress is an important apoptosis pathway. Manganese (Mn) has been shown to enhance the activity of manganese superoxide dismutase (MnSOD). To explore the potential effect of Mn on ER stress and apoptosis induced by heat stress, we examined crucial factors associated with heat stress, ER stress, and apoptosis in cultured primary chick embryonic myocardial cells that had been pretreated with 20 µM Mn for 24 h and then subjected to 4 h of heat stress. The results showed that Mn decreased (P < 0.05) heat stress-induced reactive oxygen species (ROS) production and exerted antiapoptotic effects by increasing MnSOD enzymatic activity. The heat stress-induced accumulation of intracellular calcium was dramatically reduced (P < 0.05). Mn treatment significantly decreased (P < 0.05) the expression levels of the apoptosis-related gene Bax and ER stress markers glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP) in primary chick embryonic myocardial cells. Additionally, Mn reduced oxidative stress by activating the nuclear factor E2-related factor 2 (NRF2)/SOD2 signaling pathway. Taken together, our findings indicate that Mn attenuates heat stress-induced apoptosis by inhibiting ROS generation, intracellular calcium accumulation, and the ER stress pathway and activating the NRF2/SOD2 signaling pathway to protect myocardial cells from oxidative stress during chick embryonic development.

Whole-Genome Resequencing to Study Brucellosis Susceptibility in Sheep.

Brucellosis is a zoonotic disease and a major public health problem. However, the genetic mechanism of brucellosis in sheep remains unclear. In this study, serum samples were collected from 6,358 sheep from the F2 population (Dorper sheep ♂ × Hu sheep ♀), and antibody levels were continuously measured at 14 days and 1, 2, 3, 4, 5, 6, 7, 8, 9, and 10 months after administration of brucellosis vaccine. Finally, 19 brucellosis-resistant group (BRG) sheep and 22 brucellosis-susceptible group sheep (BSG) were screened for whole-genome sequencing. Using the fixation index, Fisher's exact test, and chi-square test, a total of 205 candidate SNP sites were identified. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis suggested that 138 candidate genes were significantly enriched in adherens junction (CTNNA3, PARD3, and PTPRM), cell adhesion molecules (NLGN1, CNTNAP2, NCAM1, and PTPRM), salivary secretion (LOC101102109, PRKG1, and ADCY2), and hippo signaling pathway (CTNNA3, YAP1, and PARD3). These findings provide valuable molecular markers for brucellosis resistance breeding in sheep and novel insights into the genetic mechanism of brucellosis resistance.