Curcumin alleviates cecal oxidative injury in diquat-induced broilers by regulating the Nrf2/ARE pathway and microflora.

This study evaluated the alleviative effect of curcumin (CUR) on the diquat (DQ)-induced cecal injury in broilers. A total of 320 one-day-old Cobb broilers were selected and randomly divided into 4 treatments, namely control, DQ, CUR 100, and CUR150 groups. The control and DQ groups were fed a basal diet, while the CUR 100 and CUR150 groups were fed the basal diet supplemented with 100 and 150 mg/kg CUR, respectively. Each group had 8 replicates, with 10 broilers per replicate. On day 21 of the experiment, 1 broiler was selected from each replicate and intraperitoneally injected 20 mg/kg body weight of DQ for DQ, CUR 100, and CUR 150 groups. Broilers in control group received equivalent volume of saline. Broilers were euthanized 48h postinjection for tissue sampling. The results showed that DQ injection could cause oxidative stress and inflammatory reactions in the cecum, affecting the fatty acid production and flora structure, thus leading to cecum damage. Compared with the DQ group, the activity of superoxide dismutase, the level of interleukin 10, acetic acid, and total volatile fatty, and the abundance of nuclear factor E2-related factor 2, copper and zinc superoxide dismutase and catalase mRNA in the cecal mucosa of broilers in the CUR group increased significantly (P < 0.05). However, the levels of malondialdehyd, reactive oxygen species, tumor necrosis factor-alpha, and the expression of cysteine-aspartic acid protease-3 and tumor necrosis factor-alpha decreased significantly (P < 0.05) in the CUR group. In addition, CUR treatment alleviated the damage to the cecum and restored the flora structure, and Lactobacillus and Lactobacillaceae promoted the alleviative effect of CUR on DQ. In summary, CUR could alleviate the cecal injury caused by DQ-induced oxidative damage and inflammatory reactions by regulating the Nrf2-ARE signaling pathway and intestinal flora, thus protecting the cecum.

Protective effects of selenium yeast against cadmium-induced necroptosis through miR-26a-5p/PTEN/PI3K/AKT signaling pathway in chicken kidney.

Cadmium (Cd) is a ubiquitous environmental pollutant of increasing worldwide concern to both humans and animals. Selenium yeast (Se-Y) is an organic selenium source that has been shown an advantage in antagonizing Cd-induced liver necroptosis in chicken. Herein, we described the discovery path of Se-Y antagonism in Cd-induced renal necroptosis in chicken through targeting miR-26a-5p/PTEN/PI3K/AKT signaling pathway. We set up four groups of chickens at random: control group (0.5 mg/kg Na2SeO3), Se-Y group (0.5 mg/kg Se-Y), Se-Y+Cd group (0.5 mg/kg Se-Y and 150 mg/kg CdCl2) and Cd group (150 mg/kg CdCl2 and 0.5 mg/kg Na2SeO3). Interestingly, we found Se-Y, but not Na2SeO3, significantly blocked Cd accumulation in the kidney and alleviated Cd-induced necroptosis through inhibiting the expression of RIP1, RIP3 and MLKL. Se-Y, activated miR-26a-5p expression, thereby down-regulated the expression of PTEN, resulting in the up-regulation of PI3K/AKT signaling pathway and the inhibition of oxidative stress in both Se-Y and Cd treated chickens. Besides that, Se-Y could also specifically reduce the expression levels of heat shock protein 60 (HSP60), HSP70 and HSP90 in Se-Y and Cd co-treated chickens. Taken together, our results showed that Se-Y has an added value to antagonize Cd-induced necroptosis in chicken kidney by regulating the miR-26a-5p/PTEN/PI3K/AKT signaling pathway and HSPs, indicating that Se-Y could serve as an effective antagonist on Cd-induced renal necroptosis in chickens.

Docosahexaenoic acid (22:6 n-3)-rich microalgae along with methionine supplementation in broiler chickens: effects on production performance, breast muscle quality attributes, lipid profile, and incidence of white striping and myopathy.

The effect of docosahexaenoic acid (DHA, 22:6 n-3)-rich microalgae and methionine (Met) supplementation on production performance, incidence of breast muscle white striping (WS), and pathology, lipid profile, and meat quality aspects in broiler chickens was investigated. The hypothesis tested was that feeding Met and n-3 fatty acid (FA)-rich diet enhances muscle n-3 FA content and meat quality while attenuating breast muscle WS and myopathy in broiler chickens. One hundred and forty four (n = 144) 10-day-old Cornish cross chicks were fed a corn-soybean meal-based diet containing 0% microalgae (control), 2% microalgae (diet 1), and diet 1 + 100% more National Research Council requirement of Met (diet 2) up to day 42 of growth. All diets were isocaloric and isonitrogenous. The chicks were kept in 6 pens with 8 chicks per replicate pen. Feed consumption and feed efficiency were calculated on day 21 and 42. On day 43, 3 chicks per pen (n = 18/treatment) were euthanized. The breast muscle (pectoralis major) was visually scored for muscle WS (1 = no striping, 2 = mild, 3 = severe) and was subjected to histopathology. Breast muscle lipid profile (total lipids, FA composition, cholesterol, lipid oxidation products), quality (moisture, color, drip loss, shear force, cook loss, pH), and chemical characterization (protein, minerals) were recorded. A one-way analysis of variance was carried out with diet as the main factor and significance was set at P < 0.05. The incidence of muscle WS was lower (P < 0.02) for control vs. diet 2 and a trend for reduction in WS was observed in birds fed diet 1 vs. control (P = 0.09). Histopathological changes consisted of floccular or vacuolar degeneration, fibrosis, lipidosis, interstitial inflammation, and lysis of fibers, and were minimal in diet 2 when compared to control (P < 0.05). The total lipid content was lowest in birds fed diet 1 (P < 0.05). Total n-3 and total long chain (≥20C) n-3 FA were highest in the breast muscle of diet 2 birds (P < 0.05). Muscle drip loss and shear force were highest in diet 2 (P < 0.05). Meat color (a∗, redness) was reduced (P < 0.05) and a trend for reduction in b∗ (yellowness) was observed in diet 2 (P = 0.07). No effect of diet on body weight gain, feed efficiency, breast muscle yield, pH, moisture, lipid oxidation products, cook loss, minerals (Ca, P, Mg, Na), cholesterol, or protein content was observed (P > 0.05). The results demonstrated a significant effect of DHA-rich microalgae along with Met supplementation in reducing the incidence of breast muscle striping and myopathy, while enriching meat with n-3 FA. However, inclusion of Met in microalgae-based diets could influence meat tenderness and color.

Dietary Se deficiency dysregulates metabolic and cell death signaling in aggravating the AFB1 hepatotoxicity of chicks.

The objective of this study was to use isobaric tags for relative and absolute quantitation (iTRAQ) proteomic technology to systematically analyze the hepatotoxic mechanism of aflatoxin B1 (AFB1) and its prevention by Se in broilers. Four groups of day-old broilers were allocated into a 2 × 2 factorial design trial that fed a Se-deficient based diet (BD) or the BD + 1.0 mg AFB1/kg, 0.3 mg Se/kg, or 1.0 mg AFB1/kg plus 0.3 mg Se/kg for 3 wk. Dietary AFB1 increased serum ALT and decreased total protein and albumin concentrations, and induced hepatic histopathological lesions in Se adequate groups. Notably, Se deficiency exacerbated these AFB1-induced changes. Furthermore, Se deficiency reduced hepatic glutathione peroxidase but increased thioredoxin reductase and glutathione S-transferase activities and 8-hydroxydeoxyguanosine concentration in AFB1 administrated groups. Moreover, AFB1 dysregulated 261 co-differentially expressed proteins (DEPs) in both Se adequate and deficiency diets, and Se deficiency dysregulated 64 DEPs in AFB1 administrated diets. These DEPs are mainly related to phase I and II metabolizing enzymes, heat shock proteins, DNA repair, fatty acid metabolism and apoptosis. The in vitro study has verified that aldo-keto reductase family1, member10 plays an important role in AFB1-induced hepatotoxicity and Se-mediated detoxification of AFB1 in a chicken leghorn male hepatoma cells. Conclusively, this study has analyzed the hepatic proteome response to dietary AFB1 and Se, and thus shed new light on the mechanisms of hepatotoxicity of AFB1 and its detoxification by Se in broilers.

Lactobacillus rhamnosus JYLR-005 Prevents Thiram-Induced Tibial Dyschondroplasia by Enhancing Bone-Related Growth Performance in Chickens.

Tibial dyschondroplasia (TD) is a leg disorder caused by the abnormal development of the tibia in fast-growing poultry. Lactobacillus rhamnosus (L. rhamnosus) strains have been reported to have effects on increasing bone growth and improving osteoporosis in animals. However, whether L. rhamnosus JYLR-005 can improve bone growth in TD chickens remains unclear. In this study, we noted that L. rhamnosus JYLR-005 could not reduce the suppression of the production performance of TD broilers (p > 0.05) but had a slight protective effect on the broiler survival rate (χ2 = 5.571, p = 0.062). However, for thiram-induced TD broiler chickens, L. rhamnosus JYLR-005 could promote tibia growth by increasing tibia-related parameters, including the tibia weight (day 11, p = 0.040), tibia length (day 15, p = 0.013), and tibia mean diameter (day 15, p = 0.035). Moreover, L. rhamnosus JYLR-005 supplementation improved the normal growth and development of the tibial growth plate by maintaining the morphological structure of the chondrocytes and restored the balance of calcium and phosphorus. Taken together, these findings provide a proof of principle that L. rhamnosus JYLR-005 may represent a therapeutic strategy to treat leg disease in chickens.

Pterostilbene as a protective antioxidant attenuates diquat-induced liver injury and oxidative stress in 21-day-old broiler chickens.

This study investigated the effects of pterostilbene (PT) supplementation on growth performance, hepatic injury, and antioxidant variables in a broiler chicken model with diquat (DQ)-induced oxidative stress. There were 192 one-day-old male Ross 308 broiler chicks randomly allocated to one of two treatment groups: 1) broilers fed a basal diet and 2) broilers fed a diet supplemented with 400 mg/kg PT. At 20 D of age, half of the broilers in each group were intraperitoneally injected with DQ (20 mg per kg BW), whereas the other half were injected with an equivalent amount of sterile saline. Diquat induced a rapid loss of BW (P < 0.001) 24 h post-injection, but dietary PT supplementation improved the BW change of broilers (P = 0.014). Compared with unchallenged controls, the livers of DQ-treated broilers were in severe cellular damage and oxidative stress, with the presence of higher plasma transaminase activities (P < 0.05), a greater number of apoptotic hepatocytes (P < 0.001), and an increased malondialdehyde content (P = 0.007). Pterostilbene supplementation prevented the increases in plasma aspartate aminotransferase activity (P = 0.001), the percentage of hepatocyte apoptosis (P < 0.001), and the hepatic malondialdehyde accumulation (P = 0.011) of the DQ-treated broilers. Regarding the hepatic antioxidant function, PT significantly increased total antioxidant capacity (P = 0.007), superoxide dismutase activity (P = 0.016), reduced glutathione content (P = 0.011), and the ratio of reduced glutathione to oxidized glutathione (P = 0.003), whereas it reduced the concentration of oxidized glutathione (P = 0.017). Pterostilbene also boosted the expression levels of nuclear factor erythroid 2-related factor 2 (P = 0.010), heme oxygenase 1 (P = 0.037), superoxide dismutase 1 (P = 0.014), and the glutamate-cysteine ligase catalytic subunit (P = 0.001), irrespective of DQ challenge. In addition, PT alleviated DQ-induced adenosine triphosphate depletion (P = 0.010). In conclusion, PT attenuates DQ-induced hepatic injury and oxidative stress of broilers presumably by restoring hepatic antioxidant function.

Black bone syndrome in broilers fed ethanolic extract of mango seeds.

This study aimed to evaluate the incidence of black bone syndrome (BBS) in broiler chickens fed with ethanolic extract of mango seed (EEMS). A total of 504 one-day-old male broilers were used in a completely randomised design assigned with 7 experimental diets and 6 replicates of 12 broilers per experimental plot. The experimental diets consisted of: diet without addition of synthetic antioxidant; diet with addition of synthetic antioxidant (200 ppm); and 5 levels of EEMS: 200 ppm, 400 ppm, 600 ppm, 800 ppm, and 1,000 ppm. Two methods of cooking (roasted and boiled) were used to prepare thigh samples. According to the results, the diets did not significantly influence the performance of the broilers. BBS incidence was higher in broilers fed a diet without antioxidants and was reduced with EEMS dietary inclusion, with the lowest incidence occurring with the inclusion of 1,000 ppm. The synthetic antioxidant butylated hydroxytoluene in the diet promoted a significantly higher BBS incidence than that obtained with 800 and 1,000 ppm EEMS and did not differ from the other diets. Of the cooking methods, a higher BBS incidence was observed for the boiled method. For the meat coloration and bone parameters, there were no significant interactions between the factors, diets and cooking methods. There was a linear reduction in the darkening score and linear increase in the luminosity (L∗) of the meat with increasing EEMS in the diet. With regard to the cooking method, the boiled thighs had lower luminosity (L∗), higher parameter a∗, and lower parameter b∗ values because of more pronounced meat darkening. The roasted bones were less heavy, dense, and flexible. A negative correlation was observed between the degree of darkening of the meat that characterizes the BBS with the luminosity (L∗) and intensity of yellow. We concluded that the addition of EEMS contributes to a reduced darkening of meat that characterises the BBS and recommend the dietary inclusion of 1,000-ppm EEMS.

Obesity, insulin resistance, adiponectin, and PPAR-γ gene expression in broiler chicks fed diets supplemented with fat and green tea (Camellia sinensis) extract.

Adipose tissue is an active endocrine organ secreting several adipokines, especially adiponectin, that play an important role in regulating insulin function in the body of mammals. Therefore, this study was aimed to investigate the association between abdominal fat deposit, insulin resistance, peroxisome proliferator-activated receptor gamma (PPAR-γ), and adiponectin gene (AG) expression in broiler chicks fed diets high in unsaturated fat supplemented with green tea extract (GTE). A total of 300 one-day-old female Ross 308 broiler chicks were allocated to 6 dietary treatments in a completely randomized design with a factorial arrangement of two levels of GTE (0 and 500 mg/kg diet) × three levels of fat inclusion [without fat (control group), soybean oil (SO), and tallow (Ta)]. Each treatment was replicated five times. At the end of the experiment (day 49), two chicks from each replicate weighing an average of pen weight were bled and then slaughtered for further analysis. Abdominal fat percentage, fasting concentration of blood glucose, triglyceride and insulin, glycogen reserves of breast and liver tissues, and PPAR-γ and AG expression were determined. The insulin resistance index of the Quantitative Insulin Sensitivity Check Index (QUICKI) was calculated using the fasting plasma glucose and insulin concentrations. The highest abdominal fat percentage and the lowest carcass yield were obtained in chicks fed SO-supplemented diet (P < 0.05). Chicks fed diet supplemented with SO showed the highest PPAR-γ gene expression (P < 0.05). SO-rich diets suppressed AG expression in chickens' abdominal fat tissue, and the birds fed with SO-supplemented diet showed a significant decrease in AG expression compared with the control (P < 0.05). Chicks fed diet supplemented with SO showed lower QUICKI and breast glycogen reserve compared with the control group (P < 0.05). A significant increase in blood glucose and triglyceride concentrations was observed in birds fed SO-supplemented diets (P < 0.05). AG and PPAR-γ expression increased and decreased by GTE, respectively. QUICKI tended (P = 0.09) to be greater in GTE-supplemented chicks; however, the effect of GTE supplementation on carcass yield, abdominal fat percentage, and blood insulin and glucose concentration was not significant. The findings of this study showed that SO-rich diets via increased PPAR-γ gene expression and decreased AG expression in abdominal fat may lead to insulin resistance in female broiler chicks.

Independent and combined effects of Satureja khuzistanica essential oils and acetic acid on prevalence and intensity of fatty liver syndrome in broiler chickens.

Two hundred fifty two male Ross 308 broiler chicks were raised to examine the effects of Satureja khuzistanica essential oils (SkEO; 0, 200, 300, 400, 500 and 600 mg/bird/day) administrated via oral gavage and dietary supplementation of acetic acid (AA; 0 or 20 g/kg) in a 6 × 2 factorial fashion using a complete randomized block design with seven replicates of three birds each. In Day 34 of age, liver fat percentage decreased by increasing SkEO levels in a quadratic trend (p < .05). Oral gavag of 200 and 300 mg of SkEO decreased AST activity by 16.67% and 16.94%, respectively, compared with the control birds (p < .05). In Day 38 of age, liver percentage was greater by 0.37% in the birds received 400 mg SkEO than those given 500 mg (p < .05). Liver fat percentage decreased in the birds fed the acidified diet and received 300 and 500 mg SkEO as well as in the birds offered 200 and 400 mg of SkEO and fed non-acidified diet than those received acidified diet with no SkEO administration (p < .05). Prevalence of score zero for hepatocytic vacuolations and necrosis was 80.00% and 42.42% in the birds receiving 600 mg SkEO respectively. Median for relative frequency of scores for hepatocytic vacuolations and hepatocytic necrosis was lesser in the birds received SkEO by oral gavage compared with that of control birds (p < .05). In conclusion, administration of SkEO via oral gavage reduced liver fat in broiler chicken but no consistent dosage could be verified as the effective dosage for all ages concerned. The acidified diet per se showed no evident effect on liver fat at all ages considered. The SkEO × AA interaction exhibited promising but unreliable effects on liver colour score in market age (42 days).

Plastrum Testudinis Extract Mitigates Thiram Toxicity in Broilers via Regulating PI3K/AKT Signaling.

Tibial dyschondroplasia (TD) negatively affects broilers all over the world, in which the accretion of the growth plate (GP) develops into tibial proximal metaphysis. Plastrum testudinis extract (PTE) is renowned as a powerful antioxidant, anti-inflammatory, and bone healing agent. The current study was conducted to evaluate the efficacy of PTE for the treatment of thiram-induced TD chickens. Broilers (day old; n = 300) were raised for 3 days with normal feed. On the 4th day, three groups (n = 100 each) were sorted, namely, the control (normal diet), TD, and PTE groups (normal diet+ thiram 50 mg/kg). On the 7th day, thiram was stopped in the TD and PTE group, and the PTE group received a normal diet and PTE (30 mg/kg/day). Plastrum testudinis extract significantly restored (p < 0.05) the liver antioxidant enzymes, inflammatory cytokines, serum biochemicals, GP width, and tibia weight as compared to the TD group. The PTE administration significantly increased (p < 0.05) growth performance, vascularization, AKT (serine/threonine-protein kinase), and PI3K expressions and the number of hepatocytes and chondrocytes with intact nuclei were enhanced. In conclusion, PTE has the potential to heal TD lesions and act as an antioxidant and anti-inflammatory drug in chickens exposed to thiram via the upregulation of AKT and PI3K expressions.

The potential of acetylsalicylic acid and vitamin E in modulating inflammatory cascades in chickens under lipopolysaccharide-induced inflammation.

Distinct enzymes, including cyclooxygenase 1 and 2 (COX-1 and COX-2), lipoxygenase (LOXs), and cytochrome P450 monooxygenase (CYP450), produce different stress mediators and mediate inflammation in birds. Bioactive agents such as acetylsalicylic acid (ASA) and vitamin E (vE) may affect enzyme activities and could be used in poultry production to control the magnitude of acute phase inflammation. Here, we characterized COX, LOX, and CYP450 mRNA expression levels in chicken immune tissues in response to Escherichia coli lipopolysaccharide (LPS) challenge and investigated whether ASA and vE could alter gene expression. Additionally, for the first time in chickens, we evaluated oxygen consumption by platelet mitochondria as a biomarker of mitochondria function in response to ASA- and vE. LPS challenge compromised bird growth rates, but neither dietary ASA nor vE significantly ameliorated this effect; however, gradually increasing dietary vE levels were more effective than basal levels. ASA regulated arachidonic acid metabolism, providing an eicosanoid synthesis substrate, whereas gradually increasing vE levels evoked aspirin resistance during challenge. Gene expression in immune tissues was highly variable, indicating a complex regulatory network controlling inflammatory pathways. However, unlike COX-1, COX-2 and CYP450 exhibited increased mRNA expression in some cases, suggesting an initiation of novel anti-inflammatory and pro-resolving signals during challenge. Measuring oxygen consumption rate, we revealed that neither the ASA nor vE levels applied here exerted toxic effects on platelet mitochondria.

Effects of sodium butyrate on intestinal health and gut microbiota composition during intestinal inflammation progression in broilers.

Butyric acid is a beneficial feed additive used in animal production, including poultry production. However, there are few reports on butyric acid as a prophylactic treatment against intestinal inflammation in broilers. The current study explored the effect of sodium butyrate (SB) as a prophylactic treatment on the intestinal health and gut microbiota of broilers with intestinal inflammation induced by dextran sulfate sodium (DSS) by monitoring changes in intestinal histopathology, gut leakiness indicators, inflammatory cytokines, and gut microbiota composition. Sodium butyrate supplementation prior to DSS administration significantly reduced the lesion scores of intestinal bleeding (P < 0.05) and increased villus height and the total mucosa of the ileum (P < 0.05). Regardless of intestinal inflammation, supplementation with SB at 300 mg/kg significantly decreased the levels of D (-)-lactate (P < 0.05), interleukin-6, and interleukin-1ß (P < 0.05) but increased the level of interleukin-10 (P < 0.05). The SB treatment did not affect the alpha diversity of intestinal microbiota during intestinal inflammation progression but altered their composition, and the microbial community structure of treated broilers was similar to that of control broilers. Taken together, our results reveal the importance of SB in improving intestinal development, inducing an anti-inflammatory effect during intestinal inflammation progression, and modulating the microbial community in broilers. Sodium butyrate seems to be optimized for anti-inflammatory effects at higher doses (300 mg/kg SB).

Comparative evaluation of aflatoxin and mineral binding activity of molecular imprinted polymer designed for dummy template using in vitro and in vivo models.

The amelioration of aflatoxicosis in ducklings was examined by feeding molecular imprinted polymer (MIP) synthesized to target the aflatoxin B1 (AFB1) analog molecule [5, 7-dimethoxycoumarin (DMC)] as a smart and novel toxin binder in comparison to a commercial toxin binder (CTB). MIP was characterized with some techniques, such as scanning electron microscopy (SEM) and thermal gravimetric analysis (TGA) that showed morphology and thermal resistance of MIP, respectively. The SEM showed that more pores and big cavities were formed in the network of the MIP. TGA plots of MIP showed dehydration at temperatures of about 31 °C-200 °C and gradual decomposition until 300 °C. The in vitro and in vivo ability of MIP and CTB to adsorb some minerals (Ca, Cu, Mg, P and Zn) was evaluated. The in vivo efficacy of MIP as an aflatoxins (AFs) binder in duckling exposed to aflatoxin-contaminated feed from 4 to 18 d of age was also compared to that of the CTB. A total of 240 4-d-old ducklings were assigned to experimental diets. Each diet was replicated four times with 10 birds in each pen, and the initial body weight classes were considered as blocks. The experimental treatment diets included: 1- Control (basal diet without any additive or AFs), 2- MIP (5 g/kg diet), 3- CTB (5 g/kg diet), 4- AFs (0.2 mg/kg diet), 5- AFs + MIP (0.2 mg/kg + 5 g/kg diet), and 6- AFs + CTB (0.2 mg/kg + 5 g/kg diet). In vitro study may clearly reflect the possibility of adsorbing minerals by CTB as compared to MIP whilst the results were not confirmed by in vivo study and it seems that reduction in plasma levels of minerals is related to the adverse effects of AFs. Livers showed histopathological alterations, with bile-duct proliferation of all aflatoxin fed ducklings. Macroscopic study indicated liver of birds fed diets containing AFs showed abnormal signs including yellowish, friable and rounded shape without protective effect of MIP and CTB. The results obtained from in vivo study indicate the partial alleviation of the adverse effects of AFs in ducklings by dietary supplementation of MIP and CTB (5 g/kg) on plasma albumin, Zn, Mg and Ca.

Lead Levels in the Eggs of a Chicken With Lead Toxicosis.

A 1.5-year-old Polish hen was presented with a history of watery droppings and poor vent tone. Results of diagnostic tests revealed blood lead at levels considered to be toxic. Chelation therapy was started with calcium ethylenediaminetetraacetate. The hen was laying eggs before, during, and after chelation therapy. Eggs were tested for the presence of lead by combining yolk and albumen together. Before chelation therapy, the level of lead in the egg tested was 14 µg. Two days after the end of chelation therapy, results of a second blood lead test revealed a drop to nontoxic levels. No lead was detected in the combined yolks and albumen of eggs collected 7-11 days after the end of chelation therapy. Four weeks after the end of chelation therapy, no lead was identified in the shells of tested eggs.

Evaluation of different dietary alterations in their ability to mitigate the incidence and severity of woody breast and white striping in commercial male broilers.

The following study was conducted to define how multiple nutritional strategies affect broiler performance, meat yield, and the presence and severity of white striping (WS) and woody breast (WB) in high-yielding broilers. Relative to a commercial set of reference broiler diets (Commercial reference diet; Trt 1) that were fed in a 4-phase program, the following nutritional strategies were investigated: increasing the ratio of digestible arginine: digestible lysine (dArg: dLys ranged from 113 to 126; Trt 2), supplementing Trt 1 with 94.4 mg vitamin C/kg feed (Trt 3), doubling the vitamin pack inclusion rate (Trt 4), reducing the digestible amino acid density (dAA) of only the grower phase by 15% and feeding the same Trt 1 starter, finisher, and withdraw diets (Trt 5), and combining the 4 strategies just mentioned (Trt 6). There was no difference in performance at the end of the starter phase (P = 0.066); however, at the end of the grower and finisher phases, feeding lower dAA grower diets suppressed BW (Trts 5 and 6; P < 0.001) and increased FCR. Differences in performance amongst all treatments disappeared at day 49 (P = 0.220). No differences were observed in average breast weight (P = 0.188); however, breast yield (as a % of live weight) was greatest for Trt 1 and least for Trt 6 (P = 0.041). The WB score dropped from 1.83 in Trt 1 to 1.49, 1.27, 1.74, 1.53, and 1.43 in treatments 2 to 6, respectively (P = 0.018). These changes were the result of a shift in WB score, where the WB class that contained scores of 2 and 3 shifted from 61.3% in Trt 1 to 49.3, 35.9, 60.0, 50.8, and 38.7 in treatments 2 to 6, respectively. Given the FCR, breast weight data and the fact that high WB scores result in a devaluation of breast meat, feeding a higher ratio of dArg: dLys, higher vitamin C, or lower dAA in the grower phase results in better breast meat quality and value.

Dietary l-threonine supplementation attenuates lipopolysaccharide-induced inflammatory responses and intestinal barrier damage of broiler chickens at an early age.

This study was conducted to investigate the protective effects of l-threonine (l-Thr) supplementation on growth performance, inflammatory responses and intestinal barrier function of young broilers challenged with lipopolysaccharide (LPS). A total of 144 1-d-old male chicks were allocated to one of three treatments: non-challenged broilers fed a basal diet (control group), LPS-challenged broilers fed a basal diet without l-Thr supplementation and LPS-challenged broilers fed a basal diet supplemented with 3·0 g/kg l-Thr. LPS challenge was performed intraperitoneally at 17, 19 and 21 d of age, whereas the control group received physiological saline injection. Compared with the control group, LPS challenge impaired growth performance of broilers, and l-Thr administration reversed LPS-induced increase in feed/gain ratio. LPS challenge elevated blood cell counts related to inflammation, and pro-inflammatory cytokine concentrations in serum (IL-1ß and TNF-α), spleen (IL-1ß and TNF-α) and intestinal mucosa (jejunal interferon-γ (IFN-γ) and ileal IL-1ß). The concentrations of intestinal cytokines in LPS-challenged broilers were reduced by l-Thr supplementation. LPS administration increased circulating d-lactic acid concentration, whereas it reduced villus height, the ratio between villus height and crypt depth and goblet density in both jejunum and ileum. LPS-induced decreases in jejunal villus height, intestinal villus height:crypt depth ratio and ileal goblet cell density were reversed with l-Thr supplementation. Similarly, LPS-induced alterations in the intestinal mRNA abundances of genes related to intestinal inflammation and barrier function (jejunal toll-like receptor 4, IFN- γ and claudin-3, and ileal IL-1 ß and zonula occludens-1) were normalised with l-Thr administration. It can be concluded that l-Thr supplementation could attenuate LPS-induced inflammatory responses and intestinal barrier damage of young broilers.

Broiler responses to increasing selenium supplementation using Zn-L-selenomethionine with special attention to breast myopathies.

A study was conducted to evaluate growth performance, carcass and breast yields, and the occurrence and severity of white striping (WS) and wooden breast (WB) myopathies of broilers fed diets supplemented with increasing dietary levels of an organic source of selenium (Zn-L-SeMet). Broilers were fed 6 treatments with 12 replications of 26 birds in a 4-phase feeding program from 1 to 42 days. Corn-soy-based diets were supplemented with 0, 0.2, 0.4, 0.6, 0.8, and 1.0 ppm of Zn-L-SeMet. At 42 d, 6 birds were randomly selected from each pen (n = 72) and processed for carcass and breast yields. Breast fillets were scored for WS and WB at 42 days. Increasing Zn-L-SeMet led to quadratic responses (P < 0.05) for FCR from 1 to 7 d, BWG from 22 to 35 d, and for both responses from 8 to 21 d and 36 to 42 d, as well as in the overall period of 42 days. Carcass and breast yields presented a quadratic improvement (P < 0.01) with increasing Zn-L-SeMet supplementation and Se requirements were estimated at 0.85 and 0.86 ppm, respectively. In the overall period, estimates of Se requirements were 0.64 ppm for BWG and 0.67 ppm for FCR. White striping and WB scores presented quadratic increases (P < 0.01), and maximum scores were observed at 0.68 and 0.67 ppm, respectively. Broilers fed diets formulated without Se supplementation had a higher percentage of normal fillets compared to other Se supplementation levels (quadratic, P < 0.05). In conclusion, increasing Se supplementation to reach maximum growth performance led to higher degrees of severity of WS and WB. Selenium requirements determined in the present study were significantly higher than the present commercial recommendations.

Attenuating effect of melatonin on lipopolysaccharide-induced chicken small intestine inflammation.

Enriched melatonin (MEL) has been found in the mammalian intestine and has been recently demonstrated to alleviate rodent colitis. In this study, the effect of MEL on lipopolysaccharide (LPS)-induced intestinal inflammations was investigated in new chicken hatchlings. The chicks were fed with a diet supplemented with MEL (12.5 mg/day) from D1 to D10. Meanwhile, the chicks in the LPS or MEL + LPS groups were injected with LPS (10 mg/kg BW, i.p.) at D10. LPS treatment for 6 h increased the expression of IL-6, IL-4, caspase-3 mRNAs and TUNEL-positive cell populations, but decreased populations of the goblet and PCNA+ cells, IgA production and the expression of MUC2 mRNA in the duodenum. Compared with the LPS group, MEL pre-feeding alleviated duodenal inflammation and decreased the expression of TNF-α mRNAs by 23.6% (P = 0.004), IL-6 mRNAs by 69.4% (P = 0.001), IL-4 mRNAs by 4.1% (P = 0.824) and caspase-3 mRNAs by 45.8% (P < 0.001). Conversely, MEL pre-feeding attenuated the LPS-induced changes of IgA production by 161.6% (P = 0.013) and PCNA+ cell populations by 172.1% (P < 0.001) in the duodenum. TLR4 mRNA was also up-regulated by LPS treatment but down-regulated by MEL pre-feeding. In conclusion, dietary MEL could attenuate LPS-induced chick duodenal inflammation by down-regulating the expression of inflammatory cytokines, promoting epithelial cell proliferation, improving the immunological barrier and inhibiting epithelial apoptosis via the mediation of TLR4.

Glucose and lipid metabolism disorders in the chickens with dexamethasone-induced oxidative stress.

The purpose of this study was to investigate the effects of long-term treatment with dexamethasone (DEX) on the antioxidation and nutrition metabolism in broiler chickens. Broilers were placed on a high-nutrient diet for 41 days, and half were given orally DEX-supplemented water at 20 mg/L every other day from 19 to 41 days of age. DEX treatment downregulated superoxide dismutase activity as well as the mRNA expression of CuZn-superoxide dismutase and glutathione peroxidase with a decrease in GSH/GSSG ratio and an increase in malondialdehyde level in the liver of broilers. DEX treatment aggravated oxidative damage in the liver and, therefore, increased the sensitivity of broilers to ascites syndrome with higher mortality and reduced growth performance. Serum metabolomics analysis showed that DEX treatment significantly increased the levels of glucose, intermediates in protein metabolism (valine, proline, serine, threonine and urea) and lipid metabolism-related products (palmitic acid, stearic acid and cholesterol) while decreasing the levels of ß-hydroxy butyric acid, succinic acid and malic acid, demonstrating that DEX treatment inhibited the Krebs cycle and the oxidation of fatty acids, and promoted the de novo synthesis of fatty acids as well as protein decomposition in the liver of broilers. Additionally, detection of metabolism-related enzymes revealed that DEX treatment inhibited glycolysis and promoted glycogen decomposition. In summary, DEX treatment resulted in oxidative stress and glucose and lipid metabolism disorders in the broilers.

Liver mitochondrial dysfunction and electron transport chain defect induced by high dietary copper in broilers.

Copper is an important trace mineral in the diet of poultry due to its biological activity. However, limited information is available concerning the effects of high copper on mitochondrial dysfunction. In this study, 72 broilers were used to investigate the effects of high dietary copper on liver mitochondrial dysfunction and electron transport chain defect. Birds were fed with different concentrations [11, 110, 220, and 330 mg of copper/kg dry matter (DM)] of copper from tribasic copper chloride (TBCC). The experiment lasted for 60 d. Liver tissues on d 60 were subjected to histopathological observation. Additionally, liver mitochondrial function was recorded on d 12, 36, and 60. Moreover, a site-specific defect in the electron transport chain in liver mitochondria was also identified by using various chemical inhibitors of mitochondrial respiration. The results showed different degrees of degeneration, mitochondrial swelling, and high-density electrons in hepatocytes. In addition, the respiratory control ratio (RCR) and oxidative phosphorylation rate (OPR) in liver mitochondria increased at first and then decreased in high-dose groups. Moreover, hydrogen peroxide (H2O2) generation velocity in treated groups was higher than that in control group, which were magnified by inhibiting electron transport at Complex IV. The results indicated that high dietary copper could decline liver mitochondrial function in broilers. The presence of a site-specific defect at Complex IV in liver mitochondria may be responsible for liver mitochondrial dysfunction caused by high dietary copper.