Effects of 25-hydroxycholecalciferol on performance, gut health, and bone quality of broilers fed with reduced calcium and phosphorus diet during Eimeria challenge.

This study evaluated the effects of 25-hydroxycholecalciferol (25-OHD) on performance, gut health, and bone quality of broilers fed with reduced calcium (Ca) and phosphorus (P) diet during Eimeria spp. challenge. A total of 576 fourteen-day-old Cobb 500 male chicks were randomly distributed in a 2 × 2 × 2 factorial arrangement, with 6 replicates of 12 birds each. The main factors were 25-OHD level (0 or 3,000 IU/kg of feed), mineral level (0.84% of Ca/0.42% of P, the levels recommended for the grower phase (NOR) or 0.64% of Ca/0.22% of P (RED), and mid-high mixed Eimeria challenge or nonchallenge. 25-OHD improved phosphorus retention (P = 0.019), bone ash weight (P = 0.04), cortical bone trabecular connectivity (P = 0.043) during coccidiosis. For birds fed with reduced mineral levels, 25-OHD supplementation increased bone ash weight (P = 0.04). However, 25-OHD did not improve bone ash weight when birds were challenged and fed with reduced mineral levels. The dietary 3,000 IU of 25-OHD supplementation did not improve performance or gut morphology but support bone health during coccidiosis. Future investigations are needed for better understand 25-OHD role on bone microarchitecture and oxidative metabolism during coccidiosis.

Eimeria maxima infection impacts the protein utilisation of broiler chicks from 14 to 28 days of age.

In floor-raised broilers, coccidiosis is responsible for reducing the use of nutrients, mainly by impairing intestinal tissue function and activating the immune system. Understanding and quantifying how balanced dietary protein (BP) is used when birds are challenged will allow nutritionists to make decisions regarding challenged flocks. This study aimed to determine the effects of Eimeria maxima on broiler performance and body composition, and to calculate changes in the maintenance and efficiency of protein utilisation (Ep). A total of 2 400 male 14-day-old Cobb500 broiler chickens were randomly allotted to ten groups with six replications of 40 birds each, with a 5 × 2 factorial arrangement of treatments. Five levels of BP in reference to digestible lysine (3.6, 7.2, 10.8, 14.4, and 18.0 g/kg) were fed to unchallenged (NCH) and challenged (CH) broilers with 7 × 103E. maxima sporulated oocysts from 14 to 28 days of age. Performance and body deposition were measured using a comparative slaughter technique to compare BP maintenance requirements and Ep. ANOVA followed by a posthoc test was performed to compare the effects of BP levels, challenge, and their interactions. A monomolecular model describing the responses of NCH and CH broilers to BP intake, maintenance, and maximum protein deposition was compared. There were significant interactions between body weight gain and digestible lysine intake among the factors studied. Infection had a negative impact on all variables analysed, proving the efficacy of the challenge. The maintenance did not differ between the CH and NCH groups. Increased levels of dietary BP did not recover the maximum protein deposition in CH broilers. Eimeria maxima significantly reduced Ep by a factor of 0.09 times on Ep compared to the control group. The Eimeria maxima challenge was responsible to modify the use of BP altering the body composition and impairing broilers performance.

Dehydroepiandrosterone activates the GPER-mediated AMPK signaling pathway to alleviate the oxidative stress and inflammatory response in laying hens fed with high-energy and low-protein diets.

Fatty liver hemorrhagic syndrome (FLHS) seriously threatens the layer industry due to it can cause a sudden decline in egg production and acute death, and dietary supplement with bioactive substance is considered an effective way to prevent the FLHS occurrence. Dehydroepiandrosterone (DHEA) is a popular dietary supplement and it possesses anti-oxidative and anti-inflammatory functions; however, the effect and underlying mechanism about DHEA in protecting against the occurrence and development of FLHS remain elucidated. The current results showed that DHEA relieved HELP-induced decrease of egg productivity and liver injury in laying hens. Meanwhile, DHEA markedly enhanced the antioxidant capacity and then alleviated oxidative stress via activation of nuclear factor (erythroid-derived 2)-like 2 (NRF-2) signal in laying hens fed with HELP diets. In addition, DHEA significantly alleviated HELP-stimulated systemic inflammatory response by suppressing the overproduction of hepatic pro-inflammatory factors in laying hens, and further found this beneficial effect was achieved by blocking the activation of NF-κB pathway. Furthermore, we found that DHEA promoted the AMP-activated protein kinase α (AMPKα) activation and increased the G-protein-coupled estrogen receptor (GPER) expression level in laying hens fed with HELP diets. In summary, our data demonstrated that DHEA attenuates oxidative stress and inflammation through the activation of GPER-AMPK signal axis in laying hens fed with HELP diets. These results might facilitate an understanding of the benefits and mechanism of DHEA on the development of FLHS, and provide sufficient data to support it as a dietary supplement to control the FLHS-related metabolic diseases in chickens.

The effects of xylo-oligosaccharides on regulating growth performance, nutrient utilization, gene expression of tight junctions, nutrient transporters, and cecal short chain fatty acids profile in Eimeria-challenged broiler chickens.

A 21-d experiment was conducted to investigate the effects of xylo-oligosaccharides (XOS) on growth performance, nutrient utilization, gene expression of tight junctions, nutrient transporters, and cecal short chain fatty acids (SCFA) profile of broiler chickens challenged with mixed Eimeria spp. Two hundred fifty-two zero-day-old chicks were allocated to 6 treatments in a 3 × 2 factorial arrangement (corn-soybean meal diets supplemented with 0, 0.5, or 1.0 g/kg XOS; with or without Eimeria challenge). Challenged groups were inoculated with a solution containing E. maxima, E. acervulina, and E. tenella oocysts on d 15. During the infection period (d 15 to d 21), there was a significant (P < 0.05) Eimeria × XOS interaction for weight gain (WG). XOS significantly (P < 0.05) increased WG in the unchallenged birds but not in the challenged treatments. There was no significant Eimeria × XOS interaction for N and minerals utilization responses. XOS supplementation at 0.5 g/kg tended to alleviate Eimeria-induced depression in apparent ileal digestibility of DM (P = 0.052). Challenged birds had lower (P < 0.01) AME, AMEn, and total retention of N, Ca, and P. Eimeria upregulated (P < 0.01) gene expression of tight junction proteins claudin-1, junctional adhesion molecule-2, and glucose transporter GLUT1; but downregulated (P < 0.01) the peptide transporter PepT1, amino acid transporters rBAT, CAT2, y+LAT2, and zinc transporter ZnT1. XOS alleviated (P < 0.05) Eimeria-induced claudin-1 upregulation. Eimeria decreased (P < 0.05) cecal saccharolytic SCFA acetate, butyrate, and total SCFA, but increased (P < 0.05) branched chain fatty acids isobutyrate and isovalerate. The supplementation of XOS tended to decrease the concentration of isobutyrate (P = 0.08) and isovalerate (P = 0.062). In conclusion, 0.5 g/kg XOS supplementation alleviated depression in growth performance and nutrient utilization from the Eimeria challenge. In addition, supplemental XOS reversed the gene expression changes of claudin-1, also showed the potentials of alleviating the negative cecal fermentation pattern induced by Eimeria infection.

In ovo threonine supplementation affects ileal gene expression of nutrient transporters in broilers inoculated post-hatch with Salmonella Enteritidis.

The effect of in ovo threonine (Thr) supplementation on the ileal expression of glucose, peptide and amino acid transporters was assessed in Salmonella Enteritidis-challenged broiler chicks. At 17.5 days of incubation, fertile eggs were supplemented in the amniotic fluid with sterile saline or 3.5% threonine. Hatchlings were individually weighed, and Salmonella Enteritidis negative status was confirmed. At 2 days of age, half of the birds of each group were inoculated with sterile nutrient broth or Salmonella Enteritidis inoculum. Relative expression of sodium-dependent glucose transporter 1 (SGLT1), glucose transporter 2 (GLUT2), di- and tri-peptide transporter 1 (PepT1) and alanine, serine, cysteine, threonine transporter (ASCT1) was assessed at hatch, 2 and 9 days of age, i.e., before inoculation and 7 days post-inoculation (dpi). At 9 days of age (7dpi), threonine increased SGLT1 and GLUT2 expression, whereas GLUT2 expression decreased in Salmonella-challenged birds. There was a significant interaction between threonine and Salmonella for PepT1 and ASCT1. Threonine increased PepT1 expression only in non-challenged birds. In addition, in ovo supplementation increased expression of ASCT1 regardless of post-hatch inoculation; Salmonella inoculation resulted in decreased expression of ASCT1 only in supplemented birds. The results suggest that while intra-amniotic threonine administration in broiler embryos increases the expression of genes related to the absorption of monosaccharides and amino acids, Salmonella challenge may negatively affect the expression of protein related transporters in the ileum of broilers.

Immunohistochemical Expression of AQP2 and HSP70 in Broiler Kidney Tissue Treated with Salix tetrasperma Roxb. Extract under Heat Exposure.

The administration of plant extracts to broilers may be a way to mitigate the effects of heat stress. The importance of AQP2 and HSP70 compounds in maintaining the homeostasis of the chicken body when it is subjected to heat stress is well established. This study aims to determine the effect of giving the ethanolic extract of the leaves of Salix tetrasperma Roxb. on the immunohistochemical expression of AQP2 and HSP70 in exposed and unexposed broiler kidney tissue. This study used 36 samples of 28-day-old chicken kidneys. Chickens were kept in individual cages, provided with feed and drinking water ad libitum. The design used was a completely randomized design with 6 treatments and 6 replications: (a) chickens were reared in conditions exposed to heat (HS + 0); (b) chickens were reared in conditions exposed to heat and given Salix extract at a dose of 50 mg/L drinking water (HS + 50); (c) chickens were reared under heat-exposed conditions and given Salix extract at a dose of 100 mg/L drinking water (HS + 100); (d) chickens were reared in conditions without exposure to heat (n-HS + 0); (e) chickens were reared in conditions without exposure to heat and given Salix extract at a dose of 50 mg/L drinking water (nHS + 50); and (f) chickens were reared in conditions exposed without exposure to heat and given 100 mg/L drinking water (nHS + 100) of Salix extract. Salix extract was given for 24 hours and was renewed every 6 hours. The results showed that giving Salix extract 100 mg/L in drinking water to chickens exposed to heat (HS + 100) reduced the value of the H/L ratio. Giving Salix extract 50-100 mg/L in drinking water caused an upregulated AQP2 expression; on the other hand, it downregulated HSP-70 expression, in chicken kidney tubules both exposed to heat stress and nonexposed to heat stress. In conclusion, exposure to heat stress in broiler chickens and giving Salix extract can increase the formation of aquaporin 2 compounds and suppress the formation of HSP70.

Effect of chlorogenic acid on intestinal inflammation, antioxidant status, and microbial community of young hens challenged with acute heat stress.

Heat stress in poultry is deleterious to productive performance. Chlorogenic acid (CGA) exerts antibacterial, anti-inflammatory, and antioxidant properties. This study was conducted to evaluate the effects of dietary supplemental CGA on the intestinal health and cecal microbiota composition of young hens challenged with acute heat stress. 100-day-old Hy-line brown pullets were randomly divided into four groups. The control group (C) and heat stress group (HS) received a basal diet. HS + CGA300 group and HS + CGA600 group received a basal diet supplemented with 300- and 600-mg/kg CGA, respectively, for 2 weeks before heat stress exposure. Pullets of HS, HS + CGA300 , and HS + CGA600 group were exposed to 38°C for 4 h while the control group was maintained at 25°C. In this study, dietary CGA supplementation had effect on mitigate the decreased T-AOC and T-SOD activities and the increasing of IL-1ß and TNFα induced by acute heat stress. Dietary supplementation with 600 mg/kg CGA had better effect on increasing the relative abundance of beneficial bacterial genera, such as Rikenellaceae RC9_gut_group, Ruminococcaceae UCG-005, and Christensenellaceae R-7_group, and deceasing bacteria genera involved in inflammation, such as Sutterella species. Therefore, CGA can ameliorate acute heat stress damage through suppressing inflammation and improved antioxidant capacity and cecal microbiota composition.

Curcumin reduces enteric isoprostane 8-iso-PGF2α and prostaglandin GF2α in specific pathogen-free Leghorn chickens challenged with Eimeria maxima.

The purpose of this pilot study was to evaluate and determine the concentration of prostaglandin GF2α (PGF2α) and isoprostane 8-iso-PGF2α in plasma and intestine of specific pathogen-free (SPF) Leghorn chickens challenged with Eimeria maxima, with or without dietary supplementation of curcumin using solid-phase microextraction and ultra-performance liquid chromatography/tandem mass spectrometry. Eighty 1-day-old male SPF chickens were randomly allocated to one of four groups with four replicates (n = 5 chickens/replicate). Groups consisted of: (1) Control (no challenge), (2) Curcumin (no challenge), (3) Eimeria maxima (challenge), and (4) Eimeria maxima (challenge) + curcumin. At day 28 of age, all chickens in the challenge groups were orally gavaged with 40,000 sporulated E. maxima oocysts. No significant differences (P > 0.05) were observed in the groups regardless of the treatment or challenge with E. maxima. Enteric levels of both isoprostane 8-iso-PGF2α and PGF2α at 7 days and 9 days post-challenge were significantly increased (P < 0.01) compared to the non-challenge control chickens. Interestingly, the enteric levels of both isoprostane 8-iso-PGF2α and PGF2α at 7 days post-challenge were significantly reduced in chickens fed curcumin, compared to control chickens challenge with E. maxima. At 9 days post-challenge, only levels of isoprostane 8-iso-PGF2α in the enteric samples were significantly reduced in chickens challenged with E. maxima supplemented with curcumin, compared with E. maxima challenge chickens. No differences of isoprostane 8-iso-PGF2α or PGF2α were observed in plasma at both days of evaluation. Similarly, no significant differences were observed between the challenge control or chickens challenge with E. maxima and supplemented with curcumin at both times of evaluation. The results of this pilot study suggests that the antioxidant anti-inflammatory properties of curcumin reduced the oxidative damage and subsequent intestinal mucosal over-production of lipid oxidation products. Further studies to confirm and extend these results in broiler chickens are required.

Effects of N-acetyl-l-cysteine on heat stress-induced oxidative stress and inflammation in the hypothalamus of hens.

The purpose of this study was to discuss the effects of N-acetyl-l-cysteine (NAC) on heat stress-induced oxidative stress and inflammation in the hypothalamus of hens in different periods. A total of 120 Hy-Line variety brown laying hens (12 weeks old) were randomly assigned to 4 groups with 6 replicates. The control group (C group) (22 ± 1 °C) received a basal diet, the NAC-treated group (N group) (22 ± 1 °C) received a basal diet with 1000 mg/kg NAC, and 2 heat-stressed groups (36 ± 1 °C for 10 h per day and 22 ± 1 °C for the remaining time) were fed a basal diet (HS group) or a basal diet with 1000 mg/kg NAC (HS + N group) for 21 consecutive days. The influence of NAC on histologic changes, oxidative stress and proinflammatory cytokine production was measured and analysed in hens with heat stress-induced hypothalamic changes. NAC effectively alleviated the hypothalamic morphological changes induced by heat stress. In addition, NAC attenuated the activity of the Nf-κB pathway activated by heat stress and decreased the expression of the proinflammatory cytokines IL-6, IL-18, TNF-α, IKK, and IFN-γ. In addition, NAC treatment regulated the expression of HO-1, GSH, SOD2 and PRDX3 by regulating the activity of Nrf2 at different time points to resist oxidative stress caused by heat exposure. In summary, dietary NAC may be an effective candidate for the treatment and prevention of heat stress-induced hypothalamus injury by preventing Nf-κB activation and controlling the Nrf2 pathway.

Preparation of the peroxisome proliferator-activated receptor α polyclonal antibody: Its application in fatty liver hemorrhagic syndrome.

Peroxisome proliferator-activated receptor α (PPARα) play a key role in the regulation of metabolic homeostasis, inflammation, cellular growth, and differentiation. To further explore the potential role of PPARα in the energy homeostasis of fatty liver hemorrhagic syndrome (FLHS), we reported the prokaryotic expression and purification of chicken PPARα subunit protein, and successfully prepared a polyclonal antibody against PPARα recombinant protein. The 987 bp PPARα subunit genes were cloned into the pEASY-T3 clone vector. Then the plasmid PCR products encoding 329 amino acids were ligated to pEASY-Blunt E2 vector and transformed into BL21 to induce expression. The recombinant PPARα subunit protein, containing His-tag, was purified by affinity column chromatography using Ni-NTA affinity column. Rabbit antiserum was generated by using the concentration of recombinant PPARα subunit protein as the antigen. The results of western blotting showed that the antiserum can specifically recognize chicken endogenous PPARα protein. Immunohistochemistry and immunofluorescence showed that the PPARα mainly existed in the nucleus of hepatocytes, renal epithelial cells and hypothalamic endocrine nerve cells. More importantly, western blotting and real-time quantitative PCR indicated that FLHS significantly decreased the expression of PPARα.

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.

Dietary taurine supplementation ameliorates muscle loss in chronic heat stressed broilers via suppressing the perk signaling and reversing endoplasmic reticulum-stress-induced apoptosis.

BACKGROUND: Heat stress seriously affects animal health and induces enormous financial losses in poultry production. Exploring the appropriate means for ameliorating unfavorable effects caused by heat stress is essential. We investigated whether taurine supplementation could attenuate breast muscle loss in chronic heat-stressed broilers, as well as its mechanism. We designed three groups: a normal control group (22 °C), a heat stress group (32 °C) and a taurine treatment group (32 °C, basal diet + 5 g·kg-1 taurine). RESULTS: We found that taurine significantly moderated the decreases of breast muscle mass and yield, as well as the increases of serum aspartate aminotransferase activity and serum urine acid level in chronic heat-stressed broilers. Additionally, supplementary taurine significantly alleviated elevations of the cytoplasm Ca2+ concentration, protein expressions of GRP78 and p-PERK, mRNA expressions of Ca2+ channels (RyR1, IP3R3) and endoplasmic reticulum (ER) stress factors (GRP78, GRP94, PERK, EIF2α, ATF4, IRE1, XBP1, ATF6 and CHOP), apoptosis (Caspase-3 and TUNEL), protein catabolism, and the reduction of taurine transporter (TauT) mRNA expression in the breast muscle induced by chronic heat stress. CONCLUSION: Supplementary taurine could attenuate chronic heat stress-induced breast muscle loss via reversing ER stress-induced apoptosis and suppressing protein catabolism. © 2020 Society of Chemical Industry.

Morinda officinalis polysaccharides improve meat quality by reducing oxidative damage in chickens suffering from tibial dyschondroplasia.

Tibial dyschondroplasia (TD) is the common leg disease in commercial broilers. However, the effects of TD on meat quality and the protective of Morinda officinalis polysaccharide (MOP) are largely unknown. Three hundred broiler chicks (one-day-old) were equally allocated into control (CON), TD and MOP-treated groups for 15 days. The results indicated that TD influenced morphology and meat quality-related parameters of the breast muscle, and changed the activity and mRNA expression of antioxidant enzymes in plasma and breast muscles. Moreover, metabolomics profiling of breast muscle revealed that the main altered metabolites 4-guanidinobutyric acid and chenodeoxycholic acid, which are related to meat quality and oxidative stress. Additionally, 500 mg/L MOP effectively restored the content of meat metabolites and oxidative damage. These findings suggest that oxidative damage caused by TD may affect meat quality in broilers by changing the content of breast muscle metabolites and that MOP supplementation has a restorative effect.

Study on the morphological and metabolic changes of femur in laying hens with hypophosphatemia.

Layer fatigue syndrome caused by the lack of calcium and phosphorus can cause fracture in laying hens. The effect of phosphorus deficiency on the femur of laying hens with layer fatigue syndrome has not been studied. In this study, sixty 22-week-old Roman white layers were randomly divided into control group (group C) and low phosphorus group (group P), 30 individuals in each group. The available phosphorus content of group P was 0.18%. At the age of 26, 30 and 34 weeks, the production performance, biomechanical index, protein expression, histopathological change of femur and serological index were detected. The results showed that the laying rate, egg quality and body weight of laying hens, bone density, cortical bone thickness, rigidity, flexural modulus, flexural rigidity, the maximum load of femur and expression of osteocalcin (OCN), receptor activator of nuclear factor kappa-Β (RANK) and receptor activator of nuclear factor kappa-Β ligand (RANKL) decreased of group P. The number of osteocytes was decreased, and the voids was increased. However, cell lacunae were not obvious. The levels of phosphorus, calcium and OCN were increased, and the content of estradiol (E2), OPG and calcitonin (CT) were decreased in serum. In conclusion, the low phosphorus diet can induce layer fatigue syndrome and affect the content of OPG and E2 in serum and the expression of OCN, OPG, RANK and RANKL in femur protein, which leads to the imbalance of bone homeostasis, the thinning of femur cortex bone and the decrease of bone density.

Vitamin CNa enhances the antioxidant ability of chicken myocardium cells and induces heat shock proteins to relieve heat stress injury.

In order to explore the function of vitamin C (VC) and VC-Na in the relief of heat stress injury in chicken cardiomyocytes, 150 30-day-old specific-pathogen-free chickens were randomly divided into a control group (fed normal drinking water), a VC group (50 µg/mL VC in drinking water), and a VC-Na group (50 µg/mL VC-Na in drinking water). After 7 days of adaptation feeding, the chickens were subjected to heat stress at 40 ± 2 °C and 60%-70% humidity for 0, 1, 3, 5, and 10 h, respectively, and the sera and heart tissues of the chickens were collected immediately at the corresponding heat stress time points. The effects of VC and VC-Na supplementation on the relief of chicken myocardial cell injury following heat stress was studied by detecting the levels of LDH, CK, CK-MB, and total antioxidant capacity (T-AOC) in the sera, and through histopathological analysis and the expression of CRYAB, Hsp27, and Hsp70 in the myocardial cells. The results showed that supplementing with 50 µg/mL VC or VC-Na significantly reduced the levels of LDH, and CK-MB in serum as well as heat-stress-induced granular and vacuolar degeneration, myocardial fiber breakage, and cell necrosis, indicating effective resistance to heat-stress damage. Additionally, the levels of T-AOC in serum were increased in the VC and VC-Na groups, suggesting enhancing of antioxidant capacity. Furthermore, the expression of CRYAB were induced at 0, 3, 5, and 10 h (P < 0.01) in both VC and VC-Na group, and that of Hsp70 were induced at 0 h (P < 0.05) in VC group and at 0, 3, 5, 10 h (P < 0.01) in VC-Na group. Thus, supplementing chicken diets with VC or VC-Na presented heat-stress damage resistance by enhancing antioxidant capacity and inducing expression of CRYAB and Hsp70.

Interactive effect of dietary calcium and phytase on broilers challenged with subclinical necrotic enteritis: 3. Serum calcium and phosphorus, and bone mineralization.

Calcium is chelated by phytic acid and forms phytate-mineral complexes reducing Ca availability and the ability of phytase to hydrolyze phytate. An increased Ca concentration in the gut favors the activity of Clostridium perfringens (C. perfringens). Therefore, it was hypothesized that high dietary calcium with high dietary phytase would decrease serum Ca and P and bone mineralization during necrotic enteritis occurrence. A total of 768 one-day-old Ross 308 male chicks were randomly allocated to 8 treatments with 6 replicate pens, each housing 16 birds. A 2 × 2 × 2 factorial arrangement of treatments was applied: dietary Ca (0.6 or 1.0%), phytase (500 or 1,500 FTU/kg), and challenge (no or yes). Half of the birds (384) were challenged with Eimeria spp. on day 9 and C. perfringens strain EHE-NE18 on day 14 and 15. Blood was collected from 2 birds per pen to determine Ca, P, and parathyroid hormone in the serum. The middle toe, tibia, and femur were excised from 2 birds per pen on day 16 and 29 for determination of ash, breaking strength (BS), and mineral concentration. The challenge decreased (P < 0.05) serum Ca+ in birds regardless of dietary Ca level (day 16). There was a challenge × Ca interaction (P < 0.05) for tibial BS (day 16), with challenge being more severe in birds fed high Ca than low Ca diets. A challenge × phytase interaction (P < 0.05) was present for femur ash (day 16), with high phytase only increasing ash in challenged birds. The challenge decreased (P < 0.05) the BS of femur and tibia at each time point. Birds fed high dietary Ca had lower tibial Mg (P < 0.001), Fe (P < 0.001), Na (P < 0.001), and Zn (P < 0.05) concentrations (day 29). Altogether, high dietary Ca and phytase improved bone mineralization showing that attention to Ca and P nutrition and phytase matrix values is warranted when high levels of phytase are used.

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.

Dietary curcumin supplementation effects on blood immunological profile and liver enzymatic activity of laying hens after exposure to high temperature conditions.

Various environmental factors affect livestock production but heat stress is a major challenge in the poultry farming. Poultry exposes to high temperature alters blood immunological parameters and liver enzymatic function which in turn, suppress the immunity and disease resistance of chickens. Thus, the purpose of present study was to explore the effect of dietary curcumin supplementation on blood immunological biomarker and liver enzymatic activity of laying hens under heat stress conditions. Experimental groups contained two control groups (normal temperature control (NC) and heat stress control (HC) and 3 heat stress curcumin treatment groups (HT100, HT200 and HT300). Hens in HC group with basal diet and heat stress curcumin treatment groups were exposed 6 h/day heat stress (32 ± 1 °C) from 10:00 a.m. to 16:00 p.m. for 9 week. The results of present study showed that heat stressed curcumin treatment group had improved liver weight, WBC values and immunoglobulin level as compared to untreated HC and NC groups. The available results also indicated that laying hens supplemented with curcumin under high temperature conditions had reduced H/L ratio, serum corticosterone levels, inflammatory cytokines response and liver enzymatic activity (ALT) which enhanced the immunity of laying hens under hot climatic conditions. Therefore, it is concluded that curcumin has ability to combat harsh environmental conditions which can be used as anti-inflammatory and immune booster feed additive in the poultry nutrition.

Fumonisin-(Fusarium verticillioides)-contaminated feed causes hepatic oxidative stress and negatively affects broiler performance in the early stage: Does supplementation with açai flour residues (Euterpe oleracea) minimize these problems?

Fusarium verticillioides is often responsible for contamination of poultry feed with the mycotoxin fumonisin. The aim of this study was to determine whether oxidative stress caused by intake of fumonisin-contaminated feed affects broiler performance at an early stage of development, as well as to test whether the addition of açai residue flour to contaminated feed would minimize these negative effects of redox metabolism. Birds were divided into four groups, with four repetitions of five animals each: control (TC) - birds that received basal feed; TCA treatment - basal feed supplemented with 2% açai flour; TF treatment - feed experimentally contaminated with fumonisin (10 ppm); TFA treatment - fumonisin-contaminated feed (10 ppm) and supplemented with açai fluor (2%). The experiment lasted 20 days, that is, the first 20 days of the chicks' lives. At the end of the experiment, the birds were weighed, and blood, intestine and liver samples were collected. The TCA and TFA had greater body weights and weight gain than did TF. Further, TCA and TFA had lower feed conversion than did TF. Açai flour intake (TCA and TFA) stimulated albumin synthesis and reduced serum AST activity. Nitrate/nitrite (NOx) levels were higher in serum of fumonisin-challenged (TF) birds than in groups; NOx levels were also higher in the livers of all test groups (TF, TCA and TFA) than in TC. Serum glutathione S-transferase (GST) activity was lower in fumonisin-consuming groups (TF and TFA); this was different from what occurred in the liver, that is, higher GST activity in TF and lower activity in TFA than in TC. Catalase activity (CAT) was also higher in the fumonisin-challenged groups (TF and TFA) and the groups supplemented with açai flour (TCA) than in TC. Serum reactive species (RS) and TBARS (lipid peroxidation) levels in the liver were lower in birds supplemented with açai flour and exposed to fumonisin. These data suggest that the addition of açai flour in the feed of early chickens improves animal performance and minimizes the effects of hepatic oxidative stress in birds fed fumonisin-contaminated feed.

Influence of meat and bone meal, phytase, and antibiotics on broiler chickens challenged with subclinical necrotic enteritis: 1. growth performance, intestinal pH, apparent ileal digestibility, cecal microbiota, and tibial mineralization.

This study investigated the influence of meat and bone meal (MBM), phytase, and antibiotics (AB) on the performance, intestinal pH, ileal digestibility, cecal microbiota, and tibial mineralization in Ross 308 broilers challenged with necrotic enteritis (NE). A total of 672-day-old male Ross 308 chicks were allocated to 8 treatments with 6 replicate pens, with 14 birds each. The study employed a 2 × 2 × 2 factorial arrangement of treatments: MBM (no or yes), AB (no or yes, zinc bacitracin + salinomycin), and phytase level (500 or 1,500 FTU/kg; both using 500 matrix recommendations). Diets were based on wheat-soybean meal-canola meal. All birds were challenged with Eimeria spp on day 9 and Clostridium perfringens (C. perfringens) strain EHE-NE18 on day 14 and day 15. On day 21 (postchallenge), birds fed MBM had reduced weight gain (WG; P < 0.05) relative to without MBM. A 2-way phytase × AB interaction for WG on day 14 (P < 0.001) and day 21 (P < 0.001) and feed conversion ratio on day 21 (P < 0.001) and day 42 (P < 0.01) indicated positive effects of high phytase on bird performance in the presence of AB. On day 42, a 3-way MBM × phytase × AB interaction (P < 0.01) was observed for WG, showing high phytase increased WG with AB, relative to the birds without AB in the presence of MBM. A 2-way MBM × phytase interaction (P < 0.01) was observed for apparent ileal digestibility of Ca and P on day 16, whereby there was a notable reduction in Ca and P digestibility in birds fed MBM-free diets and a low phytase level, but with the high phytase level, Ca and P digestibility was not influenced by MBM. In conclusion, in NE challenged birds, high phytase has a beneficial effect on leg health and mineral utilization to the extent that it can replace MBM and has beneficial effects on bird performance in the presence of AB.