Individual and combined occurrences of the prevalent mycotoxins in commercial feline and canine food.

Mycotoxins, such as aflatoxin B1 (AFB1), deoxynivalenol (DON), fumonisins (FBs), ochratoxin A (OTA), T-2 toxin (T-2), and zearalenone (ZEN), can contaminate animal feeds and pose risks to animal health and production performance. These mycotoxins are commonly found in cereals and grains, with the increased use of cereals in pet food, there is a rising concern about mycotoxin contamination among pet owners. To address this, we analyzed imported brands of feline and canine food from the Chinese market produced in 2021-2022. Ninety-three samples were analyzed, comprising 45 feline food and 48 canine food samples. Among them, 14 were canned food and 79 were dry food. The results indicate that AFB1, DON, FBs, OTA, T-2, and ZEN occurred in 32.26%, 98.92%, 22.58%, 73.12%, 55.91%, and 7.53% of the samples, respectively. The most prevalent mycotoxin was DON, followed by OTA, T-2, AFB1, and FBs, whereas ZEN was less frequently detected. The mean concentrations of the six mycotoxins in pet feed samples were 3.17 µg/kg for AFB1, 0.65 mg/kg for DON, 2.15 mg/kg for FBs, 6.27 µg/kg for OTA, 20.00 µg/kg for T-2, and 30.00 µg/kg for ZEN. The levels of mycotoxins were generally below the limits of the Pet Feed Hygiene Regulations of China and the EU. Notably, a substantial majority of the pet food samples (88 out of 93) were contaminated by two or more mycotoxins. AFB1, FBs, OTA, and ZEN occurred slightly more often in feline food than in canine food. Except for OTA, the contamination rates for the other five mycotoxins in canned food were lower than those in dry food. Moreover, except for AFB1, the levels of the other five mycotoxins in canned foods were lower than those in dry foods. This study highlights the widespread contamination of pet foods with mycotoxins, which poses a significant risk to pets from continuous exposure to multiple mycotoxins.

Combined Effects of Cadmium and Lead on Growth Performance and Kidney Function in Broiler Chicken.

Cadmium (Cd) and lead (Pb) are heavy metals prevalent in the environment and feed, and they reduce production performance of domestic animals, as well as they result in residue in animal tissues. The kidney is the target tissue for Cd and Pb. And the kidney is crucial for the reabsorption of calcium (Ca), which consequently influences bone strength. However, there are relatively few studies related to the effects of Cd and Pb exposure on performance, bone strength and kidney damage in livestock. The purpose of this experiment was to explore the combined effect of Cd and Pb on growth performance and renal impairment and the possible underlying mechanism. For this, 168 1-day-old Ross 308 broilers were randomly divided into four groups of six birds each, with seven replicates in each group: control group, 50 mg Cd/kg body weight group, 200 mg Pb/kg body weight group and 50 mg Cd/kg body weight + 200 mg Pb/kg body weight group. Feed intake was recorded daily and body weight was recorded weekly. The results show that at the end of the 3rd and 6th week, one broiler from each replicate was randomly selected for sampling. Boilers co-exposed to Cd and Pb for 3 weeks and 6 weeks had significantly decreased average daily feed intake (ADFI) and average daily body weight gain (ADG) than the control group, and the ratio of feed-to-weight gain (F/G) significantly increased after 6 weeks of co-exposure to Cd and Pb. Microscopic picture and ultrastructure analyses of the kidneys showed that Cd and Pb caused kidney damage to broiler chickens, and the damage was more serious in the Cd + Pb group, which was manifested by increased renal tubular epithelial degeneration and increased interstitial stasis points. Dietary exposure to Cd and Pb impaired production performance and induced renal oxidative damage in broilers. The combined effects of Cd and Pb on the kidneys are greater than their effects alone. The PERK-ATF4 pathway mediated endoplasmic reticulum stress participates the renal oxidative damage during chronic Cd and Pb exposure.

ZnO-NPs alleviate aflatoxin B1-induced hepatoxicity in ducklings by promoting hepatic metallothionein expression.

Aflatoxin B1 (AFB1) is a mycotoxin widely present in animal feed and human food, posing a serious threat to animal and human health. This study was aim to illustrate the mechanism of the protective role of MT against AFB1-induced hepatotoxicity, as well as to explore the feasibility of enhancing the tolerance of poultry to AFB1 by upregulating the expression of hepatic MT. After being exposed to AFB1 (50 ng/kg) primary duckling hepatocytes, the cell viability, the antioxidant index (SOD and GPx) and the mRNA levels of MT downstream genes (PTGR, p53, TrxR, AR and Bcl-2) significantly (p < 0.05) decreased, while the intracellular formation of (AFBO)-DNA adduct content, apoptosis, and MDA content significantly (p < 0.05) increased. Interestingly, overexpression of MT in primary duckling hepatocytes markedly (p < 0.05) reversed the detrimental impact of AFB1 and increased the expression of MT downstream genes. HepG2 cells were applied to study the mechanism how MT works to relieve the hepatic toxicity of AFB1. The ZnO-NPs (20 µg/mL) + AFB1 (20 µg/mL) group significantly (p < 0.05) increased the cell viability, the expression of NRF2, NQO1 and SOD, and expression of MT and MTF-1, as well as significantly (p < 0.05) decreased LDH, ROS and apoptotic rate, comparing with the AFB1 group. While joint treatment with AFB1 and ZnO-NPs, the hepatic toxicity exerted by AFB1 alone was reversed, along with the translocation of MTF-1 from the cytoplasm to the nucleus and upregulated its expression. Duckling trails were further carried out. A total number of 96 1-day-old healthy Cherry Valley commercial ducklings were randomly allocated according to a 2 by 2 factorial arrangement of treatments with the main factors including oral administration of AFB1 (0 vs. 40 µg/kg) and dietary supplementation of ZnO-NPs (0 vs. 60 mg/kg) for 7 days. It showed that AFB1 exposure caused body weight loss (p < 0.05), impaired liver structure and failure in hepatic function (activity of ALT, AST and concentration of TP and GLU) (p < 0.05), and decreases in antioxidant capacity(activity of SOD, CAT and concentration of GSH) (p < 0.05), along with the decrease in hepatic concentration of Zn, increase in expression of apoptosis-related genes and protein CAS3 and mRNA Bcl-2 expression (p < 0.05), and suppressed mRNA levels of antioxidant-related genes MT, SOD1, NRF2, and NQO1 (p < 0.05). In accordance with the cell test, dietary supplementation with ZnO-NPs mitigated the toxicity exerted by AFB1. In conclusion, ZnO-NPs has the protective effects against AFB1-induced hepatocyte injury by activating the expression of MTF-1 and the ectopic induction of MT expression, providing detailed information on the detoxification ability of MT on AFB1.

Effects of Zearalenone on Production Performance, Egg Quality, Ovarian Function and Gut Microbiota of Laying Hens.

Zearalenone (ZEN) is a ubiquitous contaminant in poultry feed, since ZEN and its metabolites can interfere with estrogen function and affect the reproductive ability of animals. The estrogen-like effect of ZEN on mammal is widely reported, while little information is available, regarding the effect of relatively low dose of ZEN on estrogen function and production performance of laying hens, and the relationship between them. This work was aimed to investigate the effects of ZEN on the production performance, egg quality, ovarian function and gut microbiota of laying hens. A total of 96 Hy-line brown laying hens aged 25-week were randomly divided into 3 groups including basal diet group (BD group), basal diet supplemented with 250 µg/kg (250 µg/kg ZEN group) and 750 µg/kg (750 µg/kg ZEN group) ZEN group. Here, 750 µg/kg ZEN resulted in a significant increase in the feed conversion ratio (FCR) (g feed/g egg) (p < 0.05), a decrease in the egg production (p > 0.05), albumen height and Haugh unit (p > 0.05), compared to the BD group. The serum Follicle-stimulating hormone (FSH) levels significantly decreased in ZEN supplemented groups (p < 0.05). Serum Luteinizing hormone (LH) and Progesterone (P) levels in the 750 µg/kg ZEN group were significantly lower than those in the BD group (p < 0.05). 16S rRNA sequencing indicated that ZEN reduced cecum microbial diversity (p < 0.05) and altered gut microbiota composition. In contrast to 250 µg/kg ZEN, 750 µg/kg ZEN had more dramatic effects on the gut microbiota function. Spearman's correlation analysis revealed negative correlations between the dominant bacteria of the 750 µg/kg ZEN group and the production performance, egg quality and ovarian function of hens. Overall, ZEN was shown to exert a detrimental effect on production performance, egg quality and ovarian function of laying hens in this study. Moreover, alterations in the composition and function of the gut microbiota induced by ZEN may be involved in the adverse effects of ZEN on laying hens.

Transcriptomics and transmission ultrastructural examination reveals the nephrotoxicity of cadmium in laying hens.

The objective of this study was to reveal the effects of cadmium (Cd) on ultrastructural changes, oxidative stress, and transcriptome expression in the kidneys of laying hens. Seventy-two healthy Hy-Line brown laying hens at 41 weeks old were randomly allocated to four treatment groups with six replicates. The control group received a basal diet without additional Cd incorporation, and the other three treatment groups received diets supplemented with 15, 30, or 60 mg Cd /kg of feed. After 6 weeks of exposure, the results show that administration of 60 mg/kg Cd significantly reduced (P < 0.05) eggshell thickness. With an increase in the Cd concentration in feed, the concentrations of renal Zn and Fe also had changed. Renal histopathology and ultrastructure also showed aggravated damage to glomeruli and renal tubules and the deformation of nuclei and mitochondria in all Cd treatment groups. With an increase in Cd in feed, the activity of glutathione peroxide (GPX) and catalase (CAT) was significantly reduced (P < 0.05), while the activity of total antioxidant capacity (T -AOC) was decreased (P < 0.05) only in the 60 mg/kg Cd group. RNA-seq analysis revealed that 410 genes displayed differential expression (≥ 1.5-fold) in the 60 mg/kg supplementation group, compared to the control group. GO and KEGG pathway analysis results showed that Cd affected many genes involved in mitochondria and ion transport. In conclusion, this study elaborates the mechanisms underlying renal toxicity caused by Cd, which might provide target candidate genes for alleviating Cd poisoning in laying hens.

Selenium mitigated aflatoxin B1-induced cardiotoxicity with potential regulation of 4 selenoproteins and ferroptosis signaling in chicks.

The aim of the present study was to explore the underlying mechanism of selenium (Se)-mediated detoxification of aflatoxin B1 (AFB1)-induced cardiotoxicity in chicks. A Se-deficient, corn-soybean meal-basal diet (36 µg Se/kg, BD) and three test diets (BD+1.0 mg AFB1/kg, 0.3 mg Se/kg, or 1.0 mg AFB1/kg+0.3 mg Se/kg) were used in a 3-wk 2 × 2 factorial design trial (n = 30 chicks/group). Dietary AFB1 led to induced (P < 0.05) serum creatine kinase and creatine kinase MB isoenzyme activities and heart histopathologic lesions. However, Se deficiency aggravated most of these alterations induced by AFB1. Moreover, mRNA levels of two ferroptosis activators (solute carrier family 11 Member 2 and transferrin) were upregulated (P < 0.05) in the AFB1-treated groups. Additionally, Se deficiency reduced (P < 0.05) glutathione peroxidase (GPX) 3 and thioredoxin reductase 3 mRNA and GPX activity but increased (P < 0.05) selenoprotein M and selenophosphate synthetase 2 mRNA in the heart in AFB1-administered groups. The in vitro study showed that Se alleviated (P < 0.05) AFB1-reduced cell viability and induced (P < 0.05) ROS and ferroptosis in H9C2 cardiac cells. It also downregulated (P < 0.05) two ferroptosis activators (long-chain acyl-CoA synthetase 4 and solute carrier family 11 Member 2) in the AFB1-treated groups in the H9C2 cells. In conclusion, this study illustrated that Se alleviates AFB1-induced cardiotoxicity and cardiomyocyte damage potentially related to the regulation of redox status, 4 selenoproteins, and ferroptosis-related signaling.

Effects of dietary cadmium supplementation on production performance, cadmium residue in eggs, and hepatic damage in laying hens.

This study was conducted to investigate the adverse effects of cadmium (Cd) on the production performance, serum biochemistry, liver antioxidant status, histopathology, and egg residue in laying hens. A total of 72 healthy Hy-Line brown laying hens at 40-week-old were randomly assigned to four diets containing 0 (control diet), 15, 30, or 60 mg/kg Cd for 6 weeks. Laying hens exposed to 60 mg/kg Cd had lower egg production rate and worse feed to egg ratio (P < 0.05). Dietary Cd exposure (≥ 15 mg/kg) significantly decreased hepatic glutathione peroxide (GPX) activities, while increasing malondialdehyde (MDA) (P < 0.05). Hepatic histopathology and ultrastructure also showed damage and the symptoms were exacerbated in a dose-dependent manner. The residue of Cd in the yolk was increased with increasing dietary Cd concentration. The mRNA expression levels of mt4L, mt3, sod1, sod2, gpx1, gpx3, and gpx4 in the liver of laying hens exposed to 60 mg Cd/kg feed were significantly decreased (P < 0.05). In conclusion, dietary Cd exposure at ≥ 15 mg/kg induced hepatic damage in laying hens, indicating that the content of Cd in feed must be critically controlled.

Yeast culture promotes the production of aged laying hens by improving intestinal digestive enzyme activities and the intestinal health status.

Yeast culture (YC) positively affects the performance of laying hens. The purpose of the present study was to explore the underlying mechanism for the YC-mediated performance improvement. Sixty 67-week-old Hy-Line Brown laying hens were randomly allocated into 2 experimental groups with 5 replicates of 6 birds each. One group was fed a control diet, whereas the other received the control diet supplemented with YC at 3.0 g/kg; treatment lasted for 8 wk. The results showed that dietary YC supplementation increased (P < 0.05) the total egg weight (11.2-13.6%) and egg-laying rate (13.0-13.5%) but decreased (P < 0.05) the feed/egg ratio by 9.3 to 11.0% during weeks 5 to 6 and 7 to 8 compared with the control. However, egg quality, including eggshell strength, eggshell thickness, egg weight, albumen height, egg yolk color, and Haugh unit, was not affected (P > 0.05) by YC supplementation. Furthermore, dietary YC supplementation increased (P < 0.05) chymotrypsin and ɑ-amylase activities by 54.8 to 62.5% in the duodenal chyme and reduced (P < 0.05) plasma endotoxin by 44.1%. YC dietary supplementation also upregulated (P < 0.05) the mRNA levels of intestinal barrier-related genes (occludin and claudin 1) and antimicrobial peptides genes (ß-defensin 1 and 7 and cathelicidin 1 and 3) in the duodenum or jejunum compared with the control. In conclusion, dietary YC supplementation improved the performance of aged laying hens, potentially through the upregulation of intestinal digestive enzyme activities and intestinal health-related gene expression.

Effects of deoxynivalenol on the porcine growth performance and intestinal microbiota and potential remediation by a modified HSCAS binder.

The objectives of this study were to determine the effects of deoxynivalenol (DON) on growth performance and intestinal microbiota in weaning piglets, and potential efficacy of a modified hydrated sodium calcium aluminosilicate (HSCAS) adsorbent to reduce DON toxicity. Four groups of 21-day-old male piglets (n = 7/group) were fed either a control diet, or diet containing 1.0 or 3.0 mg/kg DON, or 3.0 mg/kg DON plus 0.05% modified HSCAS for 28 d. Compared to the control, dietary DON at 1.0 and/or 3.0 mg/kg reduced (P < 0.05) the body weight gain (16.0-60.8%) and feed intake (18.1-38.7%) during the whole experiment, and increased (P < 0.05) the feed/gain ratio (12.8-33.8%) between d 1-28. The body weight gain and feed intake were further decreased (P < 0.05) in 3.0 mg/kg DON in comparison to 1.0 mg/kg DON during d 15-28. DON exposure reshaped gut microbial structure by drastically affecting the abundance of several bacterial phyla, families and genera, including dysbiosis of Actinobacteria, Cyanobacteria, Firmicutes, and Proteobacteria in small intestine. Notably, dietary Amdetox™ supplementation alleviated the adverse effects of DON on growth performance of piglets and improved the intestinal flora disorder. Therefore, the current study has revealed that Amdetox™, the modified HSCAS binder, can alleviate DON-induced negative effects and could be used as a promising countermeasure for reducing DON toxicity.

Heavy Metal Content in Feedstuffs and Feeds in Hubei Province, China.

ABSTRACT: Heavy metal pollution threatens the health and life of animals and humans through the food chain. This study was performed to survey the heavy metal contamination in feedstuffs and feeds in Hubei Province, People's Republic of China, from 2012 to 2016. Samples were analyzed for cadmium (306 samples), mercury (117 samples), chromium (149 samples), and arsenic (4,358 samples) using atomic absorption spectrometry or atomic fluorescence spectrometry. The incidence rates of cadmium, mercury, chromium, and arsenic contamination of feedstuffs and feeds were high, and feeds were most often contaminated with chromium, followed by arsenic, cadmium, and mercury. The concentrations of heavy metals in samples positive for cadmium, mercury, chromium, and arsenic ranged from 0.001 to 1.200, 0.002 to 6.540, 0.060 to 8737.000, and 0.070 to 33.000 mg/kg, respectively. The mineral and additive samples had higher concentrations of heavy metals. The present study findings highlight the importance of monitoring heavy metals in feedstuffs and feeds and implementing feed management and bioremediation strategies to reduce heavy metal exposure.

Effect of deoxynivalenol on the porcine acquired immune response and potential remediation by a novel modified HSCAS adsorbent.

The objective of this study was to determine the immunotoxic effects of deoxynivalenol (DON) in weaning piglets, and potential efficacy of a modified hydrated sodium calcium aluminosilicate (HSCAS) adsorbent to reduce DON toxicity. Four groups of 21-day-old male piglets (n = 7/group) were fed a control diet or diet containing 1.0 or 3.0 mg DON/kg, or 3.0 mg DON/kg plus 0.05% modified HSCAS for 4 weeks. Compared to the control, the DON diets decreased serum porcine circovirus antibody titer and the dermal hypersensitivity response to OVA at day 21 or 28. DON also induced focal necrosis and proliferation of cortical lymphocytes and apoptosis and increased the total antioxidant capacity and reduced glutathione, protein carbonyl concentrations in thymus. DON increased thymus mRNA, protein and (or) enzyme levels, cytokines (IL-6, IL-10, and TNF-α) and apoptosis-related genes (Caspase-3), while hematopoietic cell kinase (HCK) decreased. Intriguingly, the modified HSCAS alleviated the DON-induced changes on serum antibody titer, and thymic histopathology, apoptosis, redox status, inflammation and apoptosis signaling. In conclusion, these findings help to explain the toxic effects and mechanisms of DON and demonstrated the modified HSCAS adsorbent could be used to reduce the toxicity of DON in weaning piglets.

The effects of dietary cottonseed meal and oil supplementation on laying performance and egg quality of laying hens.

Cottonseed meal (CSM) and cottonseed oil (CSO), two cottonseed products, are rich in protein and lipids, respectively, but their use is limited by antinutritional factors in the products. This study investigated the effect of different dietary levels of CSM and CSO supplementation on the laying performance and egg quality of laying hens. A total of 162 24-week-old Hy-Line brown laying hens were randomly assigned to diets supplemented with 0, 6%, or 12% CSM and 0, 2%, or 4% CSO in a 3 × 3 factorial design. During the 8-week feeding trial, laying performance and egg quality parameters were measured weekly. Furthermore, a texture profile analysis (TPA) of the egg yolks was conducted, and the fatty acid profiles and protein composition of the yolks were measured to further determine egg quality. CSM supplementation decreased (p < 0.01) egg production and feed efficiency and increased (p < 0.01) yolk color, eggshell rate, and shell thickness, but had no significant effects on the TPA parameters, fatty acid profiles, and protein components of egg yolks. CSO supplementation resulted in decreases (p < 0.01) in egg production, egg weight, and feed efficiency and an increase (p < 0.01) in yolk color. In addition, CSO supplementation with two weeks of cold storage changed the physical properties of boiled egg yolks, as indicated by increased (p < 0.01) hardness, springiness, cohesiveness, and chewiness. Furthermore, 4% CSO supplementation increased the ratio of saturated/monounsaturated fatty acids (SAFA/MUFA) and the protein content of egg yolks, which was accompanied by a modified protein composition. These results indicate that CSM supplementation reduces laying performance and egg quality, and CSO supplementation decreases laying performance and results in egg yolk hardening by modifying its components.

The response of glandular gastric transcriptome to T-2 toxin in chicks.

This study was conducted to determine the effect of T-2 toxin on the transcriptome of the glandular stomach in chicks using RNA-sequencing (RNA-Seq). Four groups of 1-day-old Cobb male broilers (n = 4 cages/group, 6 chicks/cage) were fed a corn-soybean-based diet (control) and control supplemented with T-2 toxin at 1.0, 3.0, and 6.0 mg/kg, respectively, for 2 weeks. The histological results showed that dietary supplementation of T-2 toxin at 3.0 and 6.0 mg/kg induced glandular gastric injury including serious inflammation, increased inflammatory cells, mucosal edema, and necrosis and desquamation of the epithelial cells in the glandular stomach of chicks. RNA-Seq analysis revealed that there were 671, 1393, and 1394 genes displayed ≥2 (P < 0.05) differential expression in the dietary supplemental T-2 toxin at 1.0, 3.0, and 6.0 mg/kg, respectively, compared with the control group. Notably, 204 differently expressed genes had shared similar changes among these three doses of T-2 toxin. GO and KEGG pathway analysis results showed that many genes involved in oxidation-reduction process, inflammation, wound healing/bleeding, and apoptosis/carcinogenesis were affected by T-2 toxin exposure. In conclusion, this study systematically elucidated toxic mechanisms of T-2 toxin on the glandular stomach, which might provide novel ideas to prevent adverse effects of T-2 toxin in chicks.

Effect of selenium nanoparticles against abnormal fatty acid metabolism induced by hexavalent chromium in chicken's liver.

The effect of selenium on excessive fatty acid-induced apoptosis and abnormal amino acid metabolism in the liver is well known, because it is an important site in the fatty acid metabolism pathway. However, the protective role of nano-elemental selenium (nano-Se) supplementation against hexavalent chromium (K2Cr2O7)-induced abnormal fatty acid metabolism has not been evaluated yet. Therefore, we conducted chicken experiments with different nano-Se supplementation doses to investigate the role of nano-Se against Cr(VI)-induced adverse effects. For this purpose, a total of 120 1-day-old chicks were randomly divided into control group, Cr(VI)-exposed group, protection group, treatment group, prevention group, and nano-Se control group. The results of RT-qPCR showed that the nano-Se supplementation notably downregulated (P < 0.01) the messenger RNA (mRNA) expression levels of fatty acid synthase (FASN), whereas nano-Se supplementation significantly upregulated (P < 0.01) the mRNA expression level of acyl-coenzyme A oxidase 1 (ACOX1) in chicken's liver at day 35 of the experiment. Similar results were further verified by western blot analysis. Moreover, nano-Se supplementation significantly enhanced and reduced the antibody expression levels of ACOX1 and FASN in immunohistochemical analysis, respectively. Thus, finally, it was concluded that nano-Se can alleviate K2Cr2O7-induced abnormal fatty acid metabolism in chicken's liver.

Selenium Deficiency Aggravates Aflatoxin B1-Induced Immunotoxicity in Chick Spleen by Regulating 6 Selenoprotein Genes and Redox/Inflammation/Apoptotic Signaling.

BACKGROUND: Selenium (Se) plays a protective role in aflatoxin B1 (AFB1)-induced splenic immunotoxicity in chicks. OBJECTIVE: This study was designed to reveal the underlying mechanism of Se-mediated protection against AFB1-induced splenic injury in broilers. METHODS: Four groups of 1-d-old Cobb male broilers (n = 5 cages/diet, 6 chicks/cage) were arranged in a 3-wk 2 × 2 factorial design trial whereby they were fed an Se-deficient, corn- and soy-based diet [base diet (BD), 36 µg Se/kg], BD plus 1.0 mg AFB1/kg, BD plus 0.3 mg Se/kg, or BD plus 1.0 mg AFB1/kg and 0.3 mg Se/kg (as 2-hydroxy-4-methylselenobutanoic acid). Serum and spleen were collected at week 3 to assay for cytokines, histology, redox status, selected inflammation- and apoptosis-related genes and proteins, and the selenogenome. RESULTS: Dietary AFB1 induced growth retardation and spleen injury, decreasing (P < 0.05) body weight gain, feed intake, feed conversion efficiency, and serum interleukin-1ß by 17.8-98.1% and increasing (P < 0.05) the spleen index and serum interleukin-6 by 37.6-113%. It also reduced the splenic lymphocyte number, the white pulp region, and histiocyte proliferation in Se-adequate groups. However, Se deficiency aggravated (P < 0.05) these AFB1-induced alterations by 16.2-103%. Moreover, Se deficiency decreased (P < 0.05) splenic glutathione peroxidase (GPX) activity and glutathione-S transferase and glutathione concentrations by 35.6-89.4% in AFB1-exposed groups. Furthermore, Se deficiency upregulated (P < 0.05) the apoptotic (Caspase 3 and Caspase 9) and antimicrobial (ß defensin 1 and 2) genes, but downregulated (P < 0.05) antiapoptotic (B-cell lymphoma 2) and inflammatory (E3 ubiquitin-protein ligase CBL-B) genes at the mRNA and/or protein level in AFB1 supplementation groups. Additionally, Se deficiency downregulated (P < 0.05) GPX3, thioredoxin reductase 1 (TXNRD 1), GPX4, and selenoprotein (SELENO) S, and upregulated (P < 0.05) SELENOT and SELENOU in spleen in AFB1 administered groups. CONCLUSIONS: Dietary Se deficiency exacerbated AFB1-induced spleen injury in chicks, partially through the regulation of oxidative stress, inflammatory and apoptotic signaling, and 6 selenoproteins.

A Novel Modified Hydrated Sodium Calcium Aluminosilicate (HSCAS) Adsorbent Can Effectively Reduce T-2 Toxin-Induced Toxicity in Growth Performance, Nutrient Digestibility, Serum Biochemistry, and Small Intestinal Morphology in Chicks.

The objective of this study was to evaluate the ability of a modified hydrated sodium calcium aluminosilicate (HSCAS) adsorbent to reduce the toxicity of T-2 toxin in broilers. Ninety-six one-day-old male broilers were randomly allocated into four experimental groups with four replicates of six birds each. The four groups, 1-4, received a basal diet (BD), a BD plus 6.0 mg/kg T-2 toxin, a BD plus 6.0 mg/kg T-2 toxin with 0.05% modified HSCAS adsorbent, and a BD plus 0.05% modified HSCAS adsorbent, respectively, for two weeks. Growth performance, nutrient digestibility, serum biochemistry, and small intestinal histopathology were analyzed. Compared to the control group, dietary supplementation of T-2 toxin decreased (p < 0.05) body weight gain, feed intake, and the feed conversion ratio by 11.4%-31.8% during the whole experiment. It also decreased (p < 0.05) the apparent metabolic rates of crude protein, calcium, and total phosphorus by 14.9%-16.1%. The alterations induced by T-2 toxin were mitigated (p < 0.05) by the supplementation of the modified HSCAS adsorbent. Meanwhile, dietary modified HSCAS adsorbent supplementation prevented (p < 0.05) increased serum aspartate aminotransferase by T-2 toxin at d 14. It also prevented (p < 0.05) T-2 toxin-induced morphological changes and damage in the duodenum, jejunum, and ileum of broilers. However, dietary supplementation of the modified HSCAS adsorbent alone did not affect (p > 0.05) any of these variables. In conclusion, these findings indicate that the modified HSCAS adsorbent could be used against T-2 toxin-induced toxicity in growth performance, nutrient digestibility, and hepatic and small intestinal injuries in chicks.

Refined cottonseed oil as a replacement for soybean oil in broiler diet.

With the shortage of common vegetable fat sources, such as soybean oil (SBO), it is urgent to find alternative oil sources for broiler producers. The objective of this study was to evaluate the potential of refined cottonseed oil (CSO) as a replacement for SBO in broiler diets. A total of 180 chickens at 1 d of age were randomly assigned to five treatments of six replicates. One treatment was the basal diet (control), and the other four experimental diets were formulated from the basal diet by replacing (w/w) 25%, 50%, 75%, and 100% of the SBO with refined CSO (only containing 0.2% cyclopropenoid fatty acids, and no free gossypol was detected). At the end of week 6, blood samples were obtained from the jugular vein and the breast muscle was aseptically isolated from two birds per replicate. The results showed that substitution of CSO for low-level SBO had no significant effect (p > 0.05) on broiler performance during the starter period (week 1-3), while 50% level of CSO inclusion significantly increased (p < 0.05) ADG and improved FCR compared with the control group during the finisher period (week 4-6). Broilers fed 100% CSO diets had lower (p < 0.05) levels of serum total protein (TP), albumin (ALB), cholesterol (CHO) concentrations, and serum alkaline phosphatase (AKP) activity than that of the control broilers. Furthermore, the serum antioxidant status appeared to be enhanced by CSO. Additionally, high levels of CSO (75 and 100%) significantly increased the proportions of C14:0 and C18:0 but decreased the proportions of C18:1n9t, C18:2n6c, and ∑ n-6 polyunsaturated fatty acids in breast muscles of broilers. Overall, the SBO could be replaced with refined CSO up to 50% in diets for broilers without adversely affecting the performance, liver functions, and breast muscle fatty acid composition of these broilers.

Grape Seed Proanthocyanidin Extract Alleviates AflatoxinB1-Induced Immunotoxicity and Oxidative Stress via Modulation of NF-κB and Nrf2 Signaling Pathways in Broilers.

Aflatoxin B1 (AFB1) is a widely spread mycotoxin contaminates food and feed, causing severe oxidative stress damages and immunotoxicity. Grape seed proanthocyanidin (GSPE), a natural antioxidant with wide range of pharmacological and medicinal properties. The goal of the present study was to investigate the protective effects of GSPE against AFB1-induced immunotoxicity and oxidative stress via NF-κB and Nrf2 signaling pathways in broiler chickens. For the experiment, 240 one-day old Cobb chicks were allocated into four dietary treatment groups of six replicates (10 birds per replicate): 1. Basal diet (control); 2. Basal diet + AFB1 1mg/kg contaminated corn (AFB1); 3. Basal diet + GSPE 250 mg/kg (GSPE); 4. Basal diet + AFB1 1 mg/kg + GSPE 250 mg/kg (AFB1 + GSPE). The results showed that GSPE significantly decreased serum inflammatory cytokines TNF-α, IFN-γ, IL-1ß, IL-10, and IL-6 induced by AFB1. Similarly, GSPE + AFB1 treated group revealed a significant decrease in mRNA expressions of pro-inflammatory cytokines (TNF-α, IFN-γ, IL-1ß, and IL-6) in the splenic tissue compared to the AFB1 treatment group. In addition, western blotting results manifested that GSPE treatment normalized the phosphorylation of nuclear factor kappa B (p65) and the degradation of IκBα protein induced by AFB1. Furthermore, GSPE enhanced the antioxidant defense system through activating the nuclear factor-erythroid-2-related factor (Nrf2) signaling pathway. The mRNA and protein expression level of Nrf2 and its down streaming associated genes were noted up-regulated by the addition of GSPE, and down-regulated in the AFB1 group. Taken together, GSPE alleviates AFB1-induced immunotoxicity and oxidative damage by inhibiting the NF-κB and activating the Nrf2 signaling pathways in broiler chickens. Conclusively, our results suggest that GSPE could be considered as a potential natural agent for the prevention of AFB1-induced immunotoxicity and oxidative damage.

Effects of dietary cottonseed oil and cottonseed meal supplementation on the structure, nutritional composition of egg yolk and gossypol residue in eggs.

The aim of this study was to evaluate the effects of dietary non-gossypol cottonseed oil (CSO) or cottonseed meal (CSM) and their interactions on the texture properties, structure, nutritional composition, and edible safety of egg yolk. A total of 162 24-wk-old Hy-line Brown laying hens were randomly allocated into 9 diet treatments with 6 replicates of 3 hens per cage. A 3 × 3 factorial design using corn soybean meal-based diets supplemented with 0, 6, or 12% CSM and 0, 2, or 4% CSO in place of soybean meal and soybean oil, respectively, was utilized. The experiment lasted for 8 wk. Eggs obtained from the CSO groups had an egg yolk gel structure, and the hardness of egg yolk increased significantly (P < 0.001) after 4°C storaged for 2 wk; the texture properties of eggs storage at 25°C had opposite trend. There were no differences in texture properties of fresh egg yolk among the different groups (P > 0.05). The saturated fatty acid (SFA) content of egg yolk increased in a CSO dose-dependent manner, whereas opposite effects (P < 0.001) were found in the monounsaturated fatty acids (MUFA) and the omega-3/omega-6 fatty acid ratio. CSO-containing diets significantly reduced the cholesterol content (P < 0.05). No significant difference was observed among the different groups on the contents of moisture, crude protein, crude fat, phospholipid, potassium, or iron (P > 0.05) in the egg yolk. Total gossypol residues were increased with the increased amount of CSM (P < 0.05), and these changes were independent of time (P > 0.05). The total gossypol concentration in the yolk was 2.01 to 5.16 mg/kg. These results suggest that CSO has a key influence on egg yolk quality, reducing both its taste and nutritional value. Egg yolk gelation was significantly associated with the change of fatty acid composition caused by CSO and storage conditions. Free gossypol will remain in the egg yolk. Although the residue is low, the edible safety risk of eggs maybe exists.