Toxic Effects Of Aflatoxin B1 Research Articles

The in vitro effects of aflatoxin B1 on physiological functions of swine alveolar macrophages.

The toxic effects of aflatoxin B1 (AFB1) on the physiological functions of swine alveolar macrophages (SAM) were investigated. Freshly isolated SAM were incubated with various AFB1 concentrations (1.6 × 10–1 – 1.6 × 105 nmol/L) and time periods, and their phagocytic ability, synthesis of DNA, RNA and protein, and cell activation by lipopolysaccharide (LPS), were analysed. Results demonstrated that a significant (p < .05) reduction (60%) in Staphylococcus aureus uptaken by SAM appeared 3 hr after AFB1 (>16 nmol/L) treatment. The synthesis of DNA, RNA and protein were markedly reduced, among which DNA and protein synthesis were affected more noticeably. The activation of SAM by LPS was significantly (p < .05) suppressed when the concentration of AFB1 reached 1.6 × 103 nmol/L. In general, most of the analysed effects were more prominent as AFB1 concentration or incubation period increased. Taken together, AFB 1could elicit significant adverse effects on the physiological functions of SAM. Exposure of pigs to aflatoxin‐contaminated feed may increase their susceptibility to various secondary infections.

AFB1 Induced Transcriptional Regulation Related to Apoptosis and Lipid Metabolism in Liver of Chicken.

Aflatoxin B1 (AFB1) leads to a major risk to poultry and its residues in meat products can also pose serious threat to human health. In this study, after feeding 165-day-old Roman laying hens for 35 days, the toxic effects of aflatoxin B1 at different concentrations were evaluated. The purpose of this study was to explore the mechanism of liver toxicosis responses to AFB1. We found that highly toxic group exposure resulted in liver fat deposition, increased interstitial space, and hepatocyte apoptosis in laying hens. Furthermore, a total of 164 differentially expressed lnRNAs and 186 differentially expressed genes were found to be highly correlated (Pearson Correlation Coefficient > 0.80, p-value < 0.05) by sequencing the transcriptome of control (CB) and highly toxic group (TB3) chickens. We also identify 29 differentially expressed genes and 19 miRNAs that have targeted regulatory relationships. Based on the liver cell apoptosis and fatty liver syndrome that this research focused on, we found that the highly toxic AFB1 led to dysregulation of the expression of PPARG and BCL6. They are cis-regulated by TU10057 and TU45776, respectively. PPARG was the target gene of gga-miR-301a-3p, gga-miR-301b-3p, and BCL6 was the target gene of gga-miR-190a-3p. In summary, highly toxic AFB1 affects the expression levels of protein-coding genes and miRNAs in the liver of Roman layer hens, as well as the expression level of long non-coding RNA in the liver, which upregulates the expression of PPARG and downregulates the expression of Bcl-6. Our study provides information on possible genetic regulatory networks in AFB1-induced hepatic fat deposition and hepatocyte apoptosis.

In vitro hepatic aflatoxicol production is related to a higher resistance to aflatoxin B1 in poultry

A study was conducted to determine the cytosolic in vitro hepatic enzymatic kinetic parameters Vmax, KM, and intrinsic clearance (CLint) for aflatoxin B1 (AFB1) reductase [aflatoxicol (AFL) production] and AFL dehydrogenase (AFB1 production) in four commercial poultry species (chicken, quail, turkey and duck). Large differences were found in AFB1 reductase activity, being the chicken the most efficient producer of AFL (highest CLint value). Oxidation of AFL to AFB1 showed only slight differences among the different poultry species. On average all species produced AFB1 from AFL at a similar rate, except for the turkey which produced AFB1 from AFL at a significantly lower rate than chickens and quail, but not ducks. Although the turkey and duck showed differences in AFL oxidation Vmax and KM parameters, their CLint values did not differ significantly. The ratio AFB1 reductase/AFL dehydrogenase enzyme activity was inversely related to the known in vivo sensitivity to AFB1 being highest for the chicken, lowest for the duck and intermediate for turkeys and quail. Since there is no evidence that AFL is a toxic metabolite of AFB1, these results suggest that AFL production is a detoxication reaction in poultry. Conversion of AFB1 to AFL prevents the formation of the AFB1-8,9-exo-epoxide which, upon conversion to AFB1-dihydrodiol, is considered to be the metabolite responsible for the acute toxic effects of AFB1.

Cloacal bursa morphology in turkey broilers challenged with aflatoxin B1 alone or co-administered with Mycotox NG

Aflatoxins are toxic metabolites of moulds from the genus Aspergillus (Aspergillus flavus and Aspergillus parasiticus being the main producers). The aim of the present investigation was to evaluate the toxic effects of aflatoxin B1 on bursa of Fabricius morphology. Also, the possibility for prevention of toxic effects of AFB1 by feed supplementation of a mycosorbent (Mycotox NB) was studied. Experiments were carried out with sixty 7-day-old female turkey broilers (meat TM strain) divided into one control and five treatment groups (n=10). Groups were as followed: Group I – control (fed standard feed according to the species and age of birds); Group II – experimental, whose feed was supplemented with 0.5 g/kg Mycotox NG, Group III– experimental, whose feed contained 0.2 mg/kg aflatoxin B1, Group IV – experimental, whose feed contained 0.4 mg/kg aflatoxin B1, Group V – experimental, supplemented with 0.2 mg/kg aflatoxin B1 and 0.5 g/kg Mycotox NG and Group VI – experimental, supplemented with 0.4 mg/kg aflatoxin B1 and 0.5 g/kg Mycotox NG. The duration of the experiments was 42 days. The changes in bursal morphology in control and treated groups were followed out after the end of the study. In birds from experimental groups ІІI and IV, atrophy and degenerative changes have occurred in the bursa of Fabricius: reduction of lymphoid cell - populations in lymphoid follicles along with dystrophy. Feed supplementation with the tested toxin binder (Groups V and VI) resulted in partial neutralisation of deleterious effects of AFB1 on severity of histological lesions: interfollicular oedema, considerably lower lymphoid follicle rarefaction.

Histological and ultrastructural study of AflatoxinB1 induced neurotoxicity in Sciatic nerve of adult male Albino rats

ABSTRACT Aflatoxins are mycotoxins produced by Aspergillus spp. which is a common contaminant of food items such as corn, spices, rice, nuts, and flour. Aflatoxin contamination of foods is a worldwide problem. Chronic aflatoxin exposure is found to be associated with Sciatic nerve damage. In vivo study was carried out to evaluate the toxic effect of aflatoxin B1 (AFB1) on the Sciatic nerve. Twenty-one adult male rats were included and divided equally into 3 groups (7 rats each): Group I (control group), group II (olive oil group) and group III: (AflatoxinB1 group). The rats received AFB1 (250 μg/kg B.W./day) orally by gastric tube 5 days/week for 4 weeks. Sciatic nerve specimens were prepared, and semi-thin sections were stained with Toluidine blue, examined by light microscope and photographed. Ultrathin sections (50–80 nm) from selected areas of the trimmed blocks were made, examined and photographed by transmission electron microscopy (JEOL-JSM-1011) in King Saud University Electron Microscopy Unit. The findings indicate that the administration of AFB1 to rats’ results in degeneration in the sciatic nerve in the form of Wallerian degeneration in the myelin sheath. Macrophages appear to engulf the degenerated myelin and neutrophils.

Evaluation of a Bacillus -Based Direct-Fed Microbial on Aflatoxin B1 Toxic Effects, Performance, Immunologic Status, and Serum Biochemical Parameters in Broiler Chickens.

The aim of the present study was to evaluate the effect of a commercial Bacillus direct-fed microbial (DFM) on aflatoxin B1 toxic effects, performance, and biochemical and immunologic parameters in broiler chickens. Ninety 1-day-old Cobb 500 male broiler chicks were raised in floor pens for a period of 21 days. Chicks were neck-tagged, individually weighed, and randomly allocated to one of three groups: Negative control (basal feed), aflatoxin B1 (basal feed + 2 ppm AFB1), and DFM (basal feed + 2 ppm AFB1 + Bacillus direct-fed microbial). Each group had three replicates of 10 chickens (n = 30/group). Body weight and body weight gain were calculated weekly, while feed intake and feed conversion ratio were determined when broilers were 21 days old. On day 21, all chickens were bled, gastrointestinal samples were collected, and spleen and bursa of Fabricius were weighed. This study confirmed that 2 ppm of AFB1 causes severe detrimental effects on performance, biochemical parameters, and immunologic parameters, generating hepatic lesions in broiler chickens (P < 0.05). However, it was also observed that DFM supplementation provided beneficial effects that might help to improve gut barrier function, anti-inflammatory and antioxidant activities, as well as humoral and cellular immunomodulation. The results of the present study suggest that this Bacillus-DFM added at a concentration of 106 spores/gram of feed can be used to counteract the negative effects that occur when birds consume diets contaminated with AFB1, showing beneficial effects on performance parameters, relative organ weights, hepatic lesions, immune response, and serum biochemical variables. The addition of this Bacillus-DFM might mitigate and decrease aflatoxicosis problems in the poultry industry, improving food security, alleviating public health problems, and providing economic benefits. Future studies are needed to fully elucidate the specific mechanisms by which this Bacillus-DFM counteracts the toxic effects of aflatoxin B1.

Toxic Effect of Aflatoxin B1 on Heart, Lung, and Testis of Male Albino Rats: Histopathology Study

The current study was carried out to investigate the toxic effects of aflatoxin B1 exposure on heart, lung, and testis of male Albino rats. Twelve healthy male Albino rats were used in the current study. They were divided equally into 2 groups (control and treated groups). The treated group was given aflatoxin B1 orally by a gastric tube at concentration 0.5 mg per kg of body weight for 7 day. The control group was given distilled water alone. At the end of experiment (1 week), the rats were killed under ether anesthesia and the internal organs(heart, lung, and testis) were collected immediately for histological examination. The histopathology examination in heart revealed that there is oedema between myocardial. In lung, there is a large number of inflammatory cells and dilated the alveolar sac with exudates. The testis revealed the excessive vacuolated cells and suppression spermatogenesis. In conclusion, oral dose of aflatoxin B1 exposure could induce a deleterious effect on the histological structure of the heart, lung, and testis of male Albino rats. High level of attention must be taken to prevent the possible contamination of our food with aflatoxin B1.

The Effect of Probiotic Supplementation on Performance and the Histopathological Changes in Liver and Kidneys in Broiler Chickens Fed Diets with Aflatoxin B₁.

The aim of the study was to investigate the toxic effects of aflatoxin B1 (AFB1) and efficacy of a probiotic preparation containing L. reuteri, L. plantarum, L. pentosus, L. rhamnosus and L. paracasei and Saccharomyces cerevisiae yeasts to ameliorate their effects in broiler chickens. A total of 168 one-day-old female Ross 308 broilers were randomly allocated to six groups. Three wheat and soybean meal-based diets were prepared: Control diet and diets contaminated with 1 or 5 mg/kg AFB1 supplied in moldy wheat. All diets were unsupplemented or supplemented with probiotic, cold pelleted and fed from 1 to 35 day of life. Feeding diet with 1 mg AFB1/kg did not affect performance, but a diet with 5 mg AFB1 resulted in a significant reduction of feed intake and BWG, both diets induced liver and kidneys enlargement. The probiotic supplementation of the diets partially ameliorated those negative effects and resulted in a significant increase of AFB1 excretion. It was accompanied by the reduced level of AFB1 residues in the liver from 8.9 to 3.7 and from 11.8 to 5.9 µg/kg, in kidneys from 7.9 to 2.5 and from 13.7 to 4.1 µg/kg in birds fed the less and more contaminated diets, respectively. AFB1 exposure caused many severe histopathological changes in the liver and kidneys of broilers, probiotic supplementation significantly reduced the changes of these organs. It may be concluded that the probiotic supplementation can be used to alleviate the negative effects of contamination of broiler feed with AFB1 on bird health and product security.

Evaluation of three mycotoxin binders to prevent the adverse effects of aflatoxin B1 in growing broilers

ABSTRACT Aflatoxins are a major problem in poultry production and are significant economic and public health burdens worldwide. Three commercial mycotoxin binders (TXB) were used to determine their efficacy in preventing the toxic effects of Aflatoxin B1 (AFB1) on broiler productivity, biochemical and hematological parameters, and liver function. A total of 600 day-old broilers were randomly allotted to 12 treatments in a 3 × 4 factorial arrangement with 3 levels of AFB1 (0, 2, and 4 µg/g) and 4 TXB (no toxin binder, 1.0 g/kg Mycosorb, 1.0 g/kg Formycin, and 20.0 g/kg Anzymit) with 5 replicates of 10 chicks each per treatment. Results indicated that AFB1, in comparison with the control, caused a significant decrease in feed intake, weight gain, feed efficiency, and hematological values. Serum proteins (globulin, albumin, and total protein) and serum Ca and P concentrations followed the same pattern. Relative weights of the heart, gizzard and liver, and AST activity in serum were increased in a dose-dependent manner, but ALT activity was not statistically affected by AFB1. Adding TXB to the AFB1 contaminated diet increased weight gain, feed efficiency, hematological values and serum proteins. The commercial mycotoxin binders decreased AST and ALT activities, but did not have a significant effect on the relative organs weight and serum Ca and P concentrations. Neither AFB1 nor commercial toxin binders affected total cholesterol, LDL, or HDL in this study. It was concluded that the addition of the commercial toxin binders to the AFB1 containing diets reduced the adverse effects of AFB1 and could be helpful as a solution to the aflatoxicosis problem in young broiler chicks.

The Toxic Effects of Aflatoxin B1 and Aflatoxin M1 on Kidney through Regulating L-Proline and Downstream Apoptosis.

The toxic effects and potential mechanisms of aflatoxin B1 (AFB1), aflatoxin M1 (AFM1), and AFB1+AFM1 in the kidney were studied and compared in HEK 293 cells model and CD-1 mice model. The 35-day subacute toxicity mice model was constructed, biochemical indicators and kidney pathological staining were detected, kidney metabonomics detection was performed, and the metabolites were analyzed, and then the related toxicity mechanism was validated. Results showed that AFB1 (0.5 mg/kg), AFM1 (3.5 mg/kg), and AFB1 (0.5 mg/kg)+AFM1 (3.5 mg/kg) activated oxidative stress and caused renal damage. The relative concentration of the metabolite L-proline was found to be lower in aflatoxins treatment groups when compared with the control (P < 0.05). Moreover, with the treatment of aflatoxins, proline dehydrogenase (PRODH) and proapoptotic factors (Bax, Caspase-3) were upregulated, while the inhibitor of apoptosis Bcl-2 was downregulated, at both the mRNA and the protein levels, comparing with the control (P < 0.05). In addition, the combined effect of AFB1 and AFM1 was validated, for the toxicity of the combination was stronger than the other two groups. In conclusion, AFB1 and AFM1 caused kidney toxicity by activating oxidative stress through altering expression of PRODH and L-proline levels, which then induced downstream apoptosis.

Aflatoxin B1 induced renal and cardiac damage in rats: Protective effect of lycopene

This study was conducted to investigate the protective effects of lycopene against the toxic effects of Aflatoxin B1 (AFB1) exposure in kidney and heart of rat by evaluating antioxidant defense systems and lipid peroxidation (LPO). Forty-two healthy three-month-old male Wistar-Albino rats were used in this study. The animals were randomly divided into six experimental groups including 7 rats in each. These groups were arranged as follows: control group, lycopene (5 mg/kg/day, orally for 15 days) group, AFB1 (0.5 mg/kg/day, orally for 7 days) group, AFB1 (1.5 mg/kg/day, orally for 3 days) group, AFB1 (0.5 mg/kg/day, orally for 7 days) + lycopene (5 mg/kg/day, orally for 15 days) group and AFB1 (1.5 mg/kg/day, orally for 3 days) + lycopene (5 mg/kg/day, orally for 15 days) group. The animals were sacrificed at the end of applications. In this study, malondialdehyde (MDA) levels significantly increased; while reduced glutathione (GSH), glutathione-S-transferase (GST), catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and glucose-6-phosphate-dehydrogenase (G6PD) activities decreased in kidney and heart tissues. The significant reduction in the activities of antioxidant enzymes and non-enzymatic antioxidant system in AF treated rats as compared to the control group could be responsible for increased MDA levels observed during AF induced kidney and heart damage. The results showed increased urea, creatinine levels, as well as reduction sodium concentrations in plasma of AFB1 treated rats. There was lycopene showed protection against AF induced nephrotoxicity and cardiotoxicity.

The toxic effect of aflatoxin B1 on early porcine embryonic development

Aflatoxin B1 (AFB1) is a type of mycotoxin produced by the fungi Aspergillus flavus and Aspergillus parasiticus. AFB1 is considered as the most toxic mycotoxin owing to its toxic effect on health. In the present study, the toxic effect of AFB1 on early porcine embryonic development and its possible mechanism were investigated. Blastocyst formation was impaired with treatment of 1 nM AFB1 compared with control, 0.01, 0.1 group (40.13 ± 2.10%, 28.21 ± 1.62%, 32.34 ± 2.07% vs 19.01 ± 1.06%). Further study showed that the presence of AFB1 induced the generation of reactive oxygen species (ROS). And excessive ROS caused DNA damage which confirmed by the comet assay. Additionally, AFB1 also disrupted the DNA damage repair through the regulation of 53BP1. The AFB1 treatment significantly increased the γH2A foci and decreased the 53BP1 foci. TUNEL assay confirmed the generation of apoptosis, further resulting in the occurrence of autophagy. Moreover, AFB1 significantly increased the expression of pro-apoptosis genes Bax and Casp3 and reduced the expression of anti-apoptotic genes Bcl2 and Bcl-xl. In addition, the AFB1 also significantly increased the expression of autophagy related genes Lc3 and Beclin1. The presence of AFB1 significantly impaired the cell proliferation, a parameter of blastocyst quality for outgrowth. These results showed that the presence of AFB1 impaired porcine early embryonic development through oxidative stress, as well as DNA damage and repair, apoptosis, autophagy.

Detoxification and immunoprotection of Zn(II)-curcumin in juvenile Pacific white shrimp (Litopenaeus vannamei) feed with aflatoxin B1

Aflatoxins, which was produced by Aspergillus flavus or Aspergillus parasiticus fungi during grain and feed processing or storage, could cause severe health problems and reduction of yield during shrimp cultures. To evaluate toxic effects of aflatoxin B1 (AFB1) in juvenile Pacific white shrimp (Litopenaeus vannamei) and potential protective effect of Zn(II)–curcumin (Zn-CM), four experimental diets (control, 500 μg/kg AFB1, 500 μg/kg AFB1+100 mg/kg Zn-CM, 500 μg/kg AFB1+200 mg/kg Zn-CM) were formulated in quadruplicate to feed the shrimp for 8 weeks. The results revealed that AFB1 could induce significant decrease in final body weight (FBW), weight gain (WG, %) and visible variations of the hepatopancreas structures in L.vannamei. Compared with AFB1 group, AFB1+100 mg/kg Zn-CM group significantly ameliorated the toxic effects of AFB1 on growth performance, while AFB1+100 mg/kg Zn-CM group had no effect on growth performance. Dietary AFB1+100 mg/kg Zn-CM enhanced phenoloxidase (PO) (P < 0.05) activity. Both dietary AFB1+100 mg/kg Zn-CM and AFB1+200 mg/kg Zn-CM reduced inducible nitric oxide synthase (iNOS) activity and glutathione (GSH) level, decreased the content of malondialdehyde (MDA) (P < 0.05) in hepatopancreas compared with AFB1 group. Transmission electron microscopy (TEM) analysis demonstrated that Zn-CM could relieve the microvilli transformation and mitochondria accumulation reduction caused by AFB1. Consequently, the results demonstrated that suitable Zn-CM could mitigate the AFB1-induced hepatotoxicity and immunotoxicity effects on L.vannamei.

Effect of probiotic supplement on aflatoxicosis and gene expression in the liver of broiler chicken

The present study aimed to investigate the toxic effect of aflatoxin B1 (AFB1) and the effectiveness of a biological mycotoxin binder (Nutritox®) in detoxifying aflatoxicosis. Ninety one-day-old chicks were chosen and divided into 3 groups. The first group received standard basal diet only, the second group received a basal diet with AFB1 (0.25 mg/kg diet), and the third group received a basal diet with AFB1 (0.25 mg/kg diet) and Nutritox® (1 kg/ton diet). AFB1 feed contamination significantly reduced growth performance and deteriorated FCR. Moreover, it significantly increased serum AST, ALT, and malondialdehyde and significantly decreased serum total protein, albumin, globulin, SOD, CAT activities and glutathione peroxidase gene expression as well. Aflatoxin residues were detected in the liver tissues. Furthermore, the liver and kidney of AFB1 treated group showed pathological changes. The supplementation of Nutritox® significantly reduced aflatoxin levels in the liver and counteracted the negative effects of AFB1.

The efficacy of raw and concentrated bentonite clay in reducing the toxic effects of aflatoxin in broiler chicks

The objective of this study was to evaluate the efficacy of two adsorbents, a raw bentonite clay (RC) and a concentrated bentonite clay (CC), in ameliorating the toxic effects of aflatoxin B1 (AFB1). Results of the in vitro study (pH 3.0) indicated the CC adsorbed more AFB1 than RC (93.39 mg/g vs. 79.30 mg/g) suggesting that CC may be more effective than RC in reducing the toxic effects of AFB1. One hundred and eighty day-old straight run broiler chicks were assigned to 6 replicate pens of 5 chicks each and assigned to 6 dietary treatments from hatch to day 21. Dietary treatments included: 1) basal diet (BD) containing no AFB1 or adsorbents; 2) BD plus 0.50% RC; 3) BD plus 0.50% CC; 4) BD plus 2.0 mg AFB1/kg; 5) BD plus 2.0 mg AFB1/kg plus 0.50% RC; and 6) BD plus 2.0 mg AFB1/kg plus 0.50% CC. Dietary AFB1 concentrations were confirmed by analysis and diets were screened for other mycotoxins prior to the start of the experiment. The addition of AFB1 to the feed reduced (P < 0.05) growth performance and increased (P < 0.05) relative liver weight (RLW) and kidney weight (RKW) of chicks fed AFB1 compared to control chicks on day 21. These changes were ameliorated (P < 0.05) by the addition of RC and CC to the AFB1 diet. Mild to moderate lesions of aflatoxicosis (2.25) were observed in chicks fed AFB1 alone on day 21. The addition of both RC and CC to the AFB1 diet decreased (P < 0.05) but did not prevent liver lesions (0.92 and 1.42, respectively). Results indicate that both RC and CC were effective in reducing the toxic effects of AFB1, however the cost of processing of CC would make the RC a more economical product for reducing the effects of AFB1 in young broiler chicks.

Protective Effects of Sporoderm-Broken Spores of Ganderma lucidum on Growth Performance, Antioxidant Capacity and Immune Function of Broiler Chickens Exposed to Low Level of Aflatoxin B₁.

This study was conducted to investigate the toxic effects of aflatoxin B1 (AFB1) and evaluate the effects of sporoderm-broken spores of Ganoderma lucidum (SSGL) in relieving aflatoxicosis in broilers. A total of 300 one-day-old male Arbor Acre broiler chickens were randomly divided into four dietary treatments; the treatment diets were: Control (a basal diet containing normal peanut meal); AFB1 (the basal diet containing AFB1-contaminated peanut meal); SSGL (basal diet with 200 mg/kg of SSGL); AFB1+SSGL (supplementation of 200 mg/kg of SSGL in AFB1 diet). The contents of AFB1 in AFB1 and AFB1+SSGL diets were 25.0 μg/kg in the starter period and 22.5 μg/kg in the finisher period. The results showed that diet contaminated with a low level of AFB1 significantly decreased (p < 0.05) the average daily feed intake and average daily gain during the entire experiment and reduced (p < 0.05) serum contents of total protein IgA and IgG. Furthermore, a dietary low level of AFB1 not only increased (p < 0.05) levels of hydrogen peroxide and lipid peroxidation, but also decreased (p < 0.05) total antioxidant capability, catalase, glutathione peroxidase, and hydroxyl radical scavenger activity in the liver and spleen of broilers. Moreover, the addition of SSGL to AFB1-contaminated diet counteracted these negative effects, indicating that SSGL has a protective effect against aflatoxicosis.

Response of yellow catfish (Pelteobagrus fulvidraco) to different dietary concentrations of aflatoxin B1 and evaluation of an aflatoxin binder in offsetting its negative effects

Aflatoxin B1 (AFB1), produced by Aspergillus flavus and Aspergillus parasiticus, is one of the major mycotoxins to affect animal health. AFB1 contamination of aquafeed is widespread, especially in countries with humid, tropical climates. The most applied method for protecting animals against aflatoxicosis is the use of clay minerals. Growth performance, immunosuppressive effects (bactericidal activity, lysozyme activity, albumin/globulin ratio, alternative complement pathway activity, and protein content), and pathology parameters were used to evaluate the response of yellow catfish (Pelteobagrus fulvidraco) to increasing concentrations of AFB1 and test the protective effect of dietary supplementation with a bentonite (dioctahedral montmorillonite) based AFB1 binder. Triplicate groups of yellow catfish with an average weight of 2.0 ± 0.1 g were fed diets containing 0, 200, 500, and 1,000 µg/kg of AFB1 alone, or diets containing 0, 200, 500, and 1,000 µg/kg of AFB1 along with 2 g/kg AFB1 binder, for 12 weeks. Results showed that diets containing increasing amounts of AFB1 had a significantly lower (P = 0.002) survival rate. There was a statistical significant reduction in weight gain, final body weight, and specific growth rate, and an increase in feed conversion ratio (FCR) influenced by the levels of AFB1 in the diet (P &lt; 0.001 for all parameters), as well as increasing protection due to the presence of the binder (P = 0.046, P = 0.014, P = 0.038, and P = 0.485, respectively). The immunosuppressive nature of AFB1 in yellow catfish diets was confirmed through observation of lower bactericidal activity (P = 0.001), lower lysozyme activity (P = 0.006), reduced total protein (P = 0.002), and enhanced albumin/globulin ratio (P = 0.004). Fish fed diets contaminated with AFB1 and supplemented with the AFB1 binder showed better improvement in FCR (P = 0.019). These results indicate that AFB1 has a negative impact on yellow catfish growth and survival rate. The AFB1 binder protected fish from the toxic effects of AFB1.

Efficacy of Mozambican bentonite and diatomaceous earth in reducing the toxic effects of aflatoxins in chicks

The effectiveness of diatomaceous earth (DE) and bentonite clay (BC) in reducing the toxic effects of aflatoxin B1 (AFB1) in chicks was assessed. A total of 150 day-old male broiler chicks were assigned to six dietary treatments, with 5 replicate pens of five chicks per treatment. Dietary treatments were: (1) a positive control basal diet (BD) containing no AFB1, no BC and no DE; (2) BD + 0.50% BC but with no AFB1 and DE; (3) BD + 0.50% DE but with no AF and BC; (4) BD + 2 mg AFB1/kg diet but with no BC and DE; (5) BD + 0.50% BC + 2 mg AFB1/kg diet but with no DE; and (6) BD + 0.50% DE + 2 mg AFB1/kg diet but with no BC. Compared with controls, feed intake (FI) and body weight gain (BWG) were depressed (P&lt;0.05) in chicks fed AFB1, with greater reduction in FI and BWG observed in birds fed the AFB1 plus 0.50% DE diet. Feed conversion ratio was similar. Chicks fed AFB1 alone had increased (P&lt;0.05) relative liver weights compared to all other dietary treatments except for chicks fed AFB1+ DE. Chicks fed AFB1 alone and those fed AFB1+ DE had heavier (P&lt;0.05) relative kidney weights compared to chicks fed other treatments. Compared with the control chicks, livers from birds fed dietary AFB1 and AFB1 plus DE were similar. Liver lesion score of chicks fed AFB1 plus BC was lower (P&lt;0.05) than that of chicks fed AFB1 but higher (P&lt;0.05) than that of control chicks. Compared to controls, serum concentrations of glucose, albumin, total protein globulin, and calcium were decreased (P&lt;0.05) in chicks fed AFB1 alone, whereas serum concentrations of aspartate amino transferase and gamma glutamyl transferase were increased (P&lt;0.05). It can be concluded that this concentration of BC was partially effective in reducing the toxic effects of 2 mg/kg AFB1, whereas DE at the same concentration was not effective in reducing the toxic effects of 2 mg/kg AFB1.

Protective Influence of Gamma Rays and Electron-Beam Irradiation with a Commercial Toxin Binder on Toxic Effects of Aflatoxin B1 in Japanese Quails

Background: This cross sectional study was conducted to evaluate the effect of &amp;gamma-rays and electron-beam irradiation with a commercial toxin binder-milbond-TX on the performance, feed components, and meat quality of Japanese quails challenged with aflatoxin B1. Methods: Overall, 168 One-d-old chicks (Japanese quails) were allocated to eight treatments with three replicates based on a completely randomized design in a 2×4 factorial arrangement. Two levels of aflatoxin (Zero and 2 ppm) were considered as the essential factor. The secondary factor was involved in four levels (Control, 27 k Gy doses of &amp;gamma-rays, electron-beam irradiation, and 0.3% commercial toxin binder-milbond-TX). Results: In vitro condition showed that experiment diets do not have any effect on meat quality and feed components such as malondialdehyde, protein, fat, ash, and the dry matter. However, the highest and the lowest levels of feed intake and body weight gain were observed in the 7th treatment (2-ppm aflatoxin B1 + electron-beam irradiation) and the 2nd treatment (2-ppm aflatoxin B1 alone), respectively in 1-15 and 29-42 days (P&amp;le0.05). In addition, the highest liver weight (1.73), spleen (0.57) and bursa (0.18) were seen in the second treatment (2 ppm aflatoxin B1) alone (P&amp;le0.05) at the age of 42 days. Conclusion: &amp;gamma-rays and electron-beam irradiation plus commercial toxin binder-milbond-TX can be used for aflatoxin B1 absorption in poultry diets.

BIOCHEMICAL, IMMUNOLOGICAL AND PATHOLOGICAL STUDIES ON BROILER FED AFLATOXIN B1 CONTAMINATED DIET TREATED BIOLOGICALLY BY LACTOBACILLUS ACIDOPHILUS OR SACCHAROMYCES CEREVISIAE

A trial was carried out to shed more light on the precautionary efficiency of Lactobacillus acidophilus and Saccharomyces cerevisiae in ameliorating the toxic effects of aflatoxin B1 (AFB1) in broiler chicks. Two hundred and forty one-day-old unsexed Cobb broilers chicks were separated randomly into four equal experimental groups; with three replicates of 20 chicks each. The first group was received basal diet without aflatoxin B1 (control negative), while the other three groups were given basal diets containing 300 ppb AFB1. Within each aflatoxin treatment, the first group (control positive) was fed the contaminated diet without any treatment; the second was fed contaminated diet treated with L. acidophilus and the third was fed contaminated diet treated with S. cerevisiae. At the end of the experiment, biochemical traits, HI titer, and histopathological profile of broilers fed contaminated diet (300ppb AFB1/kg) (treated and not treated) were studied. The results showed that serum total protein, albumin, globulin, IgG and Ig, cholesterol and triglycerides were significantly decreased in the broilers fed diet containing 300 Ppb AFB1 as compared with those fed negative control diet. However, the activity of ALT and AST in blood serum was significantly increased in the broilers fed diet containing 300 Ppb AFB1 as compared with negative control. The same trend was observed in concentration of uric acid and creatinine. Although, all groups had haemaglutination inhibiting antibodies against NDV, the highest haemaglutination inhibiting antibody titer was obtained from birds not exposed to AFB1 at 35 days of age. In addition, data showed that the biological treatment by L. acidophilus or S. cerevisiae did not influence the humoral immune response of broiler against NDV. In addition, the histopathological study showed the ability of biological treatment to reduce the negative effects of AFB1 on liver and kidney tissues. It could be recommended that using L. acidophilus and S. cerevisiae supplementation in the feed to ameliorate toxic effects of aflatoxin B1 in broilers.