The relationship of serum complement activity and bacteriostatic activity was investigated in male guinea pigs given aflatoxin and/or rubratoxin. In experiment 1, guinea pigs were given 0.6 mg of aflatoxin/kg of body weight, PO, once. In experiment 2, guinea pigs were given 0.02 mg of aflatoxin/kg, PO, and/or 8 mg of rubratoxin, PO, 11 times. Aflatoxin (0.02 mg/kg) had no effect given alone, but potentiated the effect of rubratoxin. In both experiments, changes in complement activity were accompanied by similar but not always significant (P less than 0.05) changes in bacteriostatic activity of serum. Guinea pigs given 0.06 mg of aflatoxin/kg had significant (P less than 0.05) changes in complement titers and in serum alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase activities. Guinea pigs given repeated oral doses of aflatoxin and/or rubratoxin had changes in complement titers, bacteriostasis, and alkaline phosphatase and aspartate aminotransferase activities, but not in alanine aminotransferase activities. Significant differences were detected only when average values for all guinea pigs given rubratoxin or rubratoxin with aflatoxin were compared with average values for guinea pigs not given rubratoxin.

Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for mixed feed, was added to the diets of growing wethers (mean body weight, 34.0 kg) and was evaluated for its ability to diminish the clinical signs of aflatoxicosis. The experimental design consisted of 4 treatment groups of 5 wethers each, consuming concentrations of 0 g of HSCAS and 0 g of aflatoxin (AF)/kg of feed (control; group 1); 20 g of HSCAS/kg (2.0%; group 2), 2.6 mg of AF/kg (group 3); or 20 g of HSCAS (2.0%) plus 2.6 mg of AF/kg (group 4). Wethers were maintained in indoor pens, with feed and water available ad libitum for 42 days. Lambs were observed twice daily and weighed weekly, and blood samples were obtained every 2 weeks for hematologic and serum biochemical analyses and for measurement of mitogen-induced lymphocyte-stimulation index. At the termination of the study, wethers were euthanatized and necropsied. Body weight gain was diminished significantly (P less than 0.05) by consumption of 2.6 mg of AF/kg of feed, whereas body weight of lambs consuming HSCAS plus AF did not differ from that of control wethers. The AF-alone treatment increased serum aspartate transaminase and gamma-glutamyltransferase activities, prothrombin time, and cholesterol, uric acid, and triglyceride values and decreased albumin, glucose, and urea nitrogen values, and urea-to-creatine ratio. A 27% decrease in lymphocyte stimulation index, increased spleen weight (as a percentage of body weight), and decreased liver weight were induced by AF-alone treatment. Results indicate that HSCAS may be a high-affinity sorbent for AF, that 2.6 mg of AF/kg of feed induces signs of aflatoxicosis in growing wethers, that lambs may not be as resistant to the effects of AF as previously thought, that 2.0% HSCAS can substantially reduce the toxic effects of 2.6 mg of AF/kg, and that sorbent compounds may offer a novel approach to the preventive management of aflatoxicosis in livestock.

Aflatoxins are potent hepatotoxic and carcinogenic secondary metabolites produced by toxigenic fungi. The present study investigated the protective effect of methanolic leaf extracts of Monanthotaxis caffra (MLEMC) against aflatoxin B1-induced toxicity in male Sprague-Dawley rats. The rats were randomly divided into 6 groups of 8 animals each. Five groups were administered orally for seven days with three different concentrations of MLEMC (100 mg/kg, 200 mg/kg and 300 mg/kg), curcumin (10 mg/kg) or vehicle (25% propylene glycol). The following day, these groups were administered 1 mg/kg b.w. of aflatoxin B1 (AFB1). The experiment was terminated three days after administration of AFB1. Group 6 represented untreated healthy control. Serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, creatinine and liver histopathology were evaluated. Methanolic leaf extracts of M. caffra decreased the levels of aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase and creatinine in the sera of rats as compared with the AFB1 intoxicated group. Co-administration of MLEMC improved the histological characteristics of the hepatocytes in contrast to the AFB1 treated group, which had mild to severe hepatocellular injuries including bile duct proliferation, bile duct hyperplasia, lymphoplasmacytic infiltrate and fibrosis. Extracts of M. caffra were beneficial in mitigating the hepatotoxic effects of AFB1 in rats by reducing the levels of liver enzymes and preventing hepatic injury.

Objective: The purpose of this work is to develop and validate an appropriate solvent solution and quantitative thin layer chromatography (TLC) method for determining the aflatoxins content of chicken feeds and dietary grains. Materials and Methods: To obtain the optimal mobile phase, samples were extracted with methanol/water (3:1) + 5% sodium chloride and partitioned using several solvent systems using preparative TLC. Camag TLC scanner 3 was used to scan the TLC plates at 366 nm and quantify them using JustTLC software. The method was tested for linearity, specificity, accuracy, precision, sensitivity, and robustness in accordance with ICH recommendations, and then utilized to screen 132 Nigerian poultry/food samples for total aflatoxins (TAFs). Results: The best separation of aflatoxins was achieved using acetonitrile and dichloromethane (3:17) mobile phase over an average run time of 45 min, resulting in linear calibration curves (R2 > 0.99) in the concentration range limit of quantitation (LoQ) to 50 ng/spot with a limit of detection of [J Adv Vet Anim Res 2021; 8(4.000): 656-670]

The current study is aimed to investigate the fungal contaminants in fish feed. Isolation of fungi was conducted on modified dichloran 18% glycerol agar (DG18) and potato dextrose agar (PDA). Feed samples were assayed for aflatoxins using HPLC. A total of 43 species belonging to 19 fungal genera recovered from 45 fish feed samples. Aspergillus and Penicillium were the most predominant genera with isolation frequency values indicated the retrieval capability of DG18 over PDA medium. For instance, Aspergillus spp. recorded 60%, 53.3% while Penicillium spp. were 33.3%, 17.8% on DG18 and PDA respectively via direct plating. 41.4% of the tested isolates were mycotoxin producers. Aflatoxins B1, B2, G1 and G2 were detected by 6 out of 10 screened Aspergillus isolates. Fumitremorgens, Gliotoxin, Ochratoxin A and B, and Zeralenone were also detected. The feed samples of high total count percentages (TC%) of A. flavus recorded the highest incidence of aflatoxins B2, G1 and G2 (2.3, 35.3 and 7.8 ng/g respectively). Meanwhile, the highest B1 concentration (3.7 ng/g) was recorded for the highest TC% interval studied (1:9 cfu/g). Thus, it is important to monitor the fungal load and mycotoxins in fish feed periodically using proper practical approaches.

The current research was designed to examine the protective effect of probiotic-fortified ration against aflatoxin B1 (AFB1) toxicity and its residual level in broilers' edible tissues. Sensitive high-performance liquid chromatography coupled with a fluorescence detector (HPLC-FLD) was used for measuring the toxin. Ninety, one-day-old Cobb chicks were allocated into three equal groups (n=30) with three replicates per group. The first control group (G1) was fed a balanced basal diet only and the second group (G2) received AFB1 (2 mg/kg basal diet), while the third group (G3) received a combination of AFB1 (2 mg/kg basal diet) with Saccharomyces cerevisiae (SC; 1.5 g/Kg basal diet). Experimental birds were monitored for 6 weeks, their growth performance was then compared. AFB1 residue was assessed in the meat and liver sample. AFB1 resulted in a significant (P<0.05) reduction of growth performance parameters such as body weight and carcass yield in comparison to the control and SC supplemented groups. Moreover, AFB1 residue significantly (P<0.05) diminished in SC fortified group when compared with the AFB1 group. In conclusion, probiotics such as Saccharomyces cerevisiae could be considered as a potential feed additive and a growth promoter. Besides, its role in controlling AFB1 residue in the edible tissues of boiler chicken.

The levels of aflatoxin (AFT) and ochratoxin (OCT) were assessed at different seasons in raw materials, different feed manufacture processing stages, and animal feeds in feed mills in Korea implementing the hazard analysis and critical control point (HACCP) system. Two hundred samples were collected in all four seasons from five feed mills implementing the HACCP system and examined for AFT and OCT contents. The AFT and OCT levels were analysed by using HPLC method to provide information on raw material and product stage. The AFT content of raw ingredients in the spring season was highest in corn gluten (3.84 ppb) and lowest in corn (1.82 ppb) The AFT content of corn was highest in the winter season (2.17 ppb). The content of OCT in wheat was highest in the winter season. The amounts of AFT and OCT at processing stages were higher than in the raw materials or feed. In particular, AFT content was higher in the transfer stage (3.88 ppb) than in the mixing (2.86 ppb) or filling stages (3.45 ppb) in the summer season. The means of AFT and OCT level in laying hen feed was 3.41 ppb and 1.14 ppb for broiler feed, respectively. The means of AFT and OCT level in and broiler feeds was 3.44 ppb and 1.17 ppb for broiler feed, respectively.

Aflatoxin (AF)-contaminated and fumonisin B1 (FB1)-contaminated (culture material from Fusarium moniliforme) diets were fed singly and in combination to growing cross-bred barrows. Six barrows (3 replicates of 2 each; mean body weight, 17.5 kg) per group were fed: 0 mg of AF and 0 mg of FB1/kg of feed (control); 2.5 mg of AF/kg of feed; 100 mg of FB1/kg of feed; or 2.5 mg of AF plus 100 mg of FB1/kg of feed for 35 days. The effects on production performance, serum biochemical, hematologic, immunologic, and pathologic measurements were evaluated. Body weight, gain, and feed consumption were significantly (P < 0.05) decreased by AF and AF plus FB1 diets. The FB1 diet decreased feed consumption, and although body weight was numerically decreased, it was not statistically significant. Aflatoxin increased serum gamma-glutamyltransferase (GGT) activity and total iron concentration and decreased urea nitrogen concentration and unsaturated iron-binding capacity. The FB1-alone diet increased serum GGT activity, whereas the AF plus FB1 diet increased serum aspartate transaminase, cholinesterase, alkaline phosphatase, and GGT activities, increased RBC count, triglycerides, and total iron concentrations, and decreased unsaturated iron-binding capacity and urea nitrogen concentration. For the most part, the effects of the AF plus FB1 diet on body weight and hematologic measurements could be considered additive. However, the effect of the AF plus FB1 diet on cholinesterase and alkaline phosphatase activities was greater than additive and was a synergistic response. One pig in the FB1-diet group and 2 pigs in the combination-diet group died. Postmortem lesions in pigs of the FB1-diet group consisted of ascites and increased liver weight. Observations at necropsy for pigs of the AF plus FB1-diet group consisted of hydrothorax, ascites, pulmonary edema, gastric erosions and ulceration, and increased liver and spleen weights. The AF diet increased relative liver weight and resulted in liver that was pale, rubbery, and resistant to cutting. Histologic lesions consisted of hepatic necrosis or degeneration, or both, with variable degrees of bile duct proliferation in barrows of the AF-diet groups. Renal tubular nephrosis was observed in barrows of the FB1 diet group, but this was not consistent in the AF plus FB1-diet group. Cell-mediated immunity, as measured by mitogen-induced lymphoblastogenic stimulation index, was decreased in barrows of the AF and FB1-diet groups, and values in barrows given the combination diet were significantly decreased from those in barrows given the single toxin diets. It was concluded that AF and FB1 (from culture material), singly or in combination, can adversely affect clinical performance, serum biochemical, hematologic, and immunologic values and induce lesions in growing barrows. For most of the variables we evaluated under our study conditions and dosages of toxins, measurements were affected more by the combination diet than by either single toxin diet, and the toxic responses could be described as additive or more than additive, particularly for induction of liver disease.

Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for agricultural feeds, was added to aflatoxin (AF)-contaminated diets of 3 lactating dairy cows and evaluated for its potential to reduce aflatoxin M1 (AFM1) residues in milk. During phase I, cows were fed alternating diets that consisted of 200 microgram of AF/kg of feed for 7 days, 0.5% HSCAS plus 200 microgram of AF/kg of feed for 7 days, and feed with the HSCAS removed for a final 7 days. The AFM1 milk concentrations from the intervals with HSCAS added to diets were compared with those times when HSCAS was absent. The presence of 0.5% HSCAS in feed containing 200 microgram of AF/kg reduced AFM1 secretion into the milk by an average of 0.44 microgram/L (from pretreatment of 1.85 microgram/L to 1.41 microgram/L with HSCAS, a 24% reduction). Following a 10-day period of noncontaminated feed consumption and no AFM1 residues in the milk, phase II of the study was begun. The same experimental design as phase I was used, but the dosages of HSCAS and AF were changed to 1.0% and 100 microgram/kg of feed, respectively. The addition of 1.0% HSCAS in feed containing 100 microgram of AF/kg decreased AFM1 content in the milk by an average of 0.40 microgram/L (from a pretreatment of 0.91 microgram/L to 0.51 microgram/L when HSCAS was present, a 44% reduction). These findings suggest that HSCAS, a high-affinity sorbent compound for AF in vitro, is capable of reducing the secretion of AFM1 into milk.