Efficacy of Bacillus subtilis ANSB060 Biodegradation Product for the Reduction of the Milk Aflatoxin M1 Content of Dairy Cows Exposed to Aflatoxin B1.

This study was conducted to determine the effect of Bacillus subtilis ANSB060 biodegradation product (BDP) in reducing the milk aflatoxin M1 (AFM1) content of dairy cows fed a diet contaminated with aflatoxin B1 (AFB1). Twenty-four Chinese Holstein cows (254 ± 19 d in milk; milk production 19.0 ± 1.2 kg d-1) were assigned to three dietary treatments, as follows: (1) control diet (CON), consisting of a basal total mixed ration (TMR); (2) aflatoxin diet (AF), containing CON plus 63 µg of AFB1 kg-1 of diet dry matter; and (3) aflatoxin diet plus BDP (AF + BDP), containing AF plus BDP at 0.2% of diet dry matter. The experiment lasted 12 days, including an AFB1-dosing period from days one to eight, followed by a clearance period from days nine to twelve. Milk samples were collected on days 2, 4, 6, and 8⁻12, and the plasma was sampled on day 9, before morning feeding. Short-term AFB1 exposure did not affect the milk production and composition. The plasma biochemical indices, except for lactic dehydrogenase (LDH), were also not changed by the AFB1 intake. The plasma LDH level was significantly elevated (p < 0.05) following dietary treatment with AFB1, while no significant difference was observed between the AF + BDP and CON treatments. Adding BDP to the AFB1-contaminaed diet resulted in a significant reduction in AFM1 concentration (483 vs. 665 ng L-1) in the milk, AFM1 excretion (9.14 vs. 12.71 µg d-1), and transfer rate of dietary AFB1 to milk AFM1 (0.76 vs. 1.06%). In conclusion, the addition of BDP could be an alternative method for reducing the dietary AFB1 bioavailability in dairy cows.

Study of aflatoxicosis reduction: effect of Alchornea cordifolia on biomarkers in an aflatoxin B1 exposed rats.

The toxicity of aflatoxins results in cancer and liver disease. Several natural substances such as plants exhibited their ability to inhibit the initiation of aflatoxin carcinogenesis. The aim of this study was to evaluate the effect of Alchornea cordifolia on biomarkers in an aflatoxin B1 (AFB1) exposed rats. The contents of polyphenols, flavonoids and the antioxidant activity of A. cordifolia ethanolic leaf extract (EELac) were assessed. Groups of rats were treated orally with a daily dose of a mixture of AFB1 at a dose of 150 µg/kg body weight and EELac (50, 100 and 300 mg/kg body weight) for 21 days. Biomarkers of AFB1, such as the AFB1-lysine adduct and aflatoxin M1 were assayed in blood and urine, respectively, using an HPLC system with a fluorescence detector. The contents of polyphenols and flavonoids were 6783.23 ± 272.76 µg EAG/g and 10.54 ± 3.15% of dry matter, respectively. EELac showed a good antioxidant activity (IC50 = 12.65 ± 0.13 µg/mL). The administration of the mixture (AFB1 + EELac) at different doses significantly reduced the level of AFB1-lysine adduct from 14.04 ± 2.1 to 4.13 ± 0.9 ng/mg albumin and that of Aflatoxin M1 (AFM1) from 456 ± 16 to 220 ± 24 ng/mL (p <0.05). The rate of reduction was 70.58% for AFB1-lysine adduct and 51.75% for AFM1. A. cordifolia could be used in the prevention of toxicity induced by AFB1 on account of its high content in phenolic compounds.

Effect of dietary calcium propionate on performance, hepatic enzyme activities and aflatoxin residues in broilers fed a diet containing low levels of aflatoxin B1.

This study was undertaken to the study toxic effects of aflatoxins and reducing toxic effects of calcium propionate on performance, hepatic enzyme activities and aflatoxin residues in broilers. Two hundred and seventy 1-day-old hybrid Arbor Acor broiler chickens were fed conventional feed for 3 days. Broilers were then randomly divided into nine groups of 30 birds each. The nine dietary treatments consisted of (1) conventional feed as a negative control diet, (2) 0.25% calcium propionate, (3) 0.5% calcium propionate, (4) 50 ppb aflatoxin B1, (5) 50 ppb aflatoxin B1 plus 0.25% calcium propionate, (6) 50 ppb aflatoxin B1 plus 0.5% calcium propionate, (7) 100 ppb aflatoxin B1, (8) 100 ppb aflatoxin B1 plus 0.25% calcium propionate, (9) 100 ppb aflatoxin B1 plus 0.5% calcium propionate. Test diets were offered for 6 weeks continuously and the birds were sacrificed. Decreased body weight gain, feed consumption and feed conversion ratio were observed in aflatoxin treated groups whereas aflatoxin B1-calcium propionate supplemented diet groups increased, in comparison to the control group. Significant difference was observed after 4 weeks of feeding. Serum samples were tested for gamma glutamyl transferase (gamma-GGT), aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Gamma-GGT, AST and ALT were significantly increased in aflatoxin treated groups, in comparison among the dietary treated groups. Muscle and liver tissues were analyzed for aflatoxin residues. The residual levels of aflatoxin B1 and aflatoxin M1 were significantly higher in liver than in muscle. The levels in the liver and the muscle were highest in the aflatoxin B1-supplemented groups and lower in the aflatoxin B1-calcium propionate supplemented groups. Results of this study indicate that addition of calcium propionate to diets containing aflatoxin B1 appears to be effective in reducing toxicity. Aflatoxin contamination in broiler feed may cause economic losses by lowering body weight gain. Therefore, lower levels of aflatoxin B1 in the chicken feeds should be required if all acceptable risk is to be avoided. Additionally, the risk of aflatoxins in broiler as a food appears to remain very low, although the levels of aflatoxins in human foods should be kept as low as possible to reduce the incidence of hepatic cancer.

Toxic effects of mycotoxins in humans.

Mycotoxicoses are diseases caused by mycotoxins, i.e. secondary metabolites of moulds. Although they occur more frequently in areas with a hot and humid climate, favourable for the growth of moulds, they can also be found in temperate zones. Exposure to mycotoxins is mostly by ingestion, but also occurs by the dermal and inhalation routes. Mycotoxicoses often remain unrecognized by medical professionals, except when large numbers of people are involved. The present article reviews outbreaks of mycotoxicoses where the mycotoxic etiology of the disease is supported by mycotoxin analysis or identification of mycotoxin-producing fungi. Epidemiological, clinical and histological findings (when available) in outbreaks of mycotoxicoses resulting from exposure to aflatoxins, ergot, trichothecenes, ochratoxins, 3-nitropropionic acid, zearalenone and fumonisins are discussed.

Effect of ammoniation of aflatoxin B1-contaminated cottonseed feedstock on the aflatoxin M1 content of cows' milk and hepatocarcinogenicity in the trout bioassay.

The effectiveness of ammonia in inactivating aflatoxins in contaminated cottonseed was investigated. Two aflatoxin-contaminated cottonseed lots were treated separately using an atmospheric pressure, ambient temperature ammoniation procedure (APAT) or a high pressure, high temperature ammoniation procedure (HPHT), and incorporated into dairy cow rations. Isocalorific diets containing 25% defatted, dried milk from cows fed aflatoxin-contaminated cottonseed without or with APAT or HPHT treatment, or an aflatoxin-free human grade commercial milk powder, were then fed for 12 months to rainbow trout (Oncorhynchus mykiss). Aflatoxin M1 (AFM1) concentrations in milk powders without and with seed treatment were: APAT, 85 and < 0.05 microgram/kg; HPHT, 32 and < 0.05 microgram/kg. In the APAT experiment, trout consuming the diet containing milk from cows fed the aflatoxin-contaminated cottonseed had a 42% incidence of hepatic tumours; APAT cottonseed treatment reduced this to 2.5%. Positive controls were included to demonstrate trout responsiveness. AFB1 fed continuously for 12 months at 4 micrograms/kg resulted in a 34% tumour incidence, whereas positive controls fed 20 micrograms AFB1/kg, 80 micrograms AFM1/kg, or 800 micrograms AFM1/kg for 2 wk and killed 9 months later had a 37, 5.7 and 50% incidence of tumours, respectively. These data demonstrate that APAT ammonia treatment of aflatoxin-contaminated dairy cattle cottonseed feedstock abolished the detectable transfer of AFM1 or AFB1 into milk powder, and greatly reduced the carcinogenic risk posed by any carry-over of aflatoxins or their derivatives into milk. In addition, the results confirm AFM1 to be a lower level hepatocarcinogen in comparison with AFB1 in the trout carcinogenicity assay. In the separate HPHT experiment, no tumours were observed in the livers of trout fed diets containing milk from either the ammonia-treated or untreated source, or the control diet containing 8 micrograms AFM1/kg. Positive controls fed 64 micrograms AFB1/kg for 2 wk exhibited a 29% tumour incidence 12 months later. Thus in this experiment, neither AFM1 at 8 micrograms/kg nor any HPHT-derived aflatoxin derivatives that might have been carried over into milk, represented a detectably carcinogenic hazard to trout.