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At least 127 records · Page 7Linked to original sources
PubMed1998

Aflatoxicosis in turkey poults is prevented by treatment of naturally contaminated corn with ozone generated by electrolysis.

Previous studies have demonstrated that a novel source of ozone gas (O3) maybe used to chemically degrade numerous mycotoxins, including aflatoxin (AF) B1. Subsequent in vitro analyses demonstrated detoxification of AFB1, suggesting a potential method of remediate AF-contaminated grain. The objective of this study was to evaluate the capability of electrochemically produced ozone to degrade AFB1 in naturally contaminated whole kernel corn and confirm detoxification in turkey poults. Corn was procured from the southern coastal areas of Texas and HPLC revealed 1,220 +/- 73.3 ppb AFB1. Control and contaminated corn were treated for 92 h with O3 at 200 mg/min in 30 kg batches; greater than 95% reduction of AFB1 in contaminated corn was achieved. One-day-old female turkey poults were fed 1) control corn, 2) control corn + O3, 3) AFB1 corn, or 4) AFB1 corn + O3 mixed in rations (46% by wt.) and consumed ad libitum for 3 wk. When compared with controls, turkeys fed AFB1 corn had reduced body weight gain and relative liver weight, whereas turkeys fed control corn + O3 or AFB1 corn + O3 did not differ from controls. Furthermore, alterations in the majority of relative organ weight, liver discoloration, serum enzyme activity, hematological parameters, and blood chemistry caused by AFB1 were eliminated (no difference from controls) by treatment with O3. These data demonstrate that treatment of contaminated corn with electrochemically produced O3 provided protection against AFB1 in young turkey poults. It is important to note that treatment of control corn with O3 did not alter the performance of the turkey poults.

Animal Feed↗
PubMed1997

Mycotoxins and public health: a review.

This article provides an overview of the public health implications of mycotoxins--including a review of mycotoxin-related diseases documented in humans and animals, recent associations between mycotoxin exposure and carcinogenicity, a catalogue of foodstuffs documented to have been contaminated by mycotoxins, and a description of the distribution of mycotoxins in both the United States and worldwide. The article also advocates that public health professionals utilize recent developments in the field of mycotoxicology to explore associations between these fungal metabolites and acute and chronic disease in humans.

Aflatoxins↗
PubMed1990

Risk assessment for aflatoxin: II. Implications of human epidemiology data.

A review of epidemiology literature revealed that only studies conducted in Africa and Asia included data adequate to permit quantitative assessment of the dose-response relationship between aflatoxin exposure levels and liver cancer rates. Although these studies were judged adequate, their direct use to predict risks in U.S. populations may be questioned since hepatitis B virus (HBV) infections are far more common in the studied areas than in the U.S. Recent research indicates that, if aflatoxin contributes to the development of liver cancer, it almost always does so in the presence of HBV infection. The African/Asian data do not permit us to estimate the potency of aflatoxin in the absence of HBV. Recognizing this, these data can only be used to establish upper limits for the predicted excess lifetime risk for liver cancer in the U.S. When used in conjunction with aflatoxin exposure estimates for the Southeast U.S., these data predict a liver cancer rate, due to aflatoxin alone, far above that actually observed due to all causes; this provides an indication of the conservatism of this approach. Data from the Southeast U.S. may be used to estimate an excess lifetime risk for liver cancer of 2.17 x 10(-6) x (aflatoxin intake, ng/kg/day).

Environmental Exposure↗
PubMed1975

Canine aflatoxicosis.

Poisoning with aflatoxin derived from mouldy bread was confirmed as the cause of death of one dog and was suspected as the cause of death of two other dogs on the same ration. A jaundiced carcass, firm bile-stained liver and haemorrhage into the gastro-intestinal tract were seen at autopsy. Swelling and foamy vacuolation of hepatocytes due to fatty infiltration, marked perioportal proliferation of bile ductules and some periacinar necrosis were the microscopic changes seen in the liver. Aspergillus flavus was isolated from the mouldy bread and also from a sample of vomitus. Aflatoxin B1, 6.7 ppm, was detected in the mouldy bread and extremely high levels of 100 ppm of aflatoxin B1 and 40 ppm of aflatoxin G1 were present in a sample of vomitus.

Aflatoxins↗
PubMed1981

Acute aflatoxicosis in calves fed peanut hay.

Acute aflatoxicosis was believed to be the cause of death of 12 to 90 drought-stricken Hereford calves fed peanut hay on the southern Darling Downs in Queensland. Jaundice, photosensitisation, diarrhoea, anorexia and depression were seen before death. Serum levels of enzymes of hepatic origin and bilirubin were elevated. After death haemorrhage, hepatocyte damage, bile ductule proliferation were found. Total aflatoxin levels up to 2230 microgram/kg were detected in the peanut hay with most toxin concentrated in nut-in-shell.

Aflatoxins↗
PubMed1985

Experimental combined aflatoxin B1 and ochratoxin A intoxication in pigs.

Twenty-one pigs weighing approximately 18 kg were placed in 7 groups of 3 and given diets containing respectively aflatoxin B1 alone at 0.375 and 0.0750 mg/kg, ochratoxin A alone at 1 and 2 mg/kg, 0.375 mg/kg of aflatoxin B1 plus 1 mg/kg of ochratoxin A and 0.750 mg/kg aflatoxin B1 and 2 mg/kg of ochratoxin A. The remaining group served as untreated control. At the respective dose levels, pigs receiving similar doses of ochratoxin A alone or in combination with aflatoxin B1, were similarly affected, the clinical effects of aflatoxin having been mostly obscured by those due to ochratoxin A. Mild degenerative hepatic changes typical of aflatoxicosis were observed in pigs fed this toxin alone or in combination with ochratoxin A. In kidneys of pigs fed diet containing 1 and 2 mg of ochratoxin A alone changes included interstitial fibrosis of the vortex and dystrophy and degeneration of the tubular epithelium. Similar lesions but less pronounced fibrosis were found in kidneys of pigs receiving both toxins. The respective lower dose levels of mycotoxins selected were judged to be about the no-effect levels for each dosed separately under the conditions of the trial. Such levels have been found not infrequently on mould affected grain and stock foods. The result highlights the difficulties that may be experienced in the recognition of such multimycotoxicoses as they are likely to occur in the field and indicate the need for toxicological analysis as well as pathological investigation in establishing a diagnosis.

Aflatoxin B1↗
PubMed2004

Effect of foodstuff contamination by aflatoxin on the one-humped camel (Camelus dromedarius) in Al Ain, United Arab Emirates.

Twenty young female adult one-humped racing camels (Camelus dromedarius) kept in camps scattered outside Al Ain city and aged between 3- and 6-years-old, died after a short clinical illness. Affected camels were dull, inappetant and pyrexic, with submandibular oedema and enlargement of submandibular lymph nodes. Of 100 camels within the camps, 31 showed clinical signs. At necropsy examination, the liver of dead animals appeared yellowish, enlarged, congested and friable. The main hepatic histological findings were centrolobular necrosis, haemorrhages and cellular vacuolation. Aflatoxins were detected in sera, liver, ruminal contents and in feed ingested by affected animals. Sera of symptomatic and recovered camels also showed increased levels of glutamic oxaloacetic transaminases, glutamic pyruvic transaminases, aspartate transaminases, gamma glutamyl transaminases, glucose, urea nitrogen, phosphorus and total iron. Decreased levels of albumin, calcium, cholesterol and triglycerides were also observed. It was probable that aflatoxicosis was responsible for clinical signs and subsequent death of the camels. The need for suitable and appropriate storage conditions of animal feed to prevent fungal growth and aflatoxin contamination is highlighted.

Aflatoxins↗
PubMed1980

Abnormal concentrations of B vitamins and amino acids in plasma, bile, and liver of chicks with aflatoxicosis.

Graded levels of aflatoxin fed to broiler chickens for 3 weeks decreased the levels of most B vitamins in plasma, bile, and liver and decreased all free and hydrolyzed amino acids from peptides in plasma. The levels of thiamine, riboflavin, vitamin B6, pantothenic acid, and choline decreased by more than 60% in bile; vitamin B6, pantothenic acid, and choline decreased by more than 49% in plasma; thiamine, vitamin B6, pantothenic acid, choline, folate, and niacin decreased by more than 19% in liver; and only bile and plasma levels of folate increased (78 and 12%, respectively) with a dietary level of 5 microgram of aflatoxin per g of feed. Plasma levels of cystine and cysteine, methionine, threonine, serine, and aspartic acid decreased by more than 37%, whereas valine, lysine, leucine, histidine, hydroxyproline, and alanine decreased by more than 9% with 2.5 microgram of aflatoxin per g of feed. The data suggest that aflatoxin interferes with the metabolism of B vitamins and amino acids in chicks. However, these changes may be measuring the effects of aflatoxin-induced hepatic necrosis.

Amino Acids↗
PubMed1981

Abnormal concentrations of B vitamins and amino acids in plasma and B vitamins in bile of rabbits with aflatoxicosis.

The dosages of aflatoxin B1 (AFB1) required to produce significant changes in concentrations of B vitamins in plasma and bile and of amino acids in plasma of rabbits were determined. Folate increased by 98% in plasma, whereas concentration of thiamine, vitamin B6, and biotin decreased by more than 50%. In bile, choline and biotin increased 14- and 18-fold, respectively, whereas folate and niacin decreased by more than 50%. All amino acids in plasma increased between 76 and 155%. The dosages of AFB1 required to induce these changes were usually between 12.5 and 37.5 microgram/kg of body weight per day. Except for changes in biliary concentrations of pantothenic acid, folic acid, and biotin, lower threshold dosages of aflatoxin were required to produce weight loss and anorexia (5.0 and 8.5 microgram of AFB1/kg per day, respectively) than for changes in vitamins and amino acids (approximately 25 to 50 microgram of AFB1/kg per day). The data indicated that AFB1 interfered with the metabolism of B vitamins and amino acids in rabbits.

Aflatoxin B1↗