Mycotoxins and the pet food industry: Toxicological evidence and risk assessment

Boermans, Herman J.; Leung, Maxwell C.K.

doi:10.1016/j.ijfoodmicro.2007.07.063

Cited by 94 publications

(93 citation statements)

References 33 publications

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“…Each time, the contents of the ascending colon were collected from three gilts from each experimental group. In all experimental groups, the mycotoxins were administered at NOAEL (no observable adverse effect level) doses (Schlatter 2004;Boermans and Leung 2007;Laufersweiler et al 2012). The experiment was conducted over 42 days.…”

Section: Methodsmentioning

confidence: 99%

The genotoxicity of caecal water from gilts following experimentally induced Fusarium mycotoxicosis

et al. 2015

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ABSTRACT:The examination of caecal contents allows one to investigate the exposure of colon mucosa to dietary toxins and the chemical contaminants present in animal feed. The objective of the present study was to examine the influence of Fusarium mycotoxins (zearalenone, ZEN, and deoxynivalenol, DON), administered separately and as a mixture, on the genotoxicity of caecal water (CW) from gilts fed these mycotoxins. CW genotoxicity was evaluated with the comet assay using the LLC-PK1 porcine epithelial kidney cell line. It was shown that after the first week of the experiment, the presence of DON in animal feed led to increased CW genotoxicity in the proximal colon, while the presence of DON and ZEN + DON had a similar effect in the distal colon (ANOVA, P < 0.05). After the third week of experiment, elevated genotoxicity in the distal colon was observed for all experimental groups of gilts, and it was 62%, 52.4%, and 52.8% higher for ZEN-, DON-, and ZEN + DON-fed animals, respectively, than for control group animals. However, no effect on CW genotoxicity in the proximal colon was seen. After six weeks, the presence of ZEN in the proximal colon increased CW genotoxicity by 103% in comparison with the control group. In the distal colon, after the sixth week, CW genotoxicity in all groups of animals fed with mycotoxin was significantly (by 80% to 116%) higher than in the control group. ZEN and DON administered as a mixture did not lead to an increased genotoxicity compared to either agent administered separately. Generally, the mycotoxins clearly started to increase the genotoxicity of CW from the third week of administration.

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Section: Methodsmentioning

confidence: 99%

The genotoxicity of caecal water from gilts following experimentally induced Fusarium mycotoxicosis

et al. 2015

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“…Group C pigs were fed a placebo. In the experimental group, DON was administered at a dose below NOAEL values (Boermans and Leung 2007). The mycotoxin used in the study was purified and standardized in the Department of Chemistry of the Poznań University of Life Sciences under the supervision of Professor Piotr Goliński.…”

Section: Methodsmentioning

confidence: 99%

“…The above also applies to diagnoses foods of plant and animal origin (Commission Regulation (EC) No. 1126No. /2007.…”

Section: Introductionmentioning

confidence: 99%

The effects of dietary deoxynivalenol (DON) on selected blood biochemical and hematological parameters in pre-pubertal gilts

Zielonka

Gajęcka

Tarasiuk

et al. 2015

Polish Journal of Veterinary Sciences

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The aim of this study was to determine whether exposure to low doses of DON leads to changes in serum hematological and biochemical profiles. In the experiment, pre-pubertal gilts (with body weight of up to 25 kg) were administered DON per os at a daily dose of 12 μg/kg BW (group E, n=18) or a placebo (group C, n=21) over a period of 42 days. Blood for analysis was sampled seven times at weekly intervals. Minor, but statistically significant changes were observed in selected indicators, particularly in weeks 2 and 3 in values of biochemical parameters such AlAT, AspAT, P in and Fe, and in values of hematological parameters such as RBC, MCV, MCHC, PLT, MPV, WBC, neutrophil, eosinophil, lymphocyte and monocyte counts. In group E, a decreasing trend of the values was observed in most cases, except for RBC, PLT, eosinophil, lymphocyte and monocyte counts. Similar results were obtained in the last two weeks of the experiment. Initially, exposure to DON has a stimulating effect, which is eliminated when adaptive mechanisms are triggered. The results of the study indicate that the intensity of biotransformation processes varies subjected to the body's energy resources.

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“…As reviewed by Boermans and Leung [16], aflatoxins are the most common mycotoxins to cause acute illness linked to dog food in the world. Past reports of dog aflatoxin toxicosis in the USA include contaminated dog food due to a cornmeal ingredient containing 511 ppb aflatoxin [17].…”

Section: Aflatoxin-associated Recallsmentioning

confidence: 99%

A Review of Class I and Class II Pet Food Recalls Involving Chemical Contaminants from 1996 to 2008

Rumbeiha

Morrison

2010

J. Med. Toxicol.

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Commercial pet food in USA is generally safe, but adulteration does occur. Adulterated food has to be recalled to protect pets and public health. All stakeholders, including food firms, distributors, and government agencies such as the Food and Drug Administration (FDA) participate in food recall. The objective of this review is to describe the pet food recall procedure from start to finish, and to review class I and II pet food recalls from 1996 to 2008, with a specific focus on those due to chemical contaminants/adulterants. Information was requested from the FDA by Freedom of Information Act. Only those recalls backed by the FDA scientific review were considered. The legal framework for food recalls in the Code of Federal Regulations, Title 21, Chapter 1, Part 7 and in the Food and Drug Administration Amendments Act of 2007, Title X was reviewed. From 1996 to 2008, there were a total of 22 class I and II pet food recalls. Of these, only six (27%) were due to chemical adulterants. The adulterants were aflatoxins, cholecalciferol, methionine, and melamine, and cyanuric acid. The causes of adulteration included inadequate testing of raw materials for toxins, use of wrong or faulty mixing equipment, and misformulation of raw materials.Overall, pet food manufactured in the USA is safe. Even with shortcomings in the recall process, the incidence of illness associated with pet food adulteration is low. Added changes can only make the system better in the future to safeguard pet and public safety.

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Mycotoxins and the pet food industry: Toxicological evidence and risk assessment

Cited by 94 publications

References 33 publications

The genotoxicity of caecal water from gilts following experimentally induced Fusarium mycotoxicosis

The genotoxicity of caecal water from gilts following experimentally induced Fusarium mycotoxicosis

The effects of dietary deoxynivalenol (DON) on selected blood biochemical and hematological parameters in pre-pubertal gilts

A Review of Class I and Class II Pet Food Recalls Involving Chemical Contaminants from 1996 to 2008

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