Reduction of Mutagenic Potentials in Milk: Effects of Ammonia Treatment on Aflatoxin-Contaminated Cottonseed

Jorgensen, Karen V.; Park, Douglas L.; Rua, Sam M.; Price, Ralph L.

doi:10.4315/0362-028x-53.9.777

Cited by 16 publications

(3 citation statements)

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“…A variety of physical and chemical techniques has been proposed to reduce the toxicity of aflatoxincontaminated feed (Goldblatt and Dollear, 1979;Hagler et al, 1982;Yousef and Marth, 1986;Park et al, 1988;Jorgensen et al, 1990;Salmeron et al, 1990; Samarajeewa et al, 1990;Schell et al, 1993). Modifications of mycotoxin contamination in feeds include: heat treatment (roasting and autoclaving), chemical inactivation (acid, alkalies, aldehydes, oxidizing agents, and ammonia gases), solvent extraction (ethanol, acetone, isopropanol, or a mixture of solvents), and biological inactivation (yeast, molds, and certain bacteria).…”

Section: Discussionmentioning

confidence: 99%

Dietary hydrated sodium calcium aluminosilicate reduction of aflatoxin M1 residue in dairy goat milk and effects on milk production and components1

Smith¹,

Phillips

Ellis

et al. 1994

Journal of Animal Science

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Lactating dairy goats were exposed to aflatoxin (100 and 200 ppb) and hydrated sodium calcium aluminosilicate at 1, 2, and 4% in two separate experiments. Naturally occurring low levels of aflatoxin M1 (.009 ppb) were found in the milk of the control diet, whereas there were no detectable levels of aflatoxin M1 in the milk of diets containing hydrated sodium calcium aluminosilicate in both experiments. In Exp. 1, no treatment-related differences in clinical behavior or significant difference in the feed intake, milk production, or milk component analyses were observed with 200 ppb of aflatoxin and 4% hydrated sodium calcium aluminosilicate. However, 4% hydrated sodium calcium aluminosilicate was responsible for an 86.9% reduction of aflatoxin M1 residue in the milk of diary goats. In Exp. 2, the combination of 1% hydrated sodium calcium aluminosilicate and aflatoxin at 100 ppb resulted in an overall reduction of aflatoxin M1 residue by 51.9%, which represented a mean change of aflatoxin M1 from .553 to .266 ppb of aflatoxin M1 in the milk. The diet that contained 2% hydrated sodium calcium aluminosilicate and 100 ppb of aflatoxin further reduced aflatoxin residue by a mean change from .553 to .098 of ppb aflatoxin M1, which represents an 82.2% reduction of aflatoxin M1 residue in the milk. Analysis of the data by time indicated that there were no statistical differences between days of sampling. Information regarding the ability of hydrated sodium calcium aluminosilicate to prevent or reduce the level of aflatoxin M1 residues in milk is critically needed.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 99%

Dietary hydrated sodium calcium aluminosilicate reduction of aflatoxin M1 residue in dairy goat milk and effects on milk production and components1

Smith¹,

Phillips

Ellis

et al. 1994

Journal of Animal Science

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“…On the other hand, ammoniation which refers to breaking down AFB1 in an alkaline environment is also effective in detoxification. When foods are treated with either gaseous or liquid ammonia (usually 1.5-2%), the degradation rate can sometimes reach above 99% in comparatively long time, ranging from 24 h to 15 days [124,125]. The degradation product due to ammoniation is a less mutagenic metabolite of AFB1, known as aflatoxin D1 (AFD1), formed through hydrolysis and decarboxylation, though risking a reversion back into AFB1 if reset in an acidified environment [126].…”

Section: Detoxification Strategiesmentioning

confidence: 99%

The Toxic Effects of Aflatoxin B1: An Update

Shan¹

2020

Aflatoxin B1 Occurrence, Detection and Toxicological Effects

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Aflatoxin B1 (AFB1) is the most toxic in aflatoxin family. It is well known for its involvement in hepatic carcinogenesis. Other adverse effects include immune weakness, reproduction deficiency, malnutrition, and growth impairment. The key mechanism of AFB1 carcinogenesis is supposed to be epoxidation, which produce the AFB1-8,9-epoxide (AFBO) strongly adductive to DNA molecules. Other metabolites like AFM1, AFH1, and AFL, which retain DNA adductive capability, extend its toxicity. Scientists now found that AFB1 also affected epigenetic regulation, which might shed new light into AFB1 toxicity mechanism researches. The detoxification of AFB1 has always been a hot spot in AFB1-related studies. The major methods can be categorized into physical treatment, biological treatment, chemical treatment, combination strategy, and sorbent additives. None of the methods is 100% perfect, however considering economic factors, simplicity, effectiveness, safety, and preservation of the food nutrition. This review will discuss the toxicity and toxic mechanisms of AFB1. Also, detoxification of AFB1 will be reviewed.2 as in the 1970s, its hepatocarcinogenic property has been testified in animal models [5], and there since, several epidemiological studies from Asia and Africa areas monitored intersection of high HCC incidence and AFB1 contamination, with 4.6-28.2% of HCC cases globally attributed to AFB1 exposure [6]. Moreover, hepatitis B virus (HBV) that cooperates with AFB1 can drastically increase the risk of HCC by 30-fold [7]. Recent researches also find evidences that hepatitis C virus (HCV) also has a synergistic role with AFB1 in hepatocarcinogenesis. Jeannot et al. found that the incidence of tumorous or pretumorous lesions was elevated by 2.5-fold in AFB1-treated HCV transgenic mice compared with wild-type mice [8]. Recently, a 20-year clinical follow-up study in Taiwan investigated HCC risk associated with AFB1 exposure in HCV-positive and HBV-HCV-negative individuals. HCV and AFB1 exposure were both found as independent risk factors for HCC development. Elevated serum AFB1albumin adduct levels were significantly associated with an increased risk of HCC newly developed within 8 years of follow-up in non-HBV-non-HCV participants with habitual alcohol consumption [crude OR (95% CI) for high vs. low/undetectable levels, 4.22 (1.16-15.37)], and HCV-infected participants [3.39 (1.31-8.77)], but not in non-HBV-non-HCV participants without alcohol drinking habit. Therefore, it indicated that AFB1 exposure contributes to the development of HCC in participants with significant risk factors for cirrhosis including alcohol and HCV infection [9]. What's more, AFB1 exposure can induce the increased levels of blood glucose in mice and, also, the high probability to develop liver cancer [10].Liver is not the only target organ of AFB1 toxification. Its impairment on the immune system has been established in both humans and animals. Several studies linked AFB1 exposure with reduced levels or functions of immunological factors, such as de...

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“…3 Aflatoxin-contaminated cottonseed treated with ammonia and fed to cows led to lower levels of AFB 1 and AFM 1 in milk than nontreated product. 42 When yellow dent corn naturally contaminated with 1600 ppm aflatoxin was treated with 3% NaOH at 100 • C for 4 minutes, further processed, and fried, 99% of the aflatoxin was destroyed. 14 As noted in the section below, Flavobacterium aurantiacum has been shown to remove AFB 1 from a variety of foods.…”

Section: Relative Toxicity and Mode Of Actionmentioning

confidence: 99%

Mycotoxins

Modern Food Microbiology

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A very large number of molds produce toxic substances designated mycotoxins. Some are mutagenic and carcinogenic, some display specific organ toxicity, and some are toxic by other mechanisms. Although the clear-cut toxicity of many mycotoxins for humans has not been demonstrated, the effect of these compounds on experimental animals and their effect in in vitro assay systems leaves little doubt about their real and potential toxicity for humans. At least 14 mycotoxins are known to be carcinogens, with the aflatoxins being the most potent. 84 It is generally accepted that about 93% of mutagenic compounds are carcinogens. With mycotoxins, microbial assay systems reveal an 85% level of correlation between carcinogenicity and mutagenesis. 84 Mycotoxins are produced as secondary metabolites. The primary metabolites of fungi as well as for other organisms are those compounds that are essential for growth. Secondary metabolites are formed during the end of the exponential growth phase and have no apparent significance to the producing organism relative to growth or metabolism. In general, it appears that they are formed when large pools of primary metabolic precursors such as amino acids, acetate, pyruvate, and so on, accumulate. The synthesis of mycotoxins represents one way the fungus has of reducing the pool of metabolic precursors that it no longer requires for metabolism.Some methods for the detection of mycotoxins in foods can be found in Chapter 11. For an extensive review of these substances in fruits, fruit juices, and dried fruits, see reference 27. AFLATOXINSAflatoxins are clearly the most widely studied of all mycotoxins. Knowledge of their existence dates from 1960, when more than 100,000 turkey poults died in England after eating peanut meal imported from Africa and South America. From the poisonous feed were isolated Aspergillus flavus, and a toxin produced by this organism that was designated aflatoxin (Aspergillus flavus toxin-A-fla-toxin). Studies on the nature of the toxic substances revealed the following four components:

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Reduction of Mutagenic Potentials in Milk: Effects of Ammonia Treatment on Aflatoxin-Contaminated Cottonseed

Cited by 16 publications

References 0 publications

Dietary hydrated sodium calcium aluminosilicate reduction of aflatoxin M1 residue in dairy goat milk and effects on milk production and components1

Dietary hydrated sodium calcium aluminosilicate reduction of aflatoxin M1 residue in dairy goat milk and effects on milk production and components1

The Toxic Effects of Aflatoxin B1: An Update

Mycotoxins

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