Mutagenicity and Carcinogenicity of Mycotoxins: DNA Binding as a Possible Mode of Action

Stark, Avishay‐Abraham

doi:10.1146/annurev.mi.34.100180.001315

Cited by 85 publications

(33 citation statements)

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“…(Mollenhauer et al 1989); they may affect the hemopoietic organs, the nervous system or reproductive organs (Hafez et al 1979;Clarke et al 1986;Sova et al 1989). Aflatoxins specifically affect the DNA of hepatic cells what is taken for critical target for initiation of carcinogenesis (Chu 1977;Stark 1980). Aflatoxins may affect also the immunological processes and reduce resistance of the organism particularly against infection (Edds 1983).…”

Section: Broilers Zeolite Aflatoxin Bu Hematology Liver Histologymentioning

confidence: 99%

Hematological and Histological Response to the Diet Containing Aflatoxin B1 and Zeolite in Broilers of Domestic Fowl

Sova¹,

Pohunková²,

Reisnerová³

et al. 1991

Acta Vet. Brno

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Z. Sova, Hana Pohunkova, Hana Reisnerova, AUbeta SIamova, K. Haisl: Hematological and Histological Response to the Diet Containing Aflatoxin Bl and Zeolite in Broilers of Domestic Fowl. Acta vet. Brno, 60,1991: 31-40: The experiment was performed on twenty nine healthy broilers from the school farm. The birds were divided into four groups: control group I, group II fed with diet to which 5 % of zeolite . kg-I was added, group III fed with diet containing. 5 % of zeolite and 2 . 5 mg of aflatoxin Bl • kg I, and group IV fed with diet with only 2.5 mg of aflatoxin B1 . kg-I. Three or four broilers from each group were killed after five and twelve days of the experiment. Broilers in the group IV showed both serious heterophilia and lymphopenia. In the group III this shift was not so evident. In both groups III and I V features of acute alteration of liver parenchyma charracterized by the activation of Kupffer's cells and by dilatation of bile canaliculi and cholestasis were found. Similar focal changes were revealed also in liver tissue or broilers in the group II after twelve days of experiment. Results obtained suggest not only that the addition of 5 % of zeolite. kg-l to the food does not protect liver tissue' against toxic effects of aflatoxin Bl but also that zeolite itself is not harmless for broilers. Broilers, zeolite, aflatoxin Bu hematology, liver histology

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Section: Broilers Zeolite Aflatoxin Bu Hematology Liver Histologymentioning

confidence: 99%

Hematological and Histological Response to the Diet Containing Aflatoxin B1 and Zeolite in Broilers of Domestic Fowl

Sova¹,

Pohunková²,

Reisnerová³

et al. 1991

Acta Vet. Brno

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“…The mechanism most commonly suggested is its binding to DNA (20). The earlier work done by BURMEISTER and HESSELTINE (8) and in this laboratory found gram positive organisms comparatively more susceptible to aflatoxin B1 inhibition than gram-negative organisms.…”

Section: Discussionmentioning

confidence: 81%

Mechanism of inhibitory effects of aflatoxin B1 in Escherichia coli and Salmonella typhi.

Tiwari

d'Ham

Gupta

et al. 1984

J. Gen. Appl. Microbiol.

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The inhibitory effects of aflatoxin B1 on growth, respiration and cell viability were studied in Escherichia coli, Salmonella typhi, L forms of S. typhi B-34-6 and protoplasts of E. coli and S. typhi. or EDTA (0.05 % w/v) accentuated the lethal effects of aflatoxin B1 in test organisms. The protoplasts and L forms were more sensitive than the parent strain to the inhibitory effects of aflatoxin B1. Cells from all growth phases were equally susceptible to the growth inhibition. The E, coli and S. typhi cells bound approximately 10-24% more aflatoxin B1 with Tween-80 (0.05 %) or EDTA (0.05 %) added than with aflatoxin B1 alone. Aflatoxin B1 caused a substantial decrease in oxygen uptake in test preparations and this decrease was greatest in the L forms of S. typhi, followed by protoplasts, protoplast membranes, whole cells and cell debris.Micro-organisms have been used extensively to detect and assay aflatoxins (1-7) because of the speed and simplicity of the methods. BURMEISTER and HES-SELTINE (8) found gram positive microbes to be more sensitive to aflatoxin inhibition than gram negative ones. Flavo bacterium auranticum removes aflatoxins from solutions but lacked corresponding degrading enzymes (9). Aflatoxin binds to intact cells, protoplasts and protoplast membranes with and without nucleic acid (10). Aflatoxins inhibit metabolic and biosynthetic activities in micro-organisms including respiration (6), DNA synthesis (11), histidase mRNA transcription (12), pencillinase induction (13), and decrease in DNA to protein ratio (11). Aflatoxins are proved "hepatocarcinogens" despite some analogies and differences with antibiotics (14,1 S). Despite such a large amount of literature on aflatoxins, not much information is available on the mode of action of aflatoxin B1 in procaryotes. The present study was done to explore the mode of inhibition of aflatoxin B1 in S. t yphi and E. coli. 419

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“…With respect to the genotoxicity, a number of previous in vitro genotoxicity tests of KA showed positive results in the reverse gene mutation assay (Ames test) using microorganisms in the presence or absence of rat S9 mix fraction 13,14 and in DNA-damaging and clastogenic abilities in cultured rat liver cells 19,20 , as well as sister chromatid exchange and chromosomal aberration in Chinese hamster ovary cells 14 . However, it is uncertain whether the induction of hepatocellular proliferative lesions in mice and rats is a result of the genotoxicity of KA.…”

Section: Discussionmentioning

confidence: 99%

Induction of Hepatocellular Proliferative Lesions in CBA Mice by a 26-week Dietary Administration of Kojic Acid

et al. 2005

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In our previous study in which diets containing 0, 1.5 or 3% Kojic acid (KA) were administered to heterozygous p53-deficient mice of the CBA strain [p53 (+/-) mice] and their wild-type littermates [p53 (+/+) mice] for 26 weeks, the incidences of hepatocellular adenomas as well as altered hepatocellular foci were increased in p53 (+/-) and p53 (+/+) mice of the KA treated groups without initiation, as compared to those in the untreated control mice. In order to confirm the reproducibility of the induction of hepatocellular proliferative lesions in p53 (+/+) mice given KA, male CBA mice were given dietary administration of 0, 0.5, 1 or 2% KA for 26 weeks. Body weight gain in the 2% KA group was depressed after week 20 as compared to the corresponding control group. Significant increases of absolute and relative liver weights were observed in the groups treated with 1% and 2% KA. The incidences of hepatocellular adenomas in the control and 0.5, 1 and 2% KA groups were 5, 17, 10 and 21%, respectively, and those of hepatocellular foci in these groups were 15, 39, 45 and 47%, respectively, the difference between the control and 2% KA groups being statistically significant. The mean values for multiplicity of hepatocellular adenomas in the control and 0.5, 1 and 2% KA groups were 0.05, 0.2, 0.2 and 0.2, respectively, and those for hepatocellular foci were 0.2, 0.6, 0.8 and 0.6, respectively. The results of the present study suggest that KA has a hepatocarcinogenic potential in CBA mice. (J Toxicol Pathol 2005; 18: 159-165)

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Mutagenicity and Carcinogenicity of Mycotoxins: DNA Binding as a Possible Mode of Action

Cited by 85 publications

References 0 publications

Hematological and Histological Response to the Diet Containing Aflatoxin B1 and Zeolite in Broilers of Domestic Fowl

Hematological and Histological Response to the Diet Containing Aflatoxin B1 and Zeolite in Broilers of Domestic Fowl

Mechanism of inhibitory effects of aflatoxin B1 in Escherichia coli and Salmonella typhi.

Induction of Hepatocellular Proliferative Lesions in CBA Mice by a 26-week Dietary Administration of Kojic Acid

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