Absence of a synergistic effect between fumonisin B1 and N-nitrosomethylbenzylamine in the induction of oesophageal papillomas in the rat

Wild, Christopher P.; Castegnaro, M.; Ohgaki, Hideaki; Garren, Liliane; Galendo, D.; Miller, J. David

doi:10.1002/1522-7189(1997)5:3<126::aid-nt8>3.0.co;2-q

Cited by 4 publications

References 14 publications

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Mycotoxins with a Special Focus on Aflatoxins, Ochratoxins and Fumonisins

Steyn

Gelderblom

Shephard

et al. 2009

General, Applied and Systems Toxicology

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Mycotoxins are important environmental and carcinogenic agents. They are ubiquitous in a broad range of commodities and cause toxic responses when ingested by humans and animals. A review of mycotoxins is presented with special reference to the producing species, analytical methodology, occurrence, biological activity, decontamination, regulations and the risk assessment of aflatoxins, ochratoxins and fumonisins. Some of the most recent studies regarding the mechanisms involved in fumonisin B 1 ‐induced biological effects in different cell culture systems are tabulated. The review is directed at updating the previous review of Steyn and Stander (1999) with a focus on recent findings.

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Mycotoxins with a Special Focus on Aflatoxins, Ochratoxins and Fumonisins

Steyn

Gelderblom

Shephard

et al. 2009

General, Applied and Systems Toxicology

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Implications of Apoptosis for Toxicity, Carcinogenicity, and Risk Assessment: Fumonisin B1 as an Example

Dragan

Bidlack

Cohen

et al. 2001

Toxicological Sciences

117

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The rates of cell proliferation and cell loss in conjunction with the differentiation status of a tissue are among the many factors contributing to carcinogenesis. Nongenotoxic (non-DNA reactive) chemicals may affect this balance by increasing proliferation through direct mitogenesis or through a regenerative response following loss of cells through cytotoxic (oncotic) or apoptotic necrosis. In a recent NTP study in Fischer rats and B6C3F(1) mice, the mycotoxin fumonisin B(1) caused renal carcinomas in male rats and liver cancer in female mice. In an earlier study in male BD-IX rats, fumonisin B(1) caused hepatic toxicity and hepatocellular carcinomas. An early effect of fumonisin B(1) exposure in these target organs is apoptosis. However, there is also some evidence of oncotic necrosis following fumonisin B(1) administration, especially in the liver. Induction of apoptosis may be a consequence of ceramide synthase inhibition and disruption of sphingolipid metabolism by fumonisin B(1). Fumonisin B(1) is not genotoxic in bacterial mutagenesis screens or in the rat liver unscheduled DNA-synthesis assay. Fumonisin B(1) may be the first example of an apparently nongenotoxic (non-DNA reactive) agent producing tumors through a mode of action involving apoptotic necrosis, atrophy, and consequent regeneration.

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An overview of rodent toxicities: liver and kidney effects of fumonisins and Fusarium moniliforme.

Voss

Riley

Norred

et al. 2001

Environ Health Perspect

121

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Fumonisins are produced by Fusarium moniliforme F. verticillioides) and other Fusarium that grow on corn worldwide. They cause fatal toxicoses of horses and swine. Their effects in humans are unclear, but epidemiologic evidence suggests that consumption of fumonisin-contaminated corn contributes to human esophageal cancer in southern Africa and China. Much has been learned from rodent studies about fumonisin B1(FB1), the most common homologue. FB1 is poorly absorbed and rapidly eliminated in feces. Minor amounts are retained in liver and kidneys. Unlike other mycotoxins, fumonisins cause the same liver cancer promotion and subchronic (studies (3/4) 90 days) liver and kidney effects as (italic)F. moniliforme. FB 1 induces apoptosis of hepatocytes and of proximal tubule epithelial cells. More advanced lesions in both organs are characterized by simultaneous cell loss (apoptosis and necrosis) and proliferation (mitosis). Microscopic and other findings suggest that an imbalance between cell loss and replacement develops, a condition favorable for carcinogenesis. On the molecular level, fumonisins inhibit ceramide synthase, and disrupt sphingolipid metabolism and, theoretically, sphingolipid-mediated regulatory processes that influence apoptosis and mitosis. Liver sphingolipid effects and toxicity are correlated, and ceramide synthase inhibition occurs in liver and kidney at doses below their respective no-observed-effect levels. FB1 does not cross the placenta and is not teratogenic in vivoin rats, mice, or rabbits, but is embryotoxic at high, maternally toxic doses. These data have contributed to preliminary risk evaluation and to protocol development for carcinogenicity and chronic toxicity studies of FB1 in rats and mice.

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Absence of a synergistic effect between fumonisin B1 and N-nitrosomethylbenzylamine in the induction of oesophageal papillomas in the rat

Cited by 4 publications

References 14 publications

Mycotoxins with a Special Focus on Aflatoxins, Ochratoxins and Fumonisins

Mycotoxins with a Special Focus on Aflatoxins, Ochratoxins and Fumonisins

Implications of Apoptosis for Toxicity, Carcinogenicity, and Risk Assessment: Fumonisin B1 as an Example

An overview of rodent toxicities: liver and kidney effects of fumonisins and Fusarium moniliforme.

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