Mycotoxin problem in Africa: Current status, implications to food safety and health and possible management strategies

This review presents the different mycotoxins (aflatoxins, fumonisins and ochratoxin A) produced in agricultural crops in the West African sub-region. The acute and chronic toxic effects of the various mycotoxins are presented. Maize and groundnuts have been found to be excellent substrate for aflatoxin contamination, while fumonisins are widely distributed in maize. Other food products for which mycotoxin contamination has been reported in the sub-region include dried yam chips, tiger nut, melon seeds and stored herbal plants. Mycotoxin contamination is favoured by stress factors during plant growth, late harvesting of crops, high ambient humidity preventing thorough drying, unscientific storage practices and lack of awareness. Control measures include education of the populace on the danger of mycotoxin contaminated diet, early harvesting, rapid drying, sorting, sanitation, use of improved storage structures, smoking, insect control, the use of botanicals and synthetic chemicals as storage protectants, fumigation, biological control, the use of resistant varieties and detoxification of mycotoxin contaminated grains. Key words : Mycotoxins, aflatoxins, food, fumonisins, ochratoxin A, surveillance, toxicology, prevention, control, West Africa. 
African Journal of Biotechnology Vol.2(9) 2003: 254-263

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Mycotoxins in food in West Africa: current situation and possibilities of controlling it

Fumonisin B(1) (FB(1)) is a mycotoxin produced by the fungus Fusarium verticillioides, which commonly infects corn and other agricultural products. Fusarium species can also be found in moisture-damaged buildings, and, therefore, exposure of humans to Fusarium mycotoxins including FB(1) may take place. FB(1) bears a clear structural similarity to the cellular sphingolipids, and this similarity has been shown to disturb the metabolism of sphingolipids by inhibiting the enzyme ceramide synthase leading to accumulation of sphinganine in cells and tissues. FB(1) is neurotoxic, hepatotoxic, and nephrotoxic in animals, and it has been classified as a possible carcinogen to humans. The cellular mechanisms behind FB(1)-induced toxicity include the induction of oxidative stress, apoptosis, and cytotoxicity, as well as alterations in cytokine expression. The effects of FB(1) on different parameters vary markedly depending on what types of cells are studied or what species they originate from. These aspects are important to consider when evaluating the toxic potential of FB(1).

A review of the toxic effects and mechanisms of action of fumonisin B1.

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.

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

Aflatoxin and fumonisin contamination of corn (maize, Zea mays) hybrids in Arkansas

Fumonisin B1 is a mycotoxin produced by Fusarium moniliforme, a fungus that infects corn and other grains in the U.S. Fumonisin ingestion causes a variety of effects including equine leukoencephalomalacia and porcine pulmonary edema, and has been associated epidemiologically with human esophageal cancer. Fumonisin B1 produces growth inhibition and increased apoptosis in primary human keratinocyte cultures and in HET-1A cells. In order to set the doses for a 2-year tumor bioassay, male and female F344 rats were fed fumonisin B1 (99, 163, 234, and 484 ppm) for 28 days and the organs examined histologically. There was a dose dependent decrease in liver and kidney weights in the rats. The liver weight loss was accompanied by the induction of apoptosis and hepatocellular and bile duct hyperplasia in both sexes, with the female rats being more responsive at lower doses. The induction of tubular epithelial cell apoptosis was the primary response of the kidneys to dietary fumonisin B1. Apoptosis was present at all doses in the kidneys of the male rats, and occurred in the females only at 163, 234, and 484 ppm fumonisin B1. These results demonstrate that fumonisin B1 treatment causes a similar increase in apoptosis both in vivo and in vitro.

W G Sheldon

Papers

The mycotoxin fumonisin induces apoptosis in cultured human cells and in livers and kidneys of rats.