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PubMed2006

Apiaceous vegetable constituents inhibit human cytochrome P-450 1A2 (hCYP1A2) activity and hCYP1A2-mediated mutagenicity of aflatoxin B1.

In humans, apiaceous vegetables (carrots, parsnips, celery, parsley, etc.) inhibit cytochrome P-450 1A2, a biotransformation enzyme known to activate several procarcinogens, including aflatoxin B1 (AFB). We evaluated eight phytochemicals from apiaceous vegetables for effects on human cytochrome P-450 1A2 (hCYP1A2) activity using a methoxyresorufin O-demethylase (MROD) assay and a trp-recombination assay. Saccharomyces cerevisiae was used for heterologous CYP1A2 expression and this yeast strain is also diploid and auxotrophic for tryptophan due to mutations in the trp5 alleles. When these two alleles undergo AFB-induced mitotic recombination, gene conversion occurs, allowing yeast to grow in the absence of tryptophan. The apiaceous constituents psoralen, 5-methoxypsoralen (5-MOP), 8-methoxypsoralen (8-MOP), and apigenin were potent inhibitors of hCYP1A2-mediated MROD activity in yeast microsomes, whereas quercetin was a modest hCYP1A2 inhibitor. Naringenin, caffeic acid, and chlorogenic acid did not inhibit hCYP1A2-mediated MROD activity. The 2-h pretreatment of intact yeast cells with psoralen, 5-MOP, and 8-MOP significantly improved cell survival after subsequent 4-h AFB treatment and reduced hCYP1A2-mediated mutagenicity of AFB. Apigenin also significantly decreased mutagenicity. These results suggest that in vivo CYP1A2 inhibition by apiaceous vegetables may be due to the phytochemicals present and imply that apiaceous vegetable intake may be chemopreventive by inhibiting CYP1A2-mediated carcinogen activation.

Aflatoxin B1↗

PubMed1998

Stachybotrys, a mycotoxin-producing fungus of increasing toxicologic importance.

BACKGROUND: Stachybotrys as a fungus has been implicated as a source of mycotoxins. While the toxicity of several well-known mycotoxins (aflatoxins) is well documented, recent studies on Stachybotrys have raised the question that mycotoxins produced by this fungus may be responsible for the health effects of occupants in water-damaged buildings. METHODS: Published articles regarding Stachybotrys-related mycotoxins were reviewed with particular focus on human toxicity. RESULTS: A critical review of papers, reports, and studies on Stachybotrys mycotoxins revealed only descriptive reports of suspected animal and human poisoning secondary to consumption of mold-contaminated food products. No studies of good toxicologic and epidemiologic designs answer whether airborne mycotoxins produced by Stachybotrys could produce specific human toxicity. CONCLUSIONS: Current data on the toxicology of mycotoxins produced by Stachybotrys demonstrate that this group of mycotoxins is capable of producing immunosuppression and inflammatory insults to gastrointestinal and pulmonary systems. Case control study and case reports have suggested a possible association with environmental exposure to Stachybotrys mycotoxins, although a firm causal relationship has not been firmly established. Additional studies are needed to document that humans with sufficient exposure to these mycotoxins develop compatible clinical and pathologic pictures as demonstrated in animal models.

Animals↗

PubMed1965

DETECTION OF UROCANASE IN THE BLOOD OF CHICKENS CHRONICALLY POISONED WITH TOXIC GROUNDNUT MEAL.

Chickens were fed for up to six weeks a ration containing 30 per cent of toxic groundnut meal and their controls were fed balanced commercial ration for comparable periods. Urocanase activity was determined in the blood and livers of principal and control birds killed after two, four or six weeks on these diets. Urocanase activity was detected in the blood sera of 3 out of the 9 intoxicated birds examined as early as two weeks after the initiation of the feeding trial. By the sixth week, the incidence of urocanase in the serum increased to 5 of 8 intoxicated birds. Liver urocanase concentration was uniform throughout the duration of the experiment when measured in units per gram of hepatic tissue. However, when its activity was expressed on the basis of units per total liver weight, its total activity increased toward the end of the experiment.

Aflatoxins↗

PubMed1996

Toxicological biotest on Diptera larvae to detect ciguatoxins and various other toxic substances.

A toxicological test was developed using a new animal sensitive to various toxins, especially ciguatoxin (CTX), which poisons humans who eat tropical fishes. The larvae of Parasarcophaga argyrostoma (Diptera, Sarcophagidae) were selected for their marked ability to consume spontaneously large quantities of various proteins; meat, fish flesh or liver, mussels, etc. Larvae grown on meat overnight can easily be observed without requiring optical instruments. Ten larvae were placed on 5 g of the sample to be tested, and left for 3-24 hr. Samples containing > 1 ng of CTX/g of flesh (moray.eel CTX) killed the larvae in about 3 hr; samples with lower concentrations inhibited larval growth, which can be noted with the marked eye. These readings were rendered objective by weighing the larvae before and after their being placed on the test sample and comparing the result to that of the control. The reading with the naked eye seems to be satisfactory up to 0.2 ng of CTX/g, while that by weighing was acceptable up to 0.10-0.15 ng/g. The coefficient of variation in the sensitive zone (approximately 50% of normal growth) was about 25% for a series of 11 experiments. P. argyrostoma larvae are sensitive to various other toxic substances, such as tetrodotoxin, okadaic acid, aflatoxin B1 and amanitin. The test is extremely simple in its theory and practice. It does not require complex materials or equipment and it is very inexpensive. It could be used to detect ciguatera toxins in the monitoring of fishing areas and for the commercialization of big-sized fish.

Animals↗

PubMed2004

[Safety of rice grains and mycotoxins - a historical review of yellow rice mycotoxicoses].

Aflatoxins, the most powerful mycotoxins, were brought to the attention fo the people in the early 1960s with the outbreak of the turkey "X" disease in England. However, the history of mycotoxin research in Japan began 100 years ago. In 1891, Sakaki demonstrated that moldy, unpolished rice was fatal to experimental animals, with symptoms indicating paralysis of the central nervous system (Shoshin-kakke). In 1920, Prof. I. Miyake and Dr. Takada first reported that Penicillium commune, which was known as a causal agent of "Mossy diseased rice" was found to be toxic to experimental animals by feeding the moldy rice to rabbits and rats.With such a historical background, taking the idea of "rice, fungus and toxin" as a working hypothesis, Miyake and his co-workers discovered the first sample of yellow rice grains from Taiwanese and domestic rice, from which was isolated a species of Penicillium and later identified it with P. citreonigrum (=P. toxicarium). The fungus produced a highly toxic metabolite, citreoviridin. Unfortunately because this study was published during wartime, it failed to alert the world to the potential or actual dangers of the toxicity of common molds. After World War II, Japanese people suffered for some years from a shortage in domestic rice production and depended on foreign countries to supply rice, which led to the toxicological screening on fungal isolates from polluted rice grains by Dr. Tsunoda and his co-workers. AMong the isolates from imported rice, there were two species of Penicillium which were particularly associated with high toxicity; P. islandicum responsible for brownish discolored rice, and P. citrinum responsible for yellowish rice. P. islandicum produces two hepatotoxic metabolites: luteoskyrin and cyclochlorotine, while a nephrotoxic of P. citrinum is citrinin. These toxicological characters, including the induction of cancer and chemical structures, were studied by Profs. uraguchi, Saito, Shibata, Tatsuno and their co-workers. In this way, toxic disturbances associated with the consumption of rice contaminated with these Peniciliium species occurred and became known under the collective name of the "Yellow rice syndrome". Although no human cases of poisoning were recorded, scientists in the field of mycotoxin research recommended to the Japanese Government that administrative action should be taken to protect the people against any possible hazards from "yellow rice". Consequently, mycological inspections of imported rice were started by the government. The safety control system for domestic rice during post-harvest handling and long-term storage has been progressively established after learning of these problems.

Animals↗