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At least 19 recordsLinked to original sources
PubMed1992

Content of the neurotoxins cycasin (methylazoxymethanol beta-D-glucoside) and BMAA (beta-N-methylamino-L-alanine) in cycad flour prepared by Guam Chamorros.

Exposure to cycad seed kernel is an etiologic factor for the western Pacific amyotrophic lateral sclerosis (ALS) and parkinsonism-dementia complex (PDC). Traditionally processed cycad flours (n = 17) obtained from Chamorro residents of Guam and the adjacent island of Rota at risk for neurodegenerative disease were extracted and analyzed by high-performance liquid chromatography for content of beta-N-methylamino-L-alanine (BMAA) and methyl-azoxymethanol beta-D-glucoside (cycasin). Cycasin (detection limit: picomole) was present in concentrations of 0.004 to 75.93 micrograms/g (mean, 12.45 +/- 5.0 micrograms/g), and levels of BMAA (detection limit: subpicomole) ranged from 0.00 to 18.39 micrograms/g (mean, 5.44 +/- 1.56 micrograms/g). On average, cycasin content was approximately 10 times higher than that of BMAA. The largest concentrations of cycasin were found in samples from villages with a high reported prevalence of ALS/PDC. Ingestion of cycad-derived food would result in estimated human exposure to milligram amounts of cycasin per day. The cytotoxic properties of cycasin merit consideration in relation to the etiology of western Pacific ALS/PDC.

Amino Acids, Diamino↗
PubMed1979

Mutagenicity of the naturally occurring carcinogen cycasin and synthetic methylazoxymethanol conjugates in Salmonella typhimurium.

The aglycone methylazoxymethanol of the naturally occurring carcinogenic glucoside, cycasin, has previously been shown to be mutagenic, but cycasin per se has not. In this work, cycasin was demonstrated to be mutagenic using a modification of the Ames Salmonella test in which it was preincubated with beta-glucosidase and the tester strain in liquid medium. The mutagenicity of cycasin to six histine-depedent Salmonella strains varied considerably with strain HisG46 being the most susceptible. Methylazoxymethyl-beta-D-glucosiduronic acid, which also is nonmutagenic per se, similarly became mutagenic when preincubated with beta-glucuronidase. Methylazoxymethyl acetate, which is slightly mutagenic by the Ames standard pour plate method, became highly mutagenic on preincubation. The mutagenicity of free methylazoxymethanol was confirmed, and a linear dose-response relationship was observed. The common conditions required for activation of nonmutagenic methylazoxymethanol conjugates, the glucoside cycasin and methylazoxymethyl-beta-D-glucosiduronic acid, are 90-min preincubation at 30 degrees, pH 6.5, with an appropriate hydrolase and Salmonella typhimurium HisG46.

Azo Compounds↗
PubMed1979

DNA fragmentation in some organs of rats and mice treated with cycasin.

Cycasin (methylazoxymethanol-beta-D-glucoside) is carcinogenic in several animal species. It produces a variety of malignant tumours, mainly in the liver of mice, and in the liver, kidney and large intestine in rats. It does not appear to be mutagenic in the Ames test, even in the presence of liver microsome fraction, and it is among those carcinogens (less than 10%) ranked as "false negatives" in this test. The ability of cycasin to damage in vivo liver, kidney, lung and colonic DNA of Wistar rats and C57BL/L mice was investigated by means of alkaline elution technique. Oral single-dose administration of cycasin, in the range of 50-400 mg/kg body weight, produced in the rat a clearly evident dose-dependent DNA fragmentation in the liver, and less marked damage to DNA from kidney and colon mucosa. In mice, the same treatment produced dose-dependent DNA damage only in the liver. DNA repair up to 18 h appeared to be incomplete both in mice and rats. Methylazoxymethanol acetate is considered to be an active form of cycasin. While in vivo methylazoxymethanol acetate caused DNA damage, in vitro it appeared inactive and required metabolic activation, possibly consisting in its hydrolysis by esterase activity, to be able to cause DNA fragmentation.

Animals↗
PubMed1975

Intestinal tumors of rats by gastric or intestinal administration of cycad extract and cycasin.

Sprague-Dawley rats were given gastric intubation of cycad extract (group 1), rectal infusion of cycasin (group 2), or rectal indusion of cycad extract after external colostomy at 1/3 proximal portion of the large intestine (group 3). In group 1, intestinal tumors developed in any portion of the intestinal tract ranging from the duodenum to the rectum. In group 2, tumors developed in mucosa of the large intestine. In group 3, however, tumors arose from both sites of intestinal mucosa which were in contact and not in contact directly with the cycad extract infused. Possible hypothesis for intestinal tumor development by cycad extract and cycasin was presented.

Adenocarcinoma↗
PubMed1976

Cycasin.

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Animals↗
PubMed1979

Synthesis of the glucuronic acid conjugate of methylazoxymethanol.

The glucuronic acid conjugate of methylazoxymethanol was synthesized by oxidizing the primary alcohol of the glucose moiety of cycasin (methylazoxymethanol-beta-D-glycopyranoside) to a carboxylic acid. The oxidation was carried out by bubbling oxygen gas through a cycasin solution in the presence of a platinum-on-carbon catalyst. A band at 1715 cm-1, not present in the cycasin infrared spectrum, appeared in the spectrum of the oxidized cycasin product, establishing the presence of a carboxylic acid group. The oxidation product is methylazoxymethanol-beta-D-glucosiduronic acid because, when hydrolyzed with Escherichia coli beta-glucuronidase, it produced methylazoxymethanol and glucuronic acid and also indicated retention of the beta-linkage of cycasin. Varying quantities of the synthesized methylazoxymethanol-glucosiduronic acid, injected into Wistar rats of both sexes and of varying weights, were not acutely toxic. The compound was mutagenic to Salmonella typhimurium when preincubated with E. coli beta-glucuronidase, but not when preincubated with bovine liver glucuronidase.

Animals↗
PubMed1978

[Histology, fine structure and differentiation of experimental Wilms tumors (author's transl)].

Histologic studies indicate that the cycasin-induced Wilms' tumor in the rat is equal to human nephroblastoma in appearance. Therefore, it may represent an interesting system for experimental oncology. In electron microscopy, the spindle cells of the sarcoma region mostly represent tubular cells. Besides, the author's results showed that preexisting mesenchyma cells and blood vessels also form part of the tumor. Electron microscopy studies have shown that cycasin feeding will lead to early cellular changes indicating that cycasin exercises a nucleotoxic effect. Present results do not favor the dysontogenic concept of the formation of Wilms' tumor, since this tumor can be induced diaplacentally.

Animals↗
PubMed1978

A practical procedure for testing DNA damage in vivo, proposed for a pre-screening of chemical carcinogens.

The alkaline elution method was adapted to the evaluation of DNA damage induced in vivo through a practical and reliable microfluorometric procedure, without any need for tissue pre-labeling. The DNA damage induced in vivo by treatment with a single dose of N-nitrosodimethylamine (DMNA), N-methyl-N-nitroso-urea (MNU), 1,2-dimethylhydrazine (DMH) or cycasin has been detected in different organs of mice or rats. The results obtained are rather consistent with the organotropism of these carcinogens, and show a satisfactory dose dependent of DNA damage. DMH and cycasin, both negative in the Ames' Salmonella/microsome mutagenicity test, are clearly positive with in vivo DNA damage/alkaline elution assay. This latter method, complemented with other short-term tests, may play a useful role in the pre-screening of chemical carcinogens.

Animals↗
PubMed1976

PHA response and methylazoxymethanol acetate.

Several reports have indicated the mutagenicity of the cycasin aglycone, methyl azoxymethanol (MAM). Van Den Berg and Ball (1972) have demonstrated the inhibitory effects of MAM acetate (MAMac), a more stable form of the aglycone, on DNA synthesis and cell proliferation in HeLa cells. The purpose of this study was to observe the effects of MAMac on blastogenesis in the human short-term leucocyte culture system. A depression in blastogenesis by MAMac was observed cytologically derived from two individuals. The same effect was observed utilizing [3H] thymidine as an indicator of blastogenesis in a series of cultures from 11 male individuals exposed to varying doses of MAMac, ranging from 5 through 800 mug/ml.

Azo Compounds↗
PubMedDate not supplied

Toxins and carcinogens in the environment: an observation in the tropics.

The incidence of primary liver cancer in the countries of tropical Africa is the highest in the world. There is a growing belief that the relatively high prevalence of hepatocellular carcinoma in Nigeria may have a multiple chemical factor etiology in such forms as food contaminants, herbal teas, and environmental chemicals. Major chemical toxins and carcinogens that have been identified so far in the tropical environment include sapotoxin, cycasin, mushroom toxin, capsaicin, oxalic acid, prussic acid, fluorooleic acid, N-nitroso compounds, aflatoxin, palmotoxin, pyrrolizidine alkaloids, quinine, DDT, and cyclamate.

Carcinogens, Environmental↗
PubMed1976

Leiomyomas and leiomyosarcomas of the kidney in 4-day-old BUF rats given methylazoxymethanol acetate intraperitoneally.

The effect of age and sex on the development of renal tumors was studied in inbred BUF male and female rats 4 days, 5, 8, 12, 24, or 52 weeks old. Methylazoxymethanol (MAM) acetate was injected ip (20 mg/kg body wt) once weekly for 9 weeks. Animals 52 weeks old died from hepatic and/or renal necrosis; however, animals of other ages survived 24-42 weeks. Female rats 4 days old were susceptible to the development of leiomyomas and leiomyosarcomas of the kidney, whereas 4-day-old male rats had a few leiomyomas. Adenomas and carcinomas of the kidney and nephroblastomas were not observed. It was concluded that the aglycone of cycasin, MAM, is important in the induction of leiomyosarcomas of the kidneys in 4-day-old rats.

Age Factors↗
PubMed1976

Pathogenesis of methylazoxymethanol-induced lesions in the postnatal mouse cerebellum.

Previous studies have shown that methylazoxymethanol acetate (MAM) and methylazoxymethanol glucoside (cycasin) cause destruction of differentiation cells in the postnatal mouse cerebellum. The major features of the resulting architectural disarray were Purkinje cell misalignment and granule cell deletion along with cerebellar dysfunction. Although it was clear from a number of studies that destruction of differentiation cells in the immediate postnatal period was the primary lesion, several important facets of the pathellular response to the injury was incompletely described. The relationship of the cellular response to the subsequent pathological alterations was not completely evaluated. Also, the presence of unattached Purkinje cell dendritic spine postsynpatic sites suggested that their development had occurred without presynaptic parallel fiber terminal differentiation. The possibility of early synaptogenesis and degeneration was not, however, completely ruled out.

Animals↗
PubMed1976

Naturally occuring mutagens.

Naturally occurring mutagens have usually been discovered as a result of outbreaks of disease in agricultural livestock, or as a result of epidemiological studies of cancer of the liver in man. Subsequent work has then shown that the toxic agents responsible often have mutagenic properties. Examples are the pyrrolizidine alkaloids, cyasin, a range of mycotoxins produced by various fungi, and at least two unidentified toxic agents in bracken. Commonly the toxic agent itself does not show high biological activity, but after ingestion it is converted by metabolic processes into the active mutagen or carcinogen. Some of these toxic substances have been responsible for considerable losses of agricultural livestock and therefore are of economic significance. From the view-point of genetic hazards to man, the most significant compounds are probably the mycotoxins, e.g. aflatoxin, because of the common risk of fungal contamination of food, especially in tropical regions. No information is yet available on the effects of these mutagens on natural populations of animals. Plants containing the pyrrolizidine alkaloids are found in areas of Africa and the Middle East where plagues of the migratory locust occur. Although it is known that some of the alkaloids can induce chromosomal damage in grasshoppers, whether such damage ever becomes a significant factor under ecological conditions is not known. In some cases, insects have not only evolved resistance towards mutagenic alkaloids but have become dependent on them for certain purposes. The males of certain Danaid butterflies feed on plants containing pyrrolizidine alkaloids. After ingestion, the alkaloids are metabolised to dihydropyrrolizine derivatives, which are then secreted on special organs (hair pencils) and, following dissemination into the atmosphere, act as pheromones for the stimulation of mating behaviour.

Aflatoxins↗