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At least 343 records · Page 19Linked to original sources
PubMed1984

Somatic mutation and recombination test in Drosophila melanogaster.

A novel test system for the detection of mutagenic and recombinogenic activity of chemicals is described in detail. Drosophila melanogaster larvae trans-heterozygous for the mutations multiple wing hairs (mwh) and flare (flr) are exposed to the test compounds for various periods of time ranging from 96 hr to 1 hr. Induced mutations are detected as single mosaic spots on the wing blade of surviving adults that show either the multiple wing hairs or flare phenotype. Induced recombination leads to mwh and flr twin spots and also to a certain extent, to mwh single spots. Recording of the frequency and the size of the different spots allows for a quantitative determination of the mutagenic and recombinogenic effects. This and earlier studies with a small set of well-known mutagens indicate that the test detects monofunctional and polyfunctional alkylating agents (ethyl methanesulfonate, diepoxybutane, mitomycin C, Trenimon), mutagens forming large adducts (aflatoxin B1), DNA breaking agents (bleomycin), intercalating agents (5-aminoacridine, ICR-170), spindle poisons (vinblastine), and antimetabolites (methotrexate). In addition, the test detects mutagens unstable in aqueous solution (beta-propiolactone), gaseous mutagens (1,2-dibromoethane), as well as promutagens needing various pathways of metabolic activation (aflatoxin B1, diethylnitrosamine, dimethylnitrosamine, mitomycin C, and procarbazine). The rapidity and ease of performance as well as the low costs of the test necessitate a high priority for validation of this promising Drosophila short-term test.

Animals↗
PubMedDate not supplied

Effect of dietary exposure to aflatoxin B1 on resistance of young chickens to organophosphate pesticide challenge.

White leghorn chickens were placed on a diet containing 0, 1000, or 3000 ppb aflatoxin B1 for 7 weeks. At the end of that time, the birds were challenged orally with the organophosphate pesticide malathion. A malathion dose of 215 mg/kg resulted in significant clinical signs of cholinergic poisoning in 4/10, 5/10, and 8/10 birds fed 0, 1000, and 3000 ppb aflatoxin B1, respectively, and the chickens required antidotal atropine 40 min later. Activity of brain cholinesterase was significantly lower than control levels in all birds given this dose of malathion, with activities being 28% +/- 6, 21% +/- 2, and 15% +/- 2 of control values (Mean +/- standard error, N = 5) if fed 0, 1000, and 3000 ppb aflatoxin B1, respectively. Plasma cholinesterase values paralleled those of brain, with significantly more inhibition in samples from birds given 1000 and 3000 ppb aflatoxins with malathion. Brain and plasma cholinesterase activities in birds fed aflatoxins and given a dose of malathion below the threshold for cholinergic signs (125 mg/kg) were also lower than activities in birds given malathion alone. Although aflatoxin alone had no direct effect on the activities of these enzymes, it appears that this mycotoxin may contribute to the esterase inhibition that is a manifestation of the acute toxic effects of malathion in chickens.

Aflatoxin B1↗
PubMed1975

Spontaneous and experimental aflatoxicosis in goats.

Naturally occurring aflatoxicosis is described in goats fed a concentrate mixture containing polkudu meal (defatted residue from grated coconut after juice extraction). Toxigenic strains of Aspergillus flavus were present in the concentrate and aflatoxins were recovered from the liver and urine of affected animals. Hepatic lesions in poisoned goats consisted of bile duct hyperplasia and periportal fibrosis; renal lesions included necrosis of tubular epithelial cells and proteinaceous exudation in the glomerular space. Similar lesions were produced experimentally in goats with aflatoxin and the coconut cultures of A flavus. High doses of aflatoxin B1 produced, in addition, hepatic centrilobular congestion, haemorrhage and periportal fatty change.

Aflatoxins↗
PubMed1967

The action of aflatoxin B1 on the rat liver.

The administration of a single dose of aflatoxin B(1) to the rat (7mg./kg. body wt.) results in the slow development of a periportal necrosis. Hepatic enzymes are released into the serum in the second 24hr. of the poisoning, closely preceding the onset of the necrosis, which is followed by a rise in serum alkaline-phosphatase activity and bilirubin concentration. Aflatoxin B(1) has been detected in the nucleus of the poisoned liver cell and in vitro it has been shown to interact with DNA. The toxin inhibits the production of nuclear RNA, probably by preventing the transcription of DNA by the RNA polymerase. It is proposed that the interaction of the toxin with DNA gives rise to its inhibitory action on mitosis and its necrogenic action.

Aflatoxins↗
PubMed1993

Does aflatoxin exposure in the United Kingdom constitute a cancer risk?

Although the aflatoxins were discovered more than 30 years ago, there is still considerable controversy surrounding their human health effects. Most countries have introduced legislation to control the level of aflatoxins in food, but it is not known if these permitted levels still pose a significant cancer risk. Furthermore, it is unlikely that all the sources of human aflatoxin exposure have been discovered, nor if the liver is the only, or indeed, major target organ for aflatoxin-induced cancer in man. In our laboratory we have used both immunological and HPLC methods to examine human DNA from a variety of tissues and organs to identify and quantify aflatoxin DNA-adducts. We have already detected aflatoxin B1 (AFB1)-DNA adducts in formalin-fixed tissue from an acute poisoning incident in Southeast Asia. Here we have examined human colon and rectum DNA from normal and tumorous tissue obtained from cancer patients and colon, liver, pancreas, breast, and cervix DNA from autopsy specimens. AFB1-DNA adducts were detected in all tissue types examined and ranged from 0-60 adducts/10(6) nucleotides. Where sample size allowed, the adduct levels were confirmed by HPLC analysis. Tumor tissues tended to have higher adduct levels than normal tissue from the same individual, and levels generally increased with patient age. In samples analyzed by HPLC, the adducts present had the chromatographic properties of [8,9-dihydro-8-(N5-formyl)-2',5',6'-triamino-4'-oxo-(N5-pyramidyl) -9- hydroxy-aflatoxin B1, the ring-opened form of the AFB1-guanine adduct.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxin B1↗
PubMed1975

Influence of carbon tetrachloride or riboflavin on liver carcinogenesis with a single dose of aflatoxin b1.

Liver carcinogenesis with a single dose of aflatoxin B1 (7 mg/kg body weight) has been investigated in a group of female Wistar strain rats by repeated biopsies and necropsies. Another group received a subsequent intoxication with carbon tetrachloride by inhalation (approximately 200 doses) and another one was overloaded with riboflavin (25 parts/10(6) in drinking water). The frequency of hepatomata was almost equal in the aflatoxin and aflatoxin-carbon tetrachloride group. It was lowere in the riboflavin-aflatoxin group. In these 3 groups cirrhosis was never present in neoplastic livers. Megalocytosis was the first lesion observed. All tumoral livers had previous or concomitant megalocytosis. This modification was about as frequent, intense and widespread in aflatoxin-CCl4 and aflatoxin groups but appeared much earlier, as did the first hepatoma, in the aflatoxin-CCl4 group. It was less frequent, less intense and less widespread in the riboflavin-aflatoxin group than in the aflatoxin group. There was also a lower frequency of hepatomata in the riboflavin-aflatoxin group, but the difference was not significant due to the too small number of animals involved. The facts are not a proof of the existence of an obligatory link between megalocytosis and carcinogenesis since a slight megalocytosis was observed in the riboflavin group not affected by the neoplastic process. However, the simplest explanation of our results would be to consider that the potential tumour cells are located among the megalocytic cells, without admitting that every megalocyte is obligatorily a precancerous cell. CCl4 seems to act in shortening the time of appearance of megalocytosis. The protective effect of riboflavine should be regarded with more caution.

Aflatoxins↗
PubMed1968

A study of free amino acids in rice moth larvae during mycotoxicosis.

Free amino acid pattern has been studied in rice moth larvae during aflatoxicosis and compared with normal in ground nut meal and wheat bran. It was observed that there is an increase in free amino acids in intoxicated larvae and this was directly proportional to the degree of toxicity as indicated by decrease in growth of these larvae. The study of excretary pattern of amino acids shows that intoxicated larvae excrete less amino acids than the normal larvae. The results have been discussed.

Aflatoxins↗
PubMed1984

Increased nucleoside triphosphatase activity of rat liver nuclear envelope is associated with hepatocarcinogen exposure.

Altered transport of nuclear RNA sequences is an early response to carcinogens. Nuclear envelopes (NE) were isolated and assayed for nucleoside triphosphatase activity (NTPase), on the premise that this enzymatic activity participates in RNA transport. A common feature of the action of five different carcinogens (thioacetamide, 2-acetylaminofluorene, 3'-methyl-4-dimethylaminoazobenzene, dimethylnitrosamine, and aflatoxin B1), at low doses without significant toxicity, was to increase NE NTPase activity and to increase RNA transport, as assessed by the appearance of rapidly labeled RNA in the cytoplasm and by in vitro assay. The increases in NTPase were specific for the NE fraction, and early toxic effects of higher doses initially masked the increases. The induced increases in NE NTPase were long-lived. In contrast, increases in NE NTPase were observed only during the regenerative phase of CCl4 intoxication; the CCl4-induced increase was short-lived and returned promptly to control levels. These changes in NTPase activity were not associated with parallel changes in phosphorylation/dephosphorylation of NE proteins. Increases in NE NTPase and alterations in RNA transport, without attendant nuclear replication, may relate to altered nuclear RNA restriction. This change in a regulatory phenomenon may make these cells more susceptible to further modification, potentially playing a role in the initiation phase of carcinogenesis.

2-Acetylaminofluorene↗
PubMed1965

FEEDING OF FERRETS WITH THE RAW MEAT AND LIVER OF CHICKENS CHRONICALLY POISONED WITH TOXIC GROUNDNUT MEAL.

Chickens were fed a ration containing 30 per cent of toxic groundnut meal for up to six weeks. The concentration of aflatoxin (toxic metabolites of Aspergillus flavus) in the above ration was 3.06 p.p.m. At the end of 2nd, 4th or 6th week the birds were killed. The meat was removed from the bones and put through a meat grinder. The livers of three groups were pooled together. Three control groups of birds kept on commercial pellets were treated similarly. Female ferrets, two years of age, were used in the present study. They were divided into four groups. The first three groups were given for one month meat from chickens fed the toxic ration for 2, 4, and 6 weeks, respectively. Each of these three groups contained one control ferret that was fed with the meat of chickens fed a commercial ration for a similar period of time. One half of the 4th group was fed pooled liver from intoxicated birds and one half was fed liver from control birds. No significant changes in the ferret tissues were observed as a consequence of feeding them with the meat or liver from the chickens chronically poisoned with toxic groundnut meal.

Aflatoxins↗
PubMedDate not supplied

Comparative cytotoxicity of aflatoxin B1 and saxitoxin in cell cultures.

Human and animal cell cultures were evaluated for their susceptibility to two environmental toxins found as contaminants in human food supplies: aflatoxin B1, a hepatotoxin produced by the mold Aspergillus flavus, and saxitoxin, a paralytic neurotoxin produced by the marine dinoflagellate Gonyaulax catenella. Both toxins cause food poisoning in humans and other animals. The acute cytotoxicity of both toxins was measured and compared by inhibition of cell growth and by progressive cytopathogenicity resulting in cell destruction. Aflatoxin B1 was cytotoxic to all of the 11 primary kidney cultures derived from susceptible animals. The cell growth inhibition 10% values (TD10) ranged from 0.02 to 6.0 micrograms/ml: mouse (TD10 = 0.02 micrograms), guinea pig (0.03 micrograms), rat (0.07 micrograms), hamster (0.16 micrograms), monkey (0.1 microgram), human (0.7-1.5 micrograms), chick (0.05 micrograms), and duck (6.0 micrograms). The corresponding TD50 levels were about 10 times higher concentrations and caused cell destruction within 2 d. Saxitoxin did not induce cytotoxicity manifestations in cultures derived from susceptible species--mouse kidney, human carcinoma HeLa line, chick embryo, and goldfish fin (CAR) cell line--at high concentration levels up to 5 micrograms/ml. When the same toxin preparation at only 1 microgram was injected into mice, the animals died immediately. The results indicate that animal cell cultures are useful for studies of general cytotoxins that affect common essential metabolism but cannot be used to detect environmental toxins that cause toxic manifestations by an interference with specific physiological functions of organ systems.

Aflatoxin B1↗