Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Aflatoxin Poisoning”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1988

3H-amino acid incorporation into proteins during chronic aflatoxin induced coagulation defects in rabbits.

Eighteen New Zealand White rabbits were divided equally into three groups and administered either 0.2 ml dimethyl sulfoxide (DMSO)/day, 0.06 mg/kg/day Aflatoxin B1 (AFB1) in DMSO, or 0.09 mg/kg/day AFB1 in DMSO. Incorporation of 3H-amino acids into total serum protein, fibrinogen and platelet proteins was determined during the intoxication and developing coagulation defect. Ten of 18 rabbits administered AFB1 in DMSO died or developed prolonged coagulation times. There was no significant difference in specific incorporation of 3H-amino acids into total serum protein, fibrinogen or platelet proteins between groups, nor was there a difference in incorporation between rabbits with normal coagulation times and those with prolonged coagulation times. Correlation between plasma fibrinogen concentration and specific incorporation of 3H-amino acid into fibrinogen was not significant. In vivo inhibition of 3H-amino acid incorporation into plasma proteins or platelets could not be demonstrated.

Aflatoxin B1↗
PubMed1984

Aflatoxin exposures in the industrial setting: an epidemiological study of mortality.

Mortality occurring between 1963 and 1980 in a small cohort (N = 71) of Dutch oil-press workers exposed between 1961 and 1969 to aflatoxins primarily via the respiratory route, was assessed and compared to that of a similar group of unexposed workers (N = 67). For the entire period of study, the observed mortalities for total-cancer and respiratory cancer were higher than expected in the aflatoxin-exposed group. Mortality observed in the comparison group was within the expected range. While two deaths in the exposed group were attributed to non-malignant liver disease, no primary liver tumours were observed. The greatest difference between observed and expected mortality was in the period between 1963 and 1968.

Adult↗
PubMed1984

Risk estimates of liver cancer due to aflatoxin exposure from peanuts and peanut products.

An assessment was undertaken of the risk of liver cancer in the USA associated with aflatoxin ingestion from peanuts. Both laboratory-animal data and epidemiological data collected from the scientific literature and several prominent mathematical extrapolation techniques were used. Risk estimates differed by a factor of greater than 1000 when the extrapolated results of three selected animal studies were analysed. Dose-response data for the male Fischer rat, the most sensitive mammalian species studied, produced an estimate of 158 cases of liver cancer per year in the USA at current levels of aflatoxin exposure. An estimate of 58 annual cases was predicted on the basis of epidemiological data of populations in Africa and Thailand.

Africa↗
PubMed1984

Cost-effectiveness of lowering the aflatoxin tolerance level.

The cost-effectiveness of adopting aflatoxin tolerance levels of 15, 10 and 5 ppb for peanuts and peanut products was assessed. Estimates of the annual cost to manufacturers of monitoring and controlling peanut aflatoxin levels at the current 20-ppb action level, and estimates of the projected increase in costs of establishing lower tolerances were elicited from producers by questionnaire. Exposures to peanut products were derived from the HANES I survey and from peanut production statistics. The risk of liver cancer at each tolerance level was estimated using both epidemiological and extrapolated experimental data assuming that exposure would be reduced in direct proportion to the decrease in the tolerance. It was found that the 15-ppb tolerance would cost $60,000 per cancer death averted (range $20,000-$1,700,000) and is therefore relatively cost-effective. The marginal costs per life saved for both the 10-ppb and 5-ppb levels were found to be $1.7 million (range $0.6 million-$11.4 million) and $1.6 million (range +0.6 million-$31.1 million), respectively. Conclusions on the optimal regulatory approach should be guided by comparisons of these figures with corresponding cost-effectiveness ratios for alternative regulatory uses of national resources in the interests of public health.

Arachis↗
PubMed1975

Comparative histopathological effects of aflatoxin B1 and palmotoxins B0 and G0 on some organs of different strains of the newly hatched chick (Gallus domesticus).

Aflatoxin B1 and palmotoxin B0 are equitoxic to the developing chick-embryo (Gallus domesticus) whilst palmotoxin G0 is relatively non-toxic. Toxic lesions are present in the heart, liver, skeletal muscle, brain and cartilage in varying severities. The liver and skeletal muscle show fatty change and toxic myositis, respectively. Lesions in the heart, brain and cartilage are relatively mild. The endocardial cushion-like plaques at the base of the atrioventricular valves are lesions peculiar to aflatoxin B1 and palmotoxin B0-induced cardiac damage. It appears that these mycotoxins are not selectively tissue specific in inducing organ damage in the chick-embryo. An ultrastructural study of these lesions in the chick and other species may help to elucidate the molecular mechanism of the toxicity of these mycotoxins which are suspected to be very potent human hepatocarcinogens in certain parts of the tropics. Their acute phase effects in man are, however, unknown.

Animals↗
PubMed1984

Comparative incidence of oral ochratoxicosis and aflatoxicosis on the activity of drug-metabolizing enzymes in rat liver.

Mycotoxicosis has been produced in the rat by daily oral administrations of ochratoxin A (1.5 mg/kg/day) or aflatoxin B1 (1 mg/kg/day). Hepatic microsomal cytochrome P-450 and b5 contents and many phase I and II biotransformation systems have been measured in the course of ochratoxicosis (4 to 15 dosings) and aflatoxicosis (1 to 8 dosings). In case of ochratoxicosis, decreases in cytochrome P-450 level, aminopyrine demethylase and aniline hydroxylase activities were observed in rats receiving 15 administrations of the toxin. Aflatoxicosis induced more severe decreases in cytochrome P-450, aminopyrine demethylase and ethoxycoumarin deethylase following 8 daily gavages. In the two studies, there was no significant change in activities of liver phase II biotransformation enzymes.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1984

Distal nephron function of the rat during acute aflatoxicosis.

The effect of an acute intoxication with aflatoxin B1 (AFB1) on some parameters of distal nephron function was examined in rats 48 h after a single i.p. dose of 100 micrograms/kg body wt. The parameters tested were the capacity for the excretion of fixed acids and ammonium salts during metabolic acidosis and the concentration and dilution of urine applying conventional clearance techniques. The treated rats showed a glomerular filtration rate (GFR) approx. 50% lower than the controls, but they were able to reduce the urinary pH as were nonintoxicated animals. The ammonium excretion rate per ml of GFR was unimpaired in the treated rats, but the rate of excretion of fixed acids per ml of GFR was increased. The maximal urinary osmolality was significantly diminished in the intoxicated rats as was water reabsorption, when compared with data obtained in the controls. No differences between groups were seen in the free water formation although urinary excretion of electrolytes was significantly increased. The studies support the nephrotoxicity of AFB1 in the rat probably by interfering with transport function in the collecting tubule cells together with a diffuse impairment of proximal tubule function, as observed previously.

Absorption↗
PubMed1984

The role of dietary aflatoxin in the genesis of hepatocellular cancer in developing countries.

Impaired activity of the liver microsomal mixed-function-oxidase (MFO) system is characteristic of protein malnutrition. It explains the accumulation of aflatoxin (AFB1) in livers of kwashiorkor victims, whose staple foods are usually heavily contaminated with this fungal toxin. Dietary rehabilitation of such children with high-protein foods not only increases the activity of the liver MFO system but also stimulates DNA replication and rapid regeneration of liver cells. Under such circumstances highly reactive metabolites of AFB1, such as the AFB1-epoxide, can produce malignant transformation of the cells by binding covalently with genetic macromolecules. Alternating cycles of food shortage and sufficiency, which usually characterise impoverished communities, and liver-cell hyperplasia stimulated by the non-genetic cytotoxic effects of AFB1 or parasitic infestation promote rapid replication of the transformed cells.

Aflatoxin B1↗
PubMed1990

Molds, mycotoxins, and mycotoxicosis.

Interest in mycotoxins and mycotoxicosis in humans and animals has greatly increased in recent years. Horses have long been considered very susceptible to molds. The signs, treatment, and prevention of several conditions, such as leukoencephalomalacia, aflatoxicosis, ergotism, fescue toxicity, slobbering disease, ryegrass staggers, and moldy sweet clover disease, are discussed.

Animals↗
PubMed1985

Hepatocellular carcinoma and dietary aflatoxin in Mozambique and Transkei.

Estimations of the incidence of hepatocellular carcinoma (HCC) for the period 1968-74 in the Province of Inhambane, Mozambique, have been calculated and together with rates observed in South Africa among mineworkers from the same Province indicate very high levels of incidence in certain districts of Inhambane. Exceptionally high incidence levels in adolescents and young adults are not sustained at older ages and suggest the existence of a subgroup of highly susceptible individuals. A sharp decline in incidence occurred during the period of study. Concurrently with the studies of incidence, 2183 samples of prepared food were randomly collected from 6 districts of Inhambane as well as from Manhica-Magude, a region of lower HCC incidence to the south. A further 623 samples were taken during 1976-77 in Transkei, much further south, where an even lower incidence had been recorded. The mean aflatoxin dietary intake values for the regions studied were significantly related to HCC rates. Furthermore, data on aflatoxin B1 contamination of prepared food from 5 different countries showed overall a highly significant relationship with crude HCC rates. In view of the evidence that chronic hepatitis B virus (HBV) infection may be a prerequisite for the development of virtually all cases of HCC and given the merely moderate prevalence of carrier status that has been observed in some high incidence regions, it is likely that an interaction between HBV and aflatoxin is responsible for the exceptionally high rates evident in parts of Africa and Asia. Various indications from Mozambique suggest that aflatoxin may have a late stage effect on the development of HCC. This points to avenues for intervention that could be more rapidly implemented than with vaccination alone.

Adolescent↗