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Biomedical subjects

A W Hayes

Publications and source records attributed to A W Hayes.

At least 73 records · Page 4Linked to original sources
PubMed1980

High-performance liquid chromatographic analysis of the mycotoxin citrinin and its application to biological fluids.

Citrinin is a toxic metabolite produced by several species of Penicillium and Aspergillus. Citrinin is nephrotoxic and has been implicated in disease outbreaks in animals and humans. Citrinin was resolved in a sharp peak by reversed-phase high-performance liquid chromatography on a small-article (10 micrometers) column by elution in 4.25 min with a phosphoric acid (0.25 N)-acetonitrile-2-propanol solvent (55:35:10). Detection was by ultraviolet absorbance at 340 nm. The relationship between peak height and area and quantity injected was linear over a range of 2--50 ng at 340 nm and 5--200 ng at 365 nm. Retention time and peak area were highly reproducible. As little as 2--5 ng citrinin was detectable. Complete recovery of citrinin from plasma samples containing known quantities of [14C]citrinin was obtained over a range of 5--40 micrograms/ml by treatment of the plasma with 1 N hydrochloric acid followed by extraction with ethyl acetate. The method provides for the direct analysis of citrinin in urine and bile without prior extraction.

Animals↗
PubMed1980

Effects of rubratoxin B on the hepatic monooxygenase system in phenobarbital and 3-methylcholanthrene induced male mice.

Alterations in the hepatic microsomal monooxygenase system and in the concentrations of rubratoxin B in urine and feces were examined in male mice pretreated with corn oil, phenobarbital or 3-methylcholanthrene (3MC) and then given a single i.p. dose of rubratoxin B (1 mg/2.5 ml propylene glycol/kg). Twenty-four hours later the following parameters were determined; hepatic cytochrome P-450 content, enzyme activities of NADPH-cytochrome c reductase, NADPH-dependent dehydrogenase, aniline hydroxylase and ethylmorphine N-demethylase, and hepatic microsomal protein and reduced glutathione levels. Excretion of rubratoxin B in urine and feces also was determined. Rubratoxin B reduced the elevated cytochrome P-450 (136%, 134%) and protein (128%, 112%) to control values in animals pretreated with phenobarbital or 3MC, respectively; whereas, in the corn oil pretreated group, the mycotoxin reduced cytochrome P-450 by 38%. Aniline hydroxylase activity was reduced 31% or more in all pretreated animals. Rubratoxin B did not affect ethylmorphine N-demethylase activity in mice pretreated with phenobarbital; however, the enzyme activity was decreased significantly in the 3MC group. Rubratoxin B reduced the hepatic glutathione level in animals receiving 3MC (33%) or corn oil (22%). More rubratoxin B was detected in the urine than in the feces regardless of animals from the 3MC group. These data suggest a greater effect of rubratoxin B in the 3MC pretreated mice than in the phenobarbital pretreated animals.

Aniline Hydroxylase↗
PubMed1980

Production and biological activity of secalonic Acid d.

Twenty isolates of Penicillium oxalicum produced secalonic acid as their major secondary metabolite. Fermentation conditions were determined for toxin production in grain and liquid media. The 50% lethal dose value for mice ranged from 26.5 to 51.7 mg/kg dependent on animal strain and sex, males being more susceptible than females. Secalonic acid was nontoxic and nonteratogenic to the chicken embryo and exhibited poor antibiotic properties. Its potential role in mycotoxicoses is discussed.

Journal Article↗
PubMed1980

Mutagenicity of secalonic acid D in mice.

Secalonic acid D is an acutely toxic and teratogenic mycotoxin, produced by Penicillium oxalicum in corn. Two rodent mutagenicity tests, the dominant lethal test designed to evaluate male germ cell mutations and the micronucleus test designed to evaluate somatic cell mutations, were conducted in mice to assess the carcinogenic potential of secalonic acid D. Data obtained indicate that the positive control compound triethylene melamine (TEM) induced dominant lethal mutations during weeks 1 through 4 after administration to male mice and also resulted in a greatly increased population of micronucleated polychromatic (immature) erythrocytes in bone marrow of treated male mice. Secalonic acid D, however, failed to induce dominant lethal mutations but produced a slight but statistically significant increase in the number of micronucleated polychromatic erythrocytes in mouse bone marrow at maximally tolerated doses. It is concluded that secalonic acid D may e weakly mutagenic in a mouse somatic cell mutation system.

Animals↗
PubMed1980

Aflatoxin and Reye's syndrome: a case control study.

Aflatoxin levels were determined in serum and urine of 17 patients with Reye's syndrome and in control subjects. No significant difference in aflatoxin levels was found for the two groups. However, 23% of all persons studied had levels of aflatoxin indicative of recent exposure. Aflatoxin levels were associated with ingestion of cornmeal and corn bread but not peanut-containing products. This prevalence of aflatoxin may be of public health importance.

Adolescent↗
PubMed1980

Effect of patulin on hepatic monooxygenase in male mice.

The in vivo effects of patulin on hepatic monooxygenase enzymes in male mice were examined after single and multiple exposures (i.p.) to the mycotoxin. The animals were exposed to a single dose of 1, 3 or 4.5 mg patulin/kg or daily doses of 1.0 mg/kg for 5 or 14 days. After single exposure no significant effect was observed on hexobarbital hydroxylation while aniline hydroxylase increased significantly at 3 mg/kg and at 48 hr. The demethylation of aminopyrine and ethylmorphine increased significantly 48 and 72 hr after 3.0 or 4.5 mg patulin/kg doses. A 12% increase was observed in cytochrome P-450 content 48 hr after exposure to 1 or 3 mg/kg. NADPH-cytochrome C reductase was enhanced significantly at all 3 dose levels at 48 hr. At 24 hr hepatic NADPH-dependent dehydrogenase activity increased 38 and 46% in animals exposed to a single dose of 3 mg patulin/kg, respectively. No effect of patulin was observed on the hepatic drug metabolizing enzymes examined except hexobarbital oxidation in mice exposed to multiple doses of patulin. Patulin at best was a weak inducer of the hepatic mixed function oxidase system.

Animals↗
PubMed1979

The failure of trichothecene mycotoxins and whole cultures of Fusarium tricinctum to cause experimental haemorrhagic syndromes in calves and pigs.

Piglets and calves were dosed orally with pure diacetoxyscirpenol (DAS) and T-2 toxin, crude extracts of Fusarium tricinctum containing T-2 toxin, and whole cultures of F tricinctum containing T-2 toxin at a constant daily rate of 0.1 mg toxin per kg body-weight (piglets) or 0.2 mg toxin per kg body-weight (calves). The treatment continued for periods of seven to 78 days but it failed to induce clinical haemorrhagic syndromes. Increasing the dose of F tricinctum culture five-fold for eight days following 78 days at the lower dose was equally ineffective. The lack of an effect by daily intakes of toxin that could have been ingested with naturally contaminated feedstuffs suggests that DAS, T-2 toxin and other metabolites of F tricinctum probably have little or no part to play in the aetiology of feed associated haemorrhagic disease.

Animals↗