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At least 19 recordsLinked to original sources
PubMed1979

Contact sensitivity to phenylglycidyl ether.

From among 40 workers with dermatitis who did not have contact with phenylglycidyl ether but worked with epoxy resins, 5 were positive to Epidian 5 and phenylglycidyl ether. Cross reactions between these contactants were noted in 3 of the 17 guinea pigs with primary sensitization to epoxy resin or the tested diluent. For 58 persons coming into contact with phenylglycidyl ether the frequency of sensitization to the contactant was determined and the mean period between starting work and the occurrence of dermatitis was calculated.

Animals↗
PubMed1976

Pepsinogen C and pepsin C from gastric mucosa of Japanese monkey. Purification and characterization.

A new pepsinogen component, pepsinogen C, was purified from the gastric mucosa of Japanese monkey. The chromatographic behavior of this component on DE-32 cellulose was coincident with that of pepsinogen III-2 previously reported (1), and final purification was performed by large-scale polyacrylamide disc gel electrophoresis. The molecular weight was 35,000 as determined by gel filtration. The ratios of glutamic acid to aspartic acid and of leucine to isoleucine were higher than those of other Japanese monkey pepsinogens. The activated form, pepsin C, had a molecular weight of 27,000 and contained a large number of glutamic acid residues. The optimal pH for hemoglobin digestion was 3.0. Pepsin C could scarcely hydrolyze the synthetic substrate, N-acetyl-L-phenylalanyl-3, 5-diiodo-L-tyrosine (APDT). 1, 2-Epoxy-3-(p-nitrophenoxy)propane (EPNP), p-bromophenacyl bromide, and diazoacetyl-DL-norleucine methyl ester (DAN) inhibited pepsin C [EC 3.4.23.3] in the same way as pepsin III-3 of Japanese monkey. The susceptibility to pepstatin of pepsin C was lower than that of pepsin III-3, and 500 times more pepstatin was required for the same inhibitory effect. The classification and nomenclature of Japanese monkey pepsinogens and pepsins are discussed.

Amino Acids↗
PubMed1976

The structure and function of acid proteases. VI. Effects of acid protease-specific inhibitors on the acid proteases from Aspergillus niger var. macrosporus.

1. The Type B acid protease from Aspergillus niger var. macrosporus was inactivated by reaction with diazoacetyl-DL-norleucine methyl ester (DAN), DL-1-diazo-3-tosylamido-2-heptanone (DTH), and L-1-diazo-3-tosylamido-4-phenyl-2-butanone (DTPB) in the presence of cupric ions. The reaction with DAN took place with 1:1 stoichiometry. The enzyme was also inactivated by reaction with 1, 2-epoxy-3-(p-nitrophenoxy)-propane (EPNP) with concomitant incorporation of approximately two EPNP molecules per molecule of protein. Moreover, these reactions of DAN and of EPNP were markedly inhibited by pepstatin. These results seem to indicate that, as in the case of porcine pepsin [EC 3.4.23.1] and related acid proteases, the enzyme has two essential carboxyl groups at the active site, one reactive with DAN and related diazo reagents in the presence of cupric ions and the other reactive with EPNP, and that pepstatin binds in the vicinity of these residues. 2. The Type A acid protease from the same mold, on the other hand, was found to be markedly less sensitive to these specific inhibitors. Under conditions where the Type B enzyme was completely inactivated by DAN and related diazo reagents, only partial inactivation of this enzyme occurred. The effect of prior mixing of DAN and cupric ions on the pH profile of inactivation was also different from that for the Type B enzyme. Moreover, the Type A enzyme was not inactivated by EPNP. These results thus indicate that the nature of the active site of the Type A enzyme is rather different from that of the Type B enzyme and hence that the Type A enzyme belongs to a different class of acid proteases from the Type B enzyme.

Aspergillus↗
PubMed1979

Isoepoxydon, a new metabolite of the patulin pathway in Penicillium urticae.

A patulin-negative mutant (J1) of Penicillium urticae (N.R.R.L. 2159A) was known to accumulate about 100mg per litre quantities of the 5,6-epoxygentisyl quinone, (-)-phyllostine and another metabolite (UIII). Both were derived from acetate and hence were polyketides. Purified UIII (m.p. 53 degrees C, [alpha](32) (D)+206 degrees , lambda(methanol) (max.) 240nm; epsilon 3806 litre.mol(-1).cm(-1)) was characterized as a partially reduced derivative of (-)-phyllostine and was found to be a diastereoisomer of the known phytotoxin, (+)-epoxydon. Hence its designation as (+)-iso- or epi-epoxydon. From (1)H n.m.r. and c.d. data the stereochemistry of the epoxide ring in (+)-isoepoxydon was determined to be identical with that in (+)-epoxydon (i.e. R,R) but the configuration of the secondary alcohol at C-4 was S rather than R as in (+)-epoxydon. Isoepoxydon (compound UIII) is therefore (4S,5R,6R)-5,6-epoxy-4-hydroxy-2-hydroxymethylcyclohex-2-en-1-one. The boat conformation in which the C-4 hydroxy group is axial is preferred. In the range of 1mm to 5mm, the antibiotic activity of (+)-isoepoxydon against Bacillus subtilis sp. was 56% of that obtained with patulin. Over a period of 1 to 3h, [(14)C]isoepoxydon was efficiently converted into patulin by a shake culture of the parent strain of P. urticae. The precursor relationship of isoepoxydon to patulin was confirmed by feeding unlabelled isoepoxydon (1mm) to a washed-cell suspension of a mutant (J2) in which, over a period of 3 to 5h, a better than 60% conversion into patulin was attained. The enzymic relationship between isoepoxydon and phyllostine and their positions in the late portion of the patulin biosynthetic pathway are discussed.

Acetylation↗
PubMed1979

The binding to mouse skin DNA of benzo[a]pyrene, its 7,8-diol and 7,8-diol-9,10-epoxides in relation to the tumorigenicity of these compounds.

Tritium labelled and carbon-14 labelled benzo[a]pyrene (PB), (+/-)trans 7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene (PB-7,8-diol), (+/-)-7 alpha,8 beta-dihydroxy-9 beta,10 beta-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene and (+/-)-7 alpha, 8 beta-dihydroxy-9 alpha, 10 alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]-pyrene were applied to the shaved backs of mice. After 24 h the DNA was isolated from the treated skin and the extent of hydrocarbon binding was determined. The level of DNA binding is considered in relation to the previously reported carcinogenicity of the various benzo[a]pyrene derivatives.

Animals↗
PubMed1977

Metabolic activation of mycotoxins by animals and humans: an overview.

Aflatoxins are associated with acute toxicoses in poultry and livestock and with liver cancer in human populations in Africa and Southeast Asia. Comparative metabolism studies indicate that aflatoxin B1, the most potent of these compounds, requires metabolic activation to the ultimate carcinogen. The mycotoxin (1) is oxidatively demethylated to form the phenolic derivative, (2) is hydroxylated directly at three sites, and (3) undergoes reduction of the carbonyl group in the cyclopentenone ring to a hydroxyl group; these five hydroxy derivatives all appear to be part of detoxication pathways. Considerable evidence is now available to support the hypothesis that activation of aflatoxin B1 to the ultimate carcinogen involves epoxidation of the double bond in the terminal furan ring. The epoxide decomposes to form a carbonium ion at C-2, which attacks nucleophilic sites in DNA, especially on the guanine moiety. Thus, like carcinogenic polycyclic hydrocarbons and N-nitroso compounds, aflatoxin B1 appears to be activated to an alkylating agent.

Aflatoxins↗
PubMed1979

The metabolic fate of cholesterol-5 alpha, 6 alpha-expoxide in vivo.

[14C] Cholesterol-5 alpha, 6 alpha-expoxide, administered to mice by either gastric intubation or skin painting, was rapidly and primarily excreted in the feces. Residual amonts of the epoxide and its metabolites were found in a wide variety of organs, and persisted for at least 72 hr. At some sites (principally the liver, the small intestinal contents and the combined stomach/duodenum and their contents), the labeled compound existed in a water-soluble form which could not be extracted with chloroform/methanol. Treatment of the small intestinal contents with a preparation of beta-glucuronidase/sulfatase produced a marked increase in the amount of organic-solvent-extractable cholesterol-alpha-epoxide and other polar metabolites. Unchanged epoxide was found mainly in the feces and the skin at the site of application. On the basis of these results, stool specimens, and not blood samples, should be analyzed to detect the presence of this compound and/or its metabolites in vivo.

Administration, Topical↗
PubMed1978

Mutagenicity of aliphatic epoxides.

The mutagenicity of 17 aliphatic epoxides was determined using the specially constructed mutants of Salmonella typhimurium developed by Ames. The activity of these epoxides together with those reported in the literature as mutagens in strains TA100 and TA1535 depended on the degree of substitution around the oxirane ring. Monosubstituted oxiranes were the most potent mutagens in both strains. 1,1-Disubstitution resulted in the complete loss or reduction of mutagenicity, trans-1,2-Disubstituted, and tetrasubstituted oxiranes all lacked mutagenicity, while the cis-1,2-disubstituted oxiranes tested were weakly mutagenic in strain TA100 only. For the monosubstituted compounds the presence of electron-withdrawing substituents increased mutagenicity.

Epoxy Compounds↗
PubMed1978

Contaminants in human milk.

There is a paucity of information regarding excretion of contaminants in human milk, due to experimental difficulties and until recently a general lack of interest. Because of the high fat content of milk and as its acidity is higher than that of plasma, nearly all liposoluble and basic agents consumed by the mother will be excreted in the milk. Distinction must be made between, on the one hand drugs and social toxicants such as smoking and alcohol, whose intake can be stopped or limited during pregnancy and lactation, and ecological toxicants present in a polluted environment to which the mother is exposed. Cases have occurred of heavy prenatal and postnatal intoxication of infants with hexachlorobenzene in Turkey and methylmercury in Iraq due to consumption of fungicide-treated seed wheat by pregnant and lactating mothers. Recent attention has been concentrated on contamination of milk with organochlorine compounds such as DDT and PCB's, that are found in many parts of the world. The heaviest contamination with DDT has been found in Guatemala, resulting in suckling infants consuming many times the Acceptable Daily Intake of this compound proposed by WHO, with unknown future effects.

DDT↗
PubMed1979

Effects of tetraethyl lead on the activities of drug metabolizing enzymes in different tissues of the rat.

The present study describes the effects of tetraethyl lead on various drug metabolizing enzymes in different tissues of the rat. Tetraethyl lead was administered intraperitoneally to rats (250 mumol/kg) on two consecutive days. The animals were killed on day 3. Tetraethyl lead-treatment decreased the concentration of hepatic cytochrome P-450 (to 45 per cent of the control), the hepatic activity of aryl hydrocarbon hydroxylase (to 41 per cent of the control) and ethoxycoumarin deethylase (to 45 per cent of the control). Epoxide hydratase activity was enhanced in the liver (1.3-fold), kidney (3.3-fold), and small intestinal mucosa (4.7-fold). The activity of glutathione S-transferase decreased in the liver (to 69 per cent of the control) but increased in the kidney (1.5-fold) and small intestinal mucosa (1.7-fold). The glucuronidation of o-aminophenol was enhanced (2.2-fold) in the kidney of tetraethyl lead treated rats. It is concluded that exposure to tetraethyl lead brings about widespread changes in the ability of mammals to detoxify foreign compounds.

Animals↗
PubMedDate not supplied

Mutagenic activities of 1,2,7,8-diepoxyoctane in Chinese hamster lung cells.

The mutagenicity of 1,2,7,8-diepoxyoctane (DEO) was investigated using Chinese hamster lung cells. 6-thioguanine resistance and chromosome aberrations were used as markers for mutagenicity testing. DEO was found to be genetically active and to readily from adducts with radiolabeled nucleotides, as demonstrated through thin-layer chromatography in DEO/nucleotide mixtures. Continuous disappearance of cells carrying chromosome aberrations from the cell populations was observed. Based on the expected frequency, cell death can be interpreted as a result of chromosome abberations. The mutagenic specificity of diepoxyoctane is apparently related to the compound's ability to blind with DNA.

Animals↗