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Results for “Epoxy Compounds”

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At least 127 records · Page 7Linked to original sources
PubMed1987

Allergic contact dermatitis from a nonbisphenol A epoxy in a graphite fiber reinforced epoxy laminate.

An employee of the Composites Division of an aircraft engine manufacturing firm developed dermatitis associated with the handling of a graphite fiber reinforced epoxy laminate (epoxy prepreg). Patch test investigation demonstrated that the responsible causal agent was the nonbisphenol A epoxy binder, 4-glycidyloxy-N, N-diglycidylaniline. A patch test with bisphenol A epoxy from a standard patch test screening series was negative. Subsequent interviews with employees of the Composites Division suggested that a relative lack of awareness of the cutaneous hazards of fiber reinforced epoxy laminates, compared with liquid epoxy resin systems, may be an important risk factor for allergic sensitization to these composite materials.

Adult↗
PubMed1980

Biosynthesis of 16 alpha, 17 alpha-epoxy-4-androsten-3-one in rat liver microsomes.

4,16-Androstadien-3-one was incubated with the microsomal fraction of male rat liver in the presence of a NADPH generating system and oxygen. The metabolites formed were extracted from the incubation medium and purified by thin-layer chromatography (tlc). Final identification was performed by combined gas liquid chromatography-mass spectrometry. Incubation of 4,16-androstadien-3-one resulted in the formation of a non-polar metabolite which proved to be 16 alpha, 17 alpha-epoxy-4-androsten-3-one. This epoxide is a shortlived intermediate which is rapidly hydrolysed by the microsomal epoxide hydratase to 16 beta, 17 alpha-dihydroxy-4-androsten-3-one. In order to increase the amounts of epoxide in the incubation mixtures, styrene oxide which is a potent inhibitor of the epoxide hydratase was added. Under these conditions, up to 8% of the 16-dehydro-steroid incubated was transferred to the 16 alpha, 17 alpha-epoxy-compound.

Androstane-3,17-diol↗
PubMed1994

Effect of Ep475 on changes induced by calcium activated neutral protease on erythrocyte membrane.

Increase in cytosolic calcium leads to activation of calcium activated neutral protease (CANP). CANP is known to cause many membrane abnormalities that aid erythrocyte destruction. An epoxy compound Ep475 causes the reversal of such changes induced by calcium and CANP. In absence of Ep475, CANP caused reduction in free sulfhydryl groups and glycoprotein content of the membrane to 61, and 50% respectively, compared to untreated membranes. Calcium ATPase and membrane associated CANP were increased 3 and 1.4 times respectively. Significant reversal of these changes by Ep475 suggests a possible role of this compound in reversing the calcium dependent alterations in RBC including the action of CANP.

Calpain↗
PubMed1997

Occupational asthma caused by triglycidyl isocyanurate (TGIC).

BACKGROUND: Polyester powder paints are extensively used in metal painting. Triglycidyl isocyanurate (TGIC), an epoxy compound, is often used as a hardener. Several cases of allergic eczema from occupational exposure to TGIC have been reported in the literature. OBJECTIVE: We examined a 36-year-old non-smoking man who worked mainly as a spray painter, using a polyester powder paint containing 4% TGIC. During painting he used protective clothing and a motorized breathing protector. After 4 years he developed eczema on his hands, face and body, and an occupational allergic eczema caused by TGIC was diagnosed. He also suffered from powder-paint-related asthmatic symptoms. METHODS: Occupational asthma was diagnosed in accordance with the accepted guidelines. Inhalation challenge tests were performed with the paint and TGIC. RESULTS: Spirometry showed slight obstruction; the blood eosinophils and serum IgE value were elevated. Skin-prick tests with common environmental allergens were negative. The challenge test with lactose powder was also negative. A challenge test with a paint containing TGIC (4%) induced a dual reaction in PEF and a late 23% fall in FEV1. A test with TGIC (4%) mixed with lactose induced a dual PEF reaction, and also dual changes in spirometry. The PD15 in the histamine challenge test decreased significantly after the challenge tests. CONCLUSIONS: To our knowledge this is the first diagnosed case of occupational asthma caused by TGIC. This case report emphasizes the importance of protecting both the skin and respiratory tract of workers against chemicals such as TGIC, capable of causing skin and respiratory allergy.

Adult↗
PubMed1988

Two-year carcinogenicity study on three aromatic epoxy resins applied cutaneously to CF1 mice.

The cutaneous and systemic carcinogenic potentials of pure and two technical diglycidyl ethers of bisphenol A, DGEBPA, EPON 828 and EPIKOTE 828, respectively, have been investigated in six groups each of 50 male and 50 female CF1 mice. Twice weekly over a period of 2 yr, 0.2 ml of a 1 or 10% (w/v) solution of one of the epoxy resins in acetone was applied to the dorsal skin. A group of 50 male and 50 female CF1 mice was similarly treated treated with 2% (w/v) beta-propiolactone in acetone (the positive control) while a group of 100 male and 100 female mice was treated with acetone alone (negative control). Survival of the CF1 mice to 2 yr was unaffected by cutaneous exposure to each epoxy resin. The compounds proved to be mildly irritant to murine skin, the response in males being greater than in females. There was a very low incidence of benign and malignant tumours of the skin and subcutis after exposure to any of these compounds. The number of systemic lymphoreticular/haematopoietic tumours was increased only in females treated with EPIKOTE 828 or DGEBPA. In male mice, treated with 10% EPON 828, there was a slight increase in the number of renal tumours. The incidence of other systemic tumours in either sex was not increased following cutaneous application of the purified or the two technical DGEBPA resins (1 to 10% in acetone). The significance of all these findings is fully discussed.

Administration, Topical↗
PubMed1996

Occupational allergic contact dermatitis caused by 2,4,6-tris-(dimethylaminomethyl)phenol, and review of sensitizing epoxy resin hardeners.

BACKGROUND: Epoxy resin compounds (ERC) include a large number of sensitizing chemicals such as epoxy resins (ER), hardeners (curing agents), and reactive diluents. Allergic contact dermatitis (ACD) caused by ERCS is often occupational. MATERIALS AND METHODS: We report a patient, sensitized to a hardener of a two-component epoxy paint. Three conventional patch test sessions were performed to diagnose the causative chemical. We also review the literature on sensitizing epoxy-resin hardeners. RESULTS: A 47-year-old nonatopic woman developed dermatitis from a two-component epoxy paint. Patch testing with epoxy resin was negative, but 2,4,6-tris(dimethylaminomethyl)phenol (tris-DMP), used in the paint hardener, induced an allergic patch test reaction. We also review briefly other epoxy hardeners that have caused allergic dermatitis, including: (1) aliphatic polyamines, e.g., ethylenediamine, diethylenetriamine, triethylenetetramine, 3-dimethylaminopropylamine, and trimethylhexamethylenediamine; (2) cycloaliphatic polyamines, e.g., isophoronediamine and 3,3'-dimethyl-4,4-diaminodicyclohexylmethane; (3) aromatic amines, such as 4,4'-diaminodiphenylmethane, m-phenylene diamine, and 1,3-xylylene diamine; (4) dicyanodiamide; (5) triglycidyl isocyanurate, an epoxy compound that may be used as an epoxy-resin hardener; and (6) additives in epoxy accelerators, such as hexavalent chromate. CONCLUSIONS: No one chemical can be used to screen for sensitization to the many different epoxy hardeners. Extensive patch testing may be required to reveal the hardener that has caused the allergy. The hardener, 2,4,6-tris-(dimethylaminomethyl)phenol (tris-DMP), is a new sensitizer. To verify ACD caused by tris-DMP, patch-testing at 1% in petrolatum is suggested.

Dermatitis, Allergic Contact↗
PubMed1990

Chirality-dependent DNA reactivity as the possible cause of the differential mutagenicity of the two components in an enantiomeric pair of epoxides.

Chemical compounds containing an epoxy group are very reactive substances and, in many cases, they therefore exhibit strong mutagenic properties. Very often such epoxides contain an asymmetric C atom and thus exist as racemic mixtures of optical isomers, the so-called R- and S-enantiomers. It is well known that in many cases a biological activity resides completely in one of the two enantiomeric forms of a molecule. Also, the R- and S-enantiomeric forms of epoxystyrene exhibit different mutagenic activities in Salmonella typhimurium TA100, although their chemical reactivity does not differ to a recognizable extent. Neither could the higher mutagenic activity of the R-epoxystyrene be attributed to a slower enzymatic hydrolysis reaction. Thus, the intrinsic potential for eliciting mutagenic responses may not be the same for the two enantiomers, as there is evidence of qualitative differences in the binding to DNA, pointing strongly to an intrinsic difference in mutagenic activity of the two enantiomers.

DNA, Bacterial↗
PubMed2000

COBRA-1, a rationally-designed epoxy-THF containing compound with potent tubulin depolymerizing activity as a novel anticancer agent.

A novel mono-THF containing synthetic anticancer drug, COBRA-1, was designed for targeting a previously unrecognized unique narrow binding cavity on the surface of alpha-tubulin. COBRA-1 inhibited GTP-induced tubulin polymerization in cell-free tubulin turbidity assays. Treatment of human breast cancer and brain tumor (glioblastoma) cells with COBRA-1 caused destruction of microtubule organization and apoptosis. Like other microtubule-interfering agents, COBRA-1 activated the proapoptotic c-Jun N-terminal kinase (JNK) signal transduction pathway, as evidenced by rapid induction of c-jun expression.

Antineoplastic Agents↗
PubMed2003

Characterization of sizing layers and buried polymer/sizing/substrate interfacial regions using a localized fluorescent probe.

A novel technique is described to investigate buried polymer/sizing/substrate interfacial regions, in situ, by localizing a fluorescent probe molecule in the sizing layer. Epoxy functional silane coupling agent multilayers were deposited on glass microscope cover slips and doped with small levels of a fluorescently labeled silane coupling agent (FLSCA). The emission of the grafted FLSCA was dependent on the silane layer thickness, showing blue-shifted emission with decreasing thickness. The fluorescent results suggest that thinner layers were more tightly bound to the glass surface. The layers were also characterized by scanning electron microscopy, contact angle, and thermogravimetric analysis (TGA). When the FLSCA-doped silane layers were immersed in epoxy resin, a blue shift in emission occurred during resin cure, indicating the potential to study interfacial chemistry, in situ. Thicker silane layers exhibited smaller fluorescence shifts during cure, suggesting incomplete resin penetration into the thickest silane layers.

Benzhydryl Compounds↗
PubMed1992

Stereoselective epoxidation of phenyl allyl ether by alkene-utilizing bacteria.

Eighteen newly isolated ethene- and propene-utilizing bacteria were screened for the ability to produce phenyl glycidyl ether, a common precursor for the synthesis of beta blockers, from phenyl allyl ether. These organisms included Aerococcus, Alcaligenes, Micrococcus and Staphylococcus spp. and a variety of Gram-negative, Gram-positive and Gram-variable mesophilic rods/coccobacilli not yet identified. The majority of ethene- and propene-grown cultures (14 strains) accumulated phenyl glycidyl ether (0.4-1.7 mM) as the sole oxidation product. The bioconversions with the three most promising ethene-utilizers (M26, M90C, M93A) were scaled-up to yield essentially optically pure (enantiomeric excess = 93%) S-(+)-phenyl glycidyl ether. This is currently under investigation for commercial production of optically pure beta blockers.

Alkenes↗