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Results for “TRIETHYLENE MELAMINE”

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At least 19 recordsLinked to original sources
PubMed1961

MECHANISM OF CHEMICAL MUTAGENESIS IV. : Reaction between Triethylene Melamine and Nucleic Acid Components.

Lorkiewicz, Z. (University of Wisconsin, Madison), and Waclaw Szybalski. Mechanism of chemical mutagenesis. IV. Reaction between triethylene melamine and nucleic acid components. J. Bacteriol. 82: 195-201. 1961.-Triethylene melamine interacts primarily with phosphorylated intracellular deoxyribonucleic acid (DNA) precursors and not with DNA. It was found by direct chemical and chromatographic analysis that only pyrimidine precursors of nucleic acids are attacked by triethylene melamine. In the course of the triethylene melamine-deoxycytidine reaction the mutagenicity of the reaction mixture is lost, but the mutagenicity of the triethylene melamine-thymidine reaction products significantly increases above that of the reaction substrates. Several steps are postulated to explain the mechanism of the triethylene melamine-initiated mutagenic reaction: (i) Reaction I, semireversible uptake of triethylene melamine; (ii) reaction II, chemical interaction between triethylene melamine and intracellular thymidine mono- or triphosphate with the production of a functional analogue of the latter; (iii) incorporation of this fraudulent analogue into the newly formed DNA strand; (iv) occurrence of self-perpetuating errors in the sequence of natural bases during subsequent rounds of replication of the analogue-containing DNA strand. It is postulated that the mechanism of mutagenic responses to different types of mutagens can fit either a simplified (mutagenic base analogues) or extended version (radiation) of this schema.

Journal Article↗
PubMed1951

Trisethylene-imino-s-triazine (triethylene melamine or TEM) in the treatment of neoplastic diseases.

Trisethylene-imino-s-triazine (triethylene melamine or TEM) produced minimal effects in inhibiting transplantable lymphoma and mammary adenocarcinoma in mice. In strain A mice, injection of the compound induced pulmonary tumors.TEM was tried on 32 patients with neoplastic disease, including nine patients with Hodgkin's disease and five with lymphosarcoma and lymphatic leukemia. The therapeutic and toxic effects were similar to those observed with nitrogen mustard (HN2). Satisfactory remissions of up to three months were observed in Hodgkin's disease and lymphosarcoma following parenteral administration of TEM. It is the authors' impression that the remissions obtained with TEM were not as complete and did not last as long as those obtained with HN2.TEM is effective by the oral route as well as parenterally, and produces much less emetic reaction than HN2. On the other hand, the chemotherapeutic range is narrower than that of HN2. Patients who do not respond to HN2 show no response to TEM.TEM is a drug of some clinical usefulness in the same conditions and with the same general limitations and toxic effects as HN2. The ease of administration of TEM increases its hazards, and close clinical and hematologic observations are essential on patients receiving the agent.

Animals↗
PubMed1982

Mithramycin- and triethylene melamine- induced sperm abnormalities in Lakeview hamsters.

The sperm abnormality-inducing action of two potential mutagenic agents mithramycin and triethylene melamine (TEM), in inbred Lakeview hamsters was studied and results compared with similar investigations in mouse. Test hamsters received subacute intraperitoneal exposures ranging from 0.01 to 0.25 mg/kg body weight with either agent for 5 consecutive days. Testis weights, epididymal sperm numbers, and body weights were also monitored at weeks 1, 4, and 10 after treatment. Mithramycin-treated hamsters showed 21 times more sperm abnormalities than control (25% vs. 1.2%) whereas TEM elevated sperm abnormalities by eight fold. The frequency and type of aberrant sperm varied with dose and time, being the highest at weeks 1 or 4, rather than week 10, with either agent. Sperm number and testis weights remained depressed considerably from 4 to 10 weeks after treatment with either agent. Body weights in chemically treated hamsters remained within 28% of control for the test period. Even though our findings were in general agreement with those reported for mouse, the magnitude of the response and the stage of spermatogenic sensitivity in the chemical induction of sperm abnormalities in the two species were different.

Animals↗
PubMed1987

Effects of bile acids on the mutagenicity and recombinogenicity of triethylene melamine in yeast strains MP1 and D61.M.

When Saccharomyces cerevisia MP1 was treated with bile acids alone or in combination with triethylene melamine (TEM), cholic acid was found to be comutagenic and antirecombinogenic while lithocholic acid had the opposite effect. Other bile acids enhanced the mutagenic and recombinogenic effects of TEM. Chenodeoxycholic acid, deoxycholic acid and ursodeoxycholic acid had stronger comutagenic than corecombinogenic effects; hyodeoxycholic acid did not show this difference. Ox gall and a mixture of bile acids antagonized the genotoxic effect of TEM, and it therefore seems plausible that in normal composition bile acids neutralize each other, i.e., the comutagenic (corecombinogenic) effect of one substance is antagonized by the antimutagenic (antirecombinogenic) effect of another one. However, when the composition is altered, bile acids may become harmful. Experiments with yeast strain D61.M were performed in order to test for aneuploidy caused by bile acids; no effects were observed.

Aneuploidy↗