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G Bobotas

Publications and source records attributed to G Bobotas.

6 recordsLinked to original sources

beta-Glucuronidase activation of latent aggression-promoting cues in mouse bladder urine.

The present study was designed to investigate the chemical properties of the aggression-promoting cues present in bladder urine of male mice. The results of the first experiment confirmed earlier work by demonstrating the presence of an aggression-promoting chemosignal in bladder urine. In Experiment 2, behavioral assays were separately performed on the organic and aqueous layers of bladder urine obtained by repeated dichloromethane extractions. Only the combined organic layers of the initial three extractions demonstrated behavioral activity. A fourth extraction showed no behavioral activity for both organic and aqueous layers. However, the findings of Experiment 3 showed that incubation of the aqueous layer from the third CH2Cl2 extraction in beta-glucuronidase can free additional aggression-promoting cues into a subsequent CH2Cl2 extraction. It is concluded that two forms of the aggression-promoting chemosignal are present in bladder urine. One is lipophilic and behaviorally active, whereas the other is conjugated, possessing latent chemosignal properties.

Aggression↗

Separation of 1,2-dimethylhydrazine metabolites by high-pressure liquid chromatography.

The separation of 1,2-dimethylhydrazine, azomethane, azoxymethane, methylazoxymethanol, methylazoxymethanol acetate, formaldehyde and methanol by high-pressure liquid chromatography on columns of C18/Corasil, muBondapak C18 and Aminex A-27 is described. The separations are highly reproducible and rapid and may be used for kinetic studies. An example of an application of these methods to the analysis of metabolites in rat urine derived from (14C)-1,2-dimethylhydrazine is reported.

Animals↗

Detection and estimation of azomethane in expired air of 1,2-dimethylhydrazine-treated rats.

Azomethane (AM) gas was identified as a major metabolite of 1,2-dimethylhydrazine (1,2-DMH) in the expired air of F344 rats. The compound was characterized by high-pressure liquid chromatography, gas chromatography, and mass spectrometry, in comparison to a synthetic standard. At a dose of 21 mg 1,2-DMH/kg sc, approximately 14 and 11% of the dose were exhaled as AM and CO2, respectively, in 24 hours. At 200 mg 1,2-DMH/kg, 23 and 4% of the dose appeared as AM and CO2, respectively, in the respired air within the same period. Most AM was seen in the first 6 hours, but the CO2 evolution was more progressive, especially after the higher dose of 1,2-DMH.

Animals↗

Inhibition of 1,2-dimethylhydrazine metabolism by disulfiram.

1. The effects of disulfiram on the metabolism of 1,2-dimethylhydrazine were studied in CDF rats. 2. Treatment with disulfiram causes enhanced elimination of azomethane in the expired air, inhibition of CO2 production, and decreased levels of 1,2-dimethylhydrazine metabolites in the urine. 3. These results suggest that disulfiram inhibits the N-oxidation of azomethane to azoxymethane, thus preventing further metabolism to the ultimate carcinogenic species, and provide an explanation for the observations that disulfiram inhibits 1,2-dimethylhydrazine-induced neoplasia of the large intestine.

Animals↗