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T Benjamin

Publications and source records attributed to T Benjamin.

34 records · Page 2Linked to original sources
PubMed1981

Effect of 2,2'-diaminodiphenyldisulfide, a resin hardener, on rats.

Guided by structure-activity relationships among carcinogenic aromatic amines, a sulfur-containing aromatic diamine was designed as a possible noncarcinogenic replacement for the resin hardener 4,4'-methylenebis(2-chloroaniline) (MOCA). However, in small-scale tests in rats the analog diaminodiphenyldisulfide (DDDS) caused necrotic changes in the liver, acanthosis and hyperkeratosis of the forestomach, and atrophy and hyperplasia of the ductal epithelium of the kidney. One case of hepatocellular carcinoma was also noted. Furthermore, DDDS caused alterations in the hepatocellular carcinoma was also noted. Furthermore, DDDS caused alterations in the phospholipid pattern of liver, kidney, and spleen, increasing total phospholipid and cholesterol but decreasing triglyceride levels. However, it was not mutagenic in a Salmonella test system, even in the presence of S9 and microsomal fractions from Aroclor 1254-treated rats.

Aniline Compounds↗
PubMed1980

Mutagenicity of urine from rats after administration of 2,4-diaminoanisole: the effect of microsomal enzyme inducers.

Ring 14C-labelled 2,4-diaminoanisole disulfate was administered to rats pretreated with the microsomal inducers phenobarbital (PB), beta-naphthoflavone (BNF), 3-methylcholanthrene (MC) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The 24-h urine from rats pretreated with PB showed a 2-fold increase in revertant rate over the corresponding control as measured by the Ames Salmonella test system. Pretreatment of rats with BNF, MC or TCDD decreased the mutagenicity of urine by about 70% when an activating system was used. However, in the absence of an activating system, the urine from rats induced with BNF, MC or TCDD showed a significant (P < 0.001) degree of mutagenicity compared with urine from controls or urine from phenobarbital-induced rats. Release of conjugates by beta-glucuronidase increased the mutagenicity of urine even in the absence of an activating system, but the number of revertants was almost doubled in the presence of an activating system. The urine from rats treated only with the 4 inducers did not show any mutagenicity. 2,4-Diaminoanisole itself was mutagenic only in the presence of an activating system. alpha-Naphthoflavone (ANF) (0.1 mM) inhibited by 85--90% the in vitro mutagenicity of urine, mediated by Aroclor 1254, MC or TCDD induced rat-liver microsomes. The mutagenicity mediated through PB-induced rat-liver microsomes was, however, inhibited only by 16%. Similarly, 0.1 mM metyrapone (MP) inhibited the mutagenicity of urine by Aroclor 1254, MC or TCDD induced rat-liver microsomes by 13--18%. For the same MP concentration a 50% inhibition of the mutagenicity mediated through PB-induced rat-liver microsomes was observed. The mutagenicity pattern for urine in vitro was shown to be similar with liver S9 from rats induced either with Aroclor 1254 or with MC.

Animals↗
PubMed1979

Metabolism of the dyestuff intermediate 2,4-diaminoanisole in the rat.

1. 2,4-Diamino[ring-U-14C]anisole.2HCl administered intraperitoneally to rats is excreted chiefly via the urine (79 and 85% of the dose in 24 and 48 h, respectively). The isotope in the faeces was 2.1 and 8.9% of the dose at 24 and 48 h. 2. The major metabolic pathway was acetylation of the amine groups(s), resulting in 4-acetylamino-2-aminoanisole and 2,4-diacetylaminoanisole. 3. Oxidate pathways yielded 2,4-diacetylaminophenol (O-demethylation), 5-hydroxy-2,4-diacetylaminoanisole (ring hydroxylation), and 2-methoxy-5-(glycol-amido)acetanilide or its isomer (omega-oxidation). 4. These major metabolites were excreted in the urine both as free and glucuronic acid conjugates.

Animals↗
PubMed1979

N-Formylation of an aromatic amine as a metabolic pathway.

1. Feeding 2-aminoanthraquinone (2-AAQ) in the diet to Fischer rats led to nephrotoxicity in females, caused by deposits of crystalline material in the kidney tubules. 2. This material consisted of 2-AAQ, N-acetyl-2-AAQ and N-formyl-2-AAQ. N-Formyl-2-AAQ was also identified in the ether extract of urine of rats fed 2-AAQ. 3. This represents the first case of identification of the N-formyl derivative of a primary aromatic amine as a metabolite in vivo.

Amines↗
PubMed1979

Comparison of the metabolism of 2,4-toluenediamine in rats and mice.

The excretion, distribution, and metabolism of 2,4-toluenediamine (TDA) have been compared in rats and mice. The elimination of TDA metabolites into urine was faster and more complete in mice than in rats. However, the feces of rats accounted for a greater percentage of the dose in rats than in mice. The distribution of metabolites in tissues were considerably lower in mice than in rats. The major urinary metabolites observed in the rat were 4-acetylamino-2-aminotoluene, 2,4-diacetylaminotoluene, 4-acetylamino-2-aminobenzoic acid. The major metabolites in the mice were 4-acetylamino-2-aminobenzoic acid, 4-acetylamino-2-aminotoluene and 2,4-diacetylaminobenzoic acid.

Aminobenzoates↗
PubMed1978

Tumor antigens induced by nontransforming mutants of polyoma virus.

We have studied the tumor (T) antigens induced by wild-type polyoma virus and several nontransforming mutants using immunoprecipitation with antisera from animals bearing polyomya-induced tumors followed by sodium dodecylsulfate (SDS)-polyacrylamide gel electrophoresis. In a variety of mouse cells, wild-type virus induces a major T antigen species with apparent molecular weight of 100,000 daltons, and four minor T antigen species with apparent molecular weights of 63,000, 56,000, 36,000 and 22,000 daltons. Hr-t mutants, which have an absolute defect in transformation, induce a normal 100,000 dalton T antigen but are altered in the minor T antigen species. Hr-t deletion mutants induce none of the minor T antigen species seen in wild-type virus. In their place, these mutants induce T antigen species with molecular weights in the range of 6,000--9,000 daltons. The size of the very small T antigen products does not correlate in any simple way with the size or location of the deletions in the viral DNA. Point hr-t mutants induce two of the four minor T antigen species; they make apparently normal amounts of the 56,000 dalton product and reduced amounts of the 22,000 dalton product, but none of the 63,000 or 36,000 dalton species. Ts-a mutants, which have a temperature-sensitive defect in the ability to induce stable transformation, and which complement hr-t mutants, induce T antigens with the same mobility as wild-type; however, the 100,000 dalton T antigen of ts-a mutants is thermolabile compared to wild-type. A double mutant virus carrying both a ts-a mutation and a deletion hr-t mutation induces a thermolabile 100,000 dalton product and none of the minor T antigen species. Cell fractionation studies with productively infected cells have been carried out to localize the T antigen species.

Antigens, Neoplasm↗
PubMed1976

Localization of gene functions in polyoma virus DNA.

Polyoma virus mutants of four functionally distinct groups have been mapped by the marker rescue technique using restriction enzyme fragments of wild-type viral DNA. Nontransforming host-range mutants map in the proximal part of the early region of the viral genome. The same DNA fragment that restores a normal host range also restores normal transforming ability to these mutants. ts-25D, a temperature-sensitive (ts)-a class mutant, maps in the distal part of the early region. ts-3 and ts-1260 map in the proximal and distal parts of the late region, respectively.

Chromosome Mapping↗
PubMed1975

Long-term effect of benzene in C57BL/6N mice.

Weaning male C57BL/6N mice received repeated subcutaneous injections of benzene in corn oil for 54 weeks. These mice and surviving controls were killed 104 weeks after the first injection. There was no evidence of carcinogenic activity in benzene-injected mice. A high incidence of amyloidosis developed in mice of all treated and untreated groups. Butyinitrosourea, used as a positive control, induced lymphomas or leukemias (in most exposed mice) and intestinal tumors in a few.

Amyloidosis↗
PubMed1975

Enzymic N-acetylation of 2,4-toluenediamine by liver cytosols from various species.

1. 2,4-Toluenediamine was incubated with liver cytosol from various species, or cytosol from various tissues of the hamster or rabbit, in the presence of [1-14C]acetyl-CoA. N-Acetylation occurred selectively at the p-amino group of 2,4-toluenediamine and to a much lesser extent on the o-amino group. 2. In hamsters and rabbits the highest N-acetyltransferase activity was present in the liver cytosol, followed by kidney intestinal mucosa and lung cytosols. 3. Hamster liver cytosol had the greatest activity followed by liver cytosols from guinea-pig, rabbit, mouse and rat. With human liver cytosol only a trace of an N-acetyl derivative of 2,4-toluenediamine was found while dog liver cytosol showed no activity. 4. N-Acetyltransferase activity was maximal at pH 7-5 in mouse, pH 6-0 in rat and man, and pH 7-0 in rabbit liver cytosols. 5. There was a slight difference in the levels of N-acetyltransferases in males and females; the female mouse had more enzyme activity than the male, but the male rat had more enzyme activity than the female.

Acetylation↗