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Biomedical subjects

S Venitt

Publications and source records attributed to S Venitt.

At least 91 records · Page 5Linked to original sources
PubMed1976

Chemical transformation of Chinese hamster cells: II. Appearance of marker chromosomes in transformed cells.

The chromosomes of 12 samples of cultured Chinese hamster kidney and prostate cells (4 normal and 8 transformed), whose tissue culture properties have already been described (Kirkland, 1976) have been examined for numerical change and for the appearance of abnormal markers. Six transformed kidney subclones contained a consistent telocentric marker not present in the normal parental cell, and Giemsa banding demonstrated this to be the centromere and the long (q) arm of the number 4 chromosome in all cases. Two transformed prostate subclones also contained a consistent telocentric marker, not present in similarly derived normal subclones or in the normal parental cell, and Giemsa banding demonstrated this to be a different fragment (the centromere and most of the p arm) of the number 4 chromosome. It is believed that the use of a mixed-serum culture medium, designed to stabilize the karyotype of cultured Chinese hamster cells, is at least partly responsible for the detection of these transformation-associated chromosome changes.

Carcinogens↗
PubMed1976

Mutagenicity and possible carcinogenicity of hair colourants and constituents.

Skin painting experiments showed that two semi-permanent hair colorants applied at low concentrations caused an early appearance of tumours in two strains of mice. Both colorants were mutagenic in S. typhimurium and further investigation revealed that three categories of hair colorant contained mutagenic constitutents.

Aniline Compounds↗
PubMed1975

Chromosome damage in the bone marrow of mice treated with the methylating agents methyl methanesulphonate and N-methyl-N-nitrosourea in the presence or absence of caffeine, and its relationship with thymoma induction.

A single dose (0.8 mmole/kg) of N-methyl-N-nitrosourea (MNUA) causes significantly more chromosome damage in the bone marrow of mice than a dose of equal toxicity to the animals, (1.1 mmole/kg) of methyl methanesulphonate (MMS) 6, 24 and 48 h after treatment. At these doses both agents alkylate bone-marrow DNA to similar extents, but only MNUA induces thymic lymphomata. The greater chromosome-damaging effects of MNUA are ascribed to the known differences in the pattern of DNA alkylation by each agent, in particular the much higher levels of O-6 methylguanine and phosphotriesters produced by MNUA. The greater chromosome-damaging effect of MNUA may account for its higher toxicity to the bone marrow which in turn may be a significant factor in the induction of thymomata. The enhancement by caffeine of chromosome damage seen particularly 48 h after MMS-treatment suggests that post-replication repair protects cells from the effects of DNA-methylation in vivo.

Animals↗
PubMedDate not supplied

UKEMS trial: bacterial mutation tests of 4-chloromethylbiphenyl, 4-hydroxymethylbiphenyl, and benzyl chloride, using E. coli WP2uvrA(pKM101) and S. typhimurium TA98 and TA100.

4CMB, 4HMB and BC were assayed in plate tests, using E. coli WP2urvA(pKM101), and S. typhimurium TA98 and TA100, in the presence or absence of microsomal activation. 4CMB was also assayed in fluctuation tests using E. coli WP2uvrA(pKM101). 4HMB was uniformly negative, and 4CMB was mutagenic to all 3 strains. BC was negative in TA98 and positive in TA100 and WP2uvrA(pKM101). The presence of absence of S9 made no substantial difference to the mutagenicity of 4CMB or BC.

Benzyl Compounds↗