Induction of sister chromatid exchanges by nicotinamide in Chinese hamster lung fibroblasts and human lymphoblastoid cells.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T Utakoji.
Explore the source record for details and available documents.
Karyotype analyses were conducted on spontaneous mammary tumors of 11 GR, 2 C3H, and 2 noninbred Swiss mice with the use of trypsin-Giemsa banding procedures. All tumors manifested trisomy of chromosome No 13 in most cells, and all except 1 tumor had cells with a model chromosome number of 40.
A benzimidazole derivative, Hoechst 33258 can induce decondensation of constitutive heterochromatin in the mouse derived L cell chromosomes when the compound is given in sufficiently high concentration (40 micrograms/ml) to the L cell culture. Hoechst 33258 at low concentration (1 micrograms/ml, 16 h) cannot produce this effect on L cell chromosomes. Bromodeoxyuridine (BUdR) incorporation for one cell cycle simultaneous with the Hoechst 33258 treatment at low concentration could decondense heterochromatin segments in metaphase chromosomes. The heterochromatin decondensation, however, was asymmetric; it was observed only on one chromatid and the other of a chromosome remained in condensed state. The observation of asymmetric decondensation of heterochromatin by Hoechst 33258 after BUdR incorporation for one cell cycle, the association of A-T rich satellite DNA to mouse heterochromatin, and available data on the specific binding of Hoechst 33258 to A-T base pairs of DNA and on the higher affinity of the compound to BUdR substituted DNA than to ordinary DNA implied that the binding of Hoechst 33258 molecules to A-T rich satellite DNA is the cause of heterochromatin decondensation.
Explore the source record for details and available documents.
Explore the source record for details and available documents.