PubMed Health⌕ Search

Biomedical subjects

H Matsudaira

Publications and source records attributed to H Matsudaira.

At least 37 records · Page 2Linked to original sources
PubMed1979

Induction and repair of DNA strand breaks in cultured mammalian cells following fast neutron irradiation.

Induction and repair of DNA breaks following irradiation with NIRS cyclotron neutrons were studied in cultured mammalian cells (L5178Y) in comparison to those following gamma-rays. The yield of the total single-strand breaks, 3'OH terminals and sites susceptible to S1 endonuclease following fast neutrons was found to be approximately 50 per cent of that following gamma-irradiation. On the other hand, the yield of double-strand breaks was slightly higher after fast neutrons than after gamma-rays. The percentage of the total single-strand breaks remaining unrejoined at 3 hours after post-irradiation incubation was found to be distinctly higher after the fast neutrons than after gamma-rays. The neutron-induced damage appears to carry a higher proportion of alkali-labile lesions compared to gamma-rays. It was concluded that the increase in the yield of double-strand breaks and of unrejoinable breaks is responsible for a high r.b.e. of the cyclotron neutrons.

Animals↗
PubMed1978

Induction and repair of strand breaks and 3'-hydroxy terminals in the DNA of mouse brain following gamma irradiation.

DNA was isolated from mouse brain after in vivo gamma-ray irradiation, treated with endonuclease S1 from Aspergillus oryzae if necessary, and analysed further by alkaline and neutral sucrose gradient centrifugation. In parallel, its template activity was determined by DNA polymerase (EC 2.7.7.7, enzyme A of Klenow from Escherichia coli) assay as described previously. Similar experiments were performed with cultured mouse leukaemia cells (L5178Y) irradiated in vitro at 0 degrees C. Irradiation induced single- and double-strand breaks in the DNA of the brain with a yield of 1.0 and 0.1 break per 10(12) dalton per rad (100 eV/break and 770 eV/break), respectively. The yield of single-strand breaks in the brain was lower than that found in the cultured cells, whereas the yield of double-strand breaks was found to be almost the same in both cases. Treatment of irradiated DNA with single-strand-specific S1 endonuclease gave rise to further breaks detected on neutral sucrose gradient analysis. The yield of these breaks was also higher in the brain compared to the cultured cells. The increase per unit dose in the template activity of the DNA from the brain was found to be five times as much as that found in the cultured cells. Then, the average number of deoxyribonucleotides incorporated per break was determined on DNA which had experienced different treatments. The value for the brain DNA irradiated in vivo was found to be five times as much as that found for DNA treated with pancreatic deoxyribonuclease and 10 times as much as those found for DNA from the cultured cells and isolated brain nuclei irradiated in vitro at 0 degrees C. Thus, in vivo irradiation seemed to induce gaps with 3'-OH terminals in addition to simple breaks with or without 3'-OH terminals found in the cultured cells. Radiation-induced single-strand breaks and 3'-OH terminals in the DNA of the brain were repaired following irradiation. Approx. 20--40% of the terminals or breaks induced were, however, remaining at 3 h or more after irradiation, depending on the dose administered.

Animals↗
PubMed1977

Induction and repair of strand breaks and 3'-hydroxy terminals in the DNA of mammalian cells in culture following gamma-ray irradiation.

DNA was isolated in a fairly pure and intact state from cultured mouse leukaemia cells (L5178Y) after gamma-ray irradiation using a hydroxyapatite column chromatography method, and analysed further by sucrose gradient centrifugation or DNA polymerase (EC 2.7.7.7, enzyme A of Klenow from Escherichia coli) assay. Irradiation of the cells induced single- and double-strand breaks in the DNA with an efficiency of 100 eV/break and 1300 eV/break, respecitvely. Approximately 50% of the single-strand breaks were estimated to be those arising from allali-labile lesions. A linear, dose-dependent increase was found in the template activity of the DNA, indicating the induction of 3'-OH terminals by gamma-irradiation. Post-irradiation incubation of the cells in serum-free medium allowed the majority of the breaks to rejoin within a few hours. Repair of the alkali-labile lesions was, however, found to be much slower than that of "actual" single-strand breaks. A slight increase of the DNA template activity was found during the period of post-irradiation incubation. The reason for the increase is discussed.

Animals↗
PubMed1977

Induction of hepatic tumors in a teleost (Oryzias latipes) after treatment with methylazoxymethanol acetate: brief communication.

Liver neoplasms including trabecular hepatoma and cholangioma were induced in medakas (Oryzias latipes) by the addition of methylazoxymethanol acetate to their aquarium water at levels of 0.1-3 ppm for periods ranging from 1 to 120 days. More than 80% of the surviving fish developed tumors at 3 or 5 months after commencement of the treatment, irrespective of levels of the drug, when appropriate times of exposure were chosen.

Adenoma, Bile Duct↗
PubMed1976

Evidence for caffeine-sensitive damage in methylazoxymethanol acetate-treated L5178Y cells.

The effects of methylazoxymethanol (MAM) acetate on colony survival, cell proliferation and DNA synthesis of murine lymphoma L5178Y cells are studied. Decreased sensitivity and immediate depression of cell proliferation and DNA synthesis were found in L5178Y cells in contrast to the reports on HeLa cells. Pre-labelling with 5-bromodeoxyuridine (BUdR) did not enhance significantly the carcinogen-induced cell lethality. Post-treatment with caffeine greatly enhanced cell lethality and depression of cell proliferation. These effects of caffeine were diminished when the cells had passed through two generations following the MAM acetate treatment. Experiments with synchronized cells showed that the action of caffeine was located primarily in S phase following the MAM acetate-treatment. These results strongly suggest that in L5178Y cells, MAM acetate induces damage, which is repaired by a mechanism analogous to post-replication repair of UV light-induced damage.

Azo Compounds↗