| Project/Area Number |
03671052
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Biological pharmacy
|
|---|
| Research Institution | Okayama University |
|---|
Principal Investigator |
NEGISHI Kazuo Okayama University, Gene Research Center, Associate Professor, 遺伝子実験施設, 助教授 (70116490)
|
|---|
| Project Period (FY) |
1991 – 1992
|
| Project Status |
Completed (Fiscal Year 1992)
|
| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1992: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1991: ¥1,300,000 (Direct Cost: ¥1,300,000)
|
|---|
| Keywords | Sunlight / Near UV / Transversion / Mutation spectrum / 8-oxoguanine / M13mp2 phage / Oxidative damages / UVB / 太陽光 / M13ファ-ジ / 突然変異 / スペクトラム / トランスバ-ジョン / 8ーヒドロキシグアニン |
|---|
| Research Abstract |
Sunlight is well known to be mutagenic and carcinogenic. The genetic effects of sunlight are believed to be induced by pyrimidine photoproducts produced by the action of ultraviolet portion of sunlight. However, it is still unclear whether DNA lesions other than pyrimidine photoproducts are also involved in sunlight mutagenesis and carcinogenesis. We have analyzed mutagenic potential of sunlight on single-stranded DNA phage M13mp2 with the lacZETAalpha region of the DNA as target, using an SOS-deficient recA^- strain and an SOS-induced rec^+ strain of Escherichia coli as hosts. Exposure to sunlight caused mutations ; about 10-fold increase in the mutation frequencies were observed with the use of both hosts. When the SOS functions were induced in the rec^+ host, CSH50, the mutation frequencies increased another 10-fold over those obtained with the host lacking the SOS functions. DNA sequence analysis of these mutants showed that most of the mutations were transversions, either G to C or G to T. Furthermore, 59 % of the identified sequence changes in the SOS^- host and 40 % of those in the SOS-induced host were G-to-C transversions. These results suggest the possibility that an unidentified modification of guanine in the DNA is produced by sunlight. We analyzed 8-hydroxydeoxyguanosine (8-oh-G) contents in M13mp2 DNA before and after sunlight exposure. The content of 8-oh-G increased 3- to 5-fold during a 5 h exposure to sunlight. UVB irradiation using 312 nm light showed a dose-dependent increase in the 8-oh-G contents. Additional experiments suggested that UVA portion of sunlight is also involved. However, the increase in the contents of 8-oh-G was only several-fold over the controls. Therefore, a damaged guanine other than 8-oh-G also may serve as a mutagenic lesion in sunlight mutagenesis.
|
