| Project/Area Number |
04670417
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Gastroenterology
|
|---|
| Research Institution | Tokyo Medical & Dental University |
|---|
Principal Investigator |
MIYAKAWA Hatsupei Tokyo Medical & Dental University Dept.of Medicine, Assistant, 医学部, 助手 (20219728)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
MIYAKAWA Hatsupei Tokyo Medical & Dental University Dept.of Medicine, Assistant (20219728)
|
|---|
| Project Period (FY) |
1992 – 1993
|
| Project Status |
Completed (Fiscal Year 1993)
|
| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1993: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1992: ¥1,000,000 (Direct Cost: ¥1,000,000)
|
|---|
| Keywords | free radical / 8-hydroxydeoxyguanosine / iron / 6メチルグアニンメチルトランスフェラーゼ / 慢性鉄負荷 / 肝発癌 |
|---|
| Research Abstract |
C-8 position of guanine residue in DNA is hydroxyrated to produce 8-hydroxydeoxyguanosine(8-OHdG) in vitro by various radical producing agents. The 8-OHdG residue in DNA may cause mutagenesis and/or carcinogenesis, since 8-OHdG induce misleading during DNA synthesis. To investigate whether 8-OHdG increase in iron overloaded rat, we fed rat with 3.0%(w/wt) carbonyl iron for 4 weeks. Liver DNA was separated and 8-OHdG was assayd by HPLC using electrochemical detector. We found that 8-OHdG was significanly increased in iron overloaded rat, on the other hand, only a small peak could be detected in the control rat. These result suggested that hydroxyradical formation was increased through Fenton reaction in iron overload status, which cause 8-OHdG formation in the liver. The increase of hepatic 8-OHdG in iron overloaded status may explain the higher incidence of hepatocellular carcinoma in hemochromatosis than those of other etiologies.
|
