2007 Fiscal Year Final Research Report Summary
Study for periodontal pathogenesis and apoptosis in periodontal tissues induced by volatile sulfur compounds
| Project/Area Number |
17390568
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Social dentistry
|
|---|
| Research Institution | The Nippon Dental University |
|---|
Principal Investigator |
YAEGAKI Ken The Nippon Dental University, School of Life Dentistry, Professor (40166468)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SATO Tsutomu The Nippon Dental University, School of Life Dentistry, Associate Professor (60130671)
TANAKA Tomoko The Nippon Dental University, School of Life Dentistry, Senior Assistant Professor (70307958)
OGURO Akira Meirin Junior College, Professor (90107780)
MURATA Takatoshi The Nippon Dental University, School of Life Dentistry, Senior Assistant Professor (10313529)
|
|---|
| Project Period (FY) |
2005 – 2007
|
| Keywords | Hydrogen sulfide / Apoptosis / DNA damage / Halitosis / Periodontal Pathogenesis |
|---|
| Research Abstract |
Hydrogen sulfide (H_2S) is one of the main reasons of halitosis and periodontally pathogenic. H_2S causes apoptotic cell death in aorta smooth muscle cells and other tissues, and apoptosis plays an important role in the onset and progress of periodontitis. Therefore, we investigated if H_2S causes apoptosis in human gingival fibroblasts (HGF). Materials and Methods : Necrotic cell were determined using lactate dehydrogenase assay. Apoptosis was ascertained with detecting histone-complexed DNA fragments and a flow cytometry. Caspase 3, a key enzyme in apoptotic signaling, was assessed. Reactive oxygen species (ROS) were also detected and inhibition of superoxide dismutase (SOD) by H_2S was verified. DNA damage was examined with single-cell gel electrophoresis (SCGE). Results : Necrosis was found less than 10% of HGF during 72 hours incubation with 100 ng/ml H_2S, whereas significant increment of DNA fragmentation in cytoplasm was found (p < 0.05). Apoptotic HGF cells were also increased in a flow cytometry. Caspase 3 activity was significantly increased at 72 hours incubation (p < 0.01). Tail length, %DNA in tail and Tail moment obtained by SCGE increased in HGF exposed to H_2S for 48 and 72 hours. Moreover, ROS was significantly increased at 48 and 72 hour incubation with H_2S (p < 0.005 and p < 0.001, respectively), and SOD of HGF was strongly inhibited. Conclusion : H_2S caused apoptosis in HGF, and an inhibition of SOD by H_2S increased ROS, then induced apoptosis and DNA strand breaks.
|
