論文 - 詳細
| RRC ID | 44200 |
|---|---|
| 著者 | Koh T, Machino M, Murakami Y, Umemura N, Sakagami H. |
| タイトル | Cytotoxicity of dental compounds towards human oral squamous cell carcinoma and normal oral cells. |
| ジャーナル | In Vivo |
| Abstract |
AIM:The cytotoxicity of four dental compounds, hydroquinone, benzoquinone, eugenol and phtharal towards human oral squamous cell carcinoma (OSCC) cell lines, normal human oral cells (gingival fibroblast, pulp cell, periodontal ligament fibroblast) and skin keratinocytes was investigated. MATERIALS AND METHODS:Viable cell number was determined by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) method. The concentration that reduced the viable cells by 50% (CC(50)) and the concentration that increased the viability of UV-irradiated cells to 50% (EC(50)) were determined from the dose-response curves. The tumor-specificity index (TS) was determined by the ratio of the mean CC(50) for normal cells to the one for tumor cells. Apoptosis induction was monitored by assay of internucleosomal DNA fragmentation and caspase-3/-7 activation. RESULTS:When both oral OSCC and normal oral cells were incubated for 4 h with any of hydroquinone, benzoquinone, eugenol and phtharal, irreversible cell growth inhibition, accompanied by cell death occurred without induction of apoptotic markers, although caspase-3/-7 activation was observed at 6 h or later. These compounds exhibited very low tumor-specificity (TS=0.4-1.3), as compared with anticancer drugs (5-fluorouracil, melphalan, peplomycin) (TS=4.1-9.7). Human skin keratinocytes were the most resistant to these drugs, and a long incubation time was required to induce irreversible growth inhibition. However, all dental compounds exhibited very low tumor-specificity (TS=0.4-2.4), compared to human skin keratinocytes and OSCC cell lines. None of the dental compounds exhibited any hormetic growth stimulation, nor protected the cells from UV-induced damage. CONCLUSION:These results suggest that apoptosis is not involved in the early stage of growth inhibition induced by dental compounds. |
| 巻・号 | 27(1) |
| ページ | 85-95 |
| 公開日 | 2013-1-1 |
| PII | 27/1/85 |
| PMID | 23239856 |
| MeSH | Apoptosis / drug effects* Benzoquinones / chemistry Benzoquinones / pharmacology Blotting, Western Carcinoma, Squamous Cell / metabolism Carcinoma, Squamous Cell / pathology Caspase 3 / metabolism Caspase 7 / metabolism Cell Line, Tumor Cell Survival / drug effects Cells, Cultured DNA Fragmentation / drug effects* Dose-Response Relationship, Drug Enzyme Activation / drug effects Eugenol / chemistry Eugenol / pharmacology HL-60 Cells Humans Hydroquinones / chemistry Hydroquinones / pharmacology Molecular Structure Mouth / cytology Mouth / metabolism Mouth Neoplasms / metabolism Mouth Neoplasms / pathology Oral Hygiene* Organic Chemicals / chemistry Organic Chemicals / pharmacology* Time Factors |
| IF | 1.541 |
| 引用数 | 6 |
| WOS 分野 | MEDICINE, RESEARCH & EXPERIMENTAL |
| リソース情報 | |
| ヒト・動物細胞 | HL60(RCB0041) |