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| 題名: | Oral administration of 5-methoxypsoralen affects the distribution and metabolism of 2-aminofluorene in Sprague-Dawley rats |
| 作者: | Lee, YM;Chen, SF;Li, YC;Lin, SS;Chung, JG |
| 貢獻者: | 醫學院醫學系微生物學科;China Med Coll, Dept Microbiol, Taichung 400, Taiwan;Chungtai Inst Hlth Sci & Technol, Dept Med Technol, Taichung 406, Taiwan;China Jr Coll Med Technol, Dept Med Technol, Tainan 701, Taiwan;Chungtai Inst Hlth Sci & Technol, Dept Radiol Technol, Taichung 406, Taiwan |
| 日期: | 2002 |
| 上傳時間: | 2010-09-24 15:01:09 (UTC+8) |
| 出版者: | INT INST ANTICANCER RESEARCH |
| 摘要: | Humic acid (HA) has been implicated as an etiologic factor in the vasculopathy of Blackfoot disease. In this study, the ability of HA to induce apoptosis was studied in cultured human umbilical vein endothelial cells. Treatment of endothelial cells with a variety of concentrations of HA (50-200 mug/ml) resulted in dose- and time-dependent sequences of events marked by apoptosis as shown by loss of cell viability, chromatin condensation, and internucleosomal DNA fragmentation. Antioxidants (superoxide dismutase, vitamin C, and vitamin E) and Ca2+ chelator (BAPTA) effectively suppressed HA-induced DNA fragmentation (apoptosis). Further studies have shown that HA induced dramatic Ca2+-dependent caspase activation (2, 3, 6, 8, and 9). In contrast, negligible caspase-1 activation was observed. The increase in HA-induced apoptosis correlated with a reduction in Bcl-2, a potent cell death inhibitor, and an increase in Bax protein levels, which heterodimerizes with and thereby inhibits Bcl-2. Both of the antioxidants vitamin C and vitamin E prevented the dysregulation of Bcl-2 and Bax in HA-treated endothelial cells. Furthermore, the increase in p53 protein levels correlated with an increase in HA-induced apoptosis. We concluded that both Ca2+ and oxidative stress were mediators of apoptosis caused by HA and the induction of apoptotic cell death on endothelial cells may be important to the etiology of HA-induced vascular disorder of Blackfoot disease. 0 2002 Elsevier Science (USA). |
| 關聯: | IN VIVO 16(3):201-213 |
| 顯示於類別: | [醫學系] 期刊論文
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