(34.204.201.220) 您好!臺灣時間:2021/04/19 18:18
字體大小: 字級放大   字級縮小   預設字形  
回查詢結果

詳目顯示:::

我願授權國圖
: 
twitterline
研究生:黃興強
研究生(外文):Hsing-Chiang Huang
論文名稱:粒線體基因突變及氧化傷害與子宮內膜異位症相關性之研究
論文名稱(外文):Mitochondrial DNA mutations and oxidative damages in endometriosis
指導教授:高淑慧高淑慧引用關係
指導教授(外文):Shu-Huei Kao, Ph. D.
學位類別:碩士
校院名稱:臺北醫學大學
系所名稱:生物醫學技術研究所
學門:醫藥衛生學門
學類:醫學技術及檢驗學類
論文種類:學術論文
論文出版年:2003
畢業學年度:91
語文別:中文
論文頁數:95
中文關鍵詞:子宮內膜異位症粒線體基因
外文關鍵詞:EndometriosisMitochondrial DNA
相關次數:
  • 被引用被引用:0
  • 點閱點閱:118
  • 評分評分:系統版面圖檔系統版面圖檔系統版面圖檔系統版面圖檔系統版面圖檔
  • 下載下載:0
  • 收藏至我的研究室書目清單書目收藏:0
根據資料顯示婦女罹患子宮內膜異位症的發生率愈來愈高,其發生率約佔婦女人口的15﹪~50﹪。依據研究顯示,子宮內膜異位症常為女性不孕的主要原因,大約有50﹪的不孕婦女患有此一疾病。所謂子宮內膜異位症是子宮內膜上皮細胞及腺體生長於子宮以外的部位。迄今,對於子宮異位性內膜症的致病機轉及成因尚未清楚。許多學者認為子宮內膜異位症與氧化壓力(oxidative stress)有關,在異位的組織受到發炎反應影響而有較高的氧化壓力,使oxidatively modified complexes增加,並產生氧化性傷害(oxidative damage)。此外,在免疫系統上,經由cytokine及chemokine活化巨噬細胞macrophage也會造成發炎反應及增加氧化性傷害。我們的研究證明在子宮內膜異位症患者的病灶處的檢體中,檢測出高含量的氧化性傷害物質,如8-OH-deoxyguanosine (8-OHdG)及脂質過氧化物(lipoperoxide)及粒線體DNA突變(mitochondrial DNA mutation)的堆積。尤其於巧克力囊腫(chocolate cyst)的組織中,檢測出遠高於正常值5.5倍的8-OHdG含量。正常人週邊血球為1.66 ± 0.02, chocolate cyst group則為9.12 ± 3.22 8-OHdG/10-5dG。並且檢測出6.2倍的lipoperoxide含量增加。正常人週邊血球值為0.18±0.02 pmol/μg protein, chocolate cyst group為1.66±0.80 pmol/μg protein。此外,於病灶處標本中檢測出4977 bp, 7599 bp及兩種新的粒線體基因斷損突變(5335 bp及5756 bp 斷損)。此新的斷損突變經DNA序列分析,於5355 bp deletion其斷損位置為nucleotide position (np) 8273至np13607,斷損兩側有5’-CCTATAGCAC-3’的direct repeat。於5756 bpdeletion斷損位置為np 8065至np13820,斷損兩側有5’-CTT-3’的direct repeat。異位組織其斷損突變的發生(frequency) 為41﹪,29﹪及55﹪(n=23,16及31)。巧克力囊腫及子宮腺肌瘤的8-OHdG氧化性傷害與mtDNA deletion呈正相關性,MDA與mtDNA mutation則無明顯相關性。此外,我們分析glutathione-S-transferase M1 (GSTM1) 和catechol-O-methyltransferase (COMT) gene的基因多型性與子宮內膜異位症之間氧化性傷害的關係。患有子宮內膜異位症婦女中有48.6﹪(n=18)為GSTM1 null type。統計後,發現子宮內膜異位症與GSTM1 null type並無明顯相關性。而患有子宮內膜異位症婦女的COMT polymorphism分別為GG (43%), AG (43%), 及AA (14%) 。非子宮內膜異位症者的基因多型性則為GG (78%), AG (22%), 及AA (0%)。此種低活性COMTLL僅於患有子宮內膜異位症婦女發現。根據實驗結果顯示,子宮內膜異位組織中存在著高量的氧化傷害,及粒線體DNA的斷損突變,我們確認氧化性傷害確實與子宮內膜異位症的形成有關,而氧化性壓力的來源及粒線體功能的缺損與子宮內膜異位症的形成機轉需進一步探討,以期能提供更有效的療程。
Endometriosis, one of frequent diseases in gynecology, is a considerable threat to the physical, psychological and social integrity of women. Moreover, up to 50% of infertile patients have this disease .The etiology and pathogenesis of this important disease, defined as the ectopic location of the endometrium-like glandular epithelium and stroma outside the uterine cavity, is poorly understood. To date, however, little is known about the pathogenesis of endometriosis. It still remains an open question as to what extent the factors influences the establishment and/or progression of endometriosis. As a result of such a stress, a sterile, inflammatory reaction with secretion of growth factors, cytokines, and chemokines is generated, which is deleterious especially to successful reproduction. In this study, the significantly higher amounts of oxidative damages were detected in endometriotic lesions than in controlled normal endometrium such as the mitochondrial DNA rearrangement, 8-OH deoxyguanosine (8-OHdG), and lipoperoxide contents. Our central hypothesis proposes that oxidative damages might be anticipated in the pathogensis of endometriosis. The study was conducted to investigate mtDNA mutation and oxidative damage in endometriotic tissue of women with endometriosis. Large-scale deletion of mtDNA were detected and occurred at a high frequency in the endometriotic tissue. We detected four types of mtDNA deletions in the endometriotic tissue such as 4977 bp. 7599 bp, and two novel deletions (5335 bp and 5756 bp). Using primer-shift PCR and DNA sequencing, we identified and characterized mutiple deletions of mtDNA in the endometriotic tissue. The 5335 bp deletion, which occurred between nucleotide position (np) 8,273 and np 13,607, was flanked by a 10-bp direct repeat of 5’-CCTATAGCAC-3’. The 5756 bp deletion, which occurred between np 8,065 and np 13,820, was flanked by a 3-bp direct repeat of 5’-CTT-3’. The propotion of mtDNA was found to correlate positively with of the 8-OHdG. The amount of 8-OHdG in chocolate cyst was significantly higher than the control group (9.12 ± 3.22 vs 1.65 ± 0.02 8-OHdG/10-5dG). Moreover, we found that average contents of lipoperoxide in chocolate cyst were higher than the control group (1.14±0.68 vs 0.18±0.02 pmol/μg protein). Furthermore, we examined glutathione S-transferase M1 (GSTM1) and catechol-O- methyltransferase (COMT) gene polymorphism. The frequencies of GSTM1 null genotype were 48.6% and 55.6% for women with or without endometriosis, respectively. We found the higher contents of 8-OHdG and MDA were detected in the tissue with GSTM1 null type. The frequencies of COMT genotype COMTHH, COMTHL, COMTLL were 43%, 43%, and 14% in the endometriotic tissue. On the other hand, the frequency were and 78%, 22% and 0% in women without endometriosis. The frequency of lowly active COMTLL was increased in the chocolate cyst. GSTM1 null type and COMT activity may predisposes to increased oxidative damages to the women with endometriosis. According to these finding, we suggest that endometriosis leads to mtDNA mutations together with oxidative damage to DNA and lipids.
表目錄 II
圖目錄 III
縮寫表 V
中文摘要 VII
Abstract X
壹、緒論 1
子宮內膜異位症(endometriosis) 1
致病學說(Theories of endometriosis) 2
氧化傷害(Oxidative damage) 6
粒線體及粒線體基因突變 6
Glutathione-S-tansferase M1 9
Catechol-O-methyltransferase (COMT) 10
貳、實驗材料與方法 30
叁、結果 30
肆、討論 30
伍、文獻參考 76
Anderson, S., Bankier, A.T., Barrell, B.G., de Bruijn, M.H., Coulson, A.R., Drouin, J., Eperon, I.C., Nierlich, D.P., Roe, B.A., Sanger, F., Schreier, P.H., Smith, A.J., Staden, R. and Young, I.G. (1981) Sequence and organization of the human mitochondrial genome. Nature, 290, 457-65.
Arvanitis, D.A., Koumantakis, G.E., Goumenou, A.G., Matalliotakis, I.M., Koumantakis, E.E. and Spandidos, D.A. (2003) CYP1A1, CYP19, and GSTM1 polymorphisms increase the risk of endometriosis. Fertil Steril, 79 Suppl 1, 702-9.
Ayres S, Abplanalp W, Liu JH, Subbiah MT. 1998) Mechanisms involved in the protective effect of estradiol-17beta on lipid peroxidation and DNA damage Am J Physiol. 274, E1002-8..
Ball, P. and Knuppen, R. (1980) Catecholoestrogens (2-and 4 hydroxyoestrogens): chemistry, biogenesis, metabolism, occurrence and physiological significance. Acta Endocrinol. Suppl. (Copenh), 232, 1-127.
Baranova, H., Bothorishvilli, R., Canis, M., Albuisson, E., Perriot, S., Glowaczower, E., Bruhat, M.A., Baranov, V. and Malet, P. (1997) Glutathione S-transferase M1 gene polymorphism and susceptibility to endometriosis in a French population. Mol Hum Reprod, 3, 775-80.
Baranova, H., Canis, M., Ivaschenko, T., Albuisson, E., Bothorishvilli, R., Baranov, V., Malet, P. and Bruhat, M.A. (1999) Possible involvement of arylamine N-acetyltransferase 2, glutathione S- transferases M1 and T1 genes in the development of endometriosis. Mol Hum Reprod, 5, 636-41.
Baxter, S.W., Thomas, E.J. and Campbell, I.G. (2001) GSTM1 null polymorphism and susceptibility to endometriosis and ovarian cancer. Carcinogenesis, 22, 63-5.
Bizebard, T., Gigant, B., Rigolet, P., Rasmussen, B., Diat, O., Bosecke, P., Wharton, S.A., Skehel, J.J. and Knossow, M. (1995) Structure of influenza virus haemagglutinin complexed with a neutralizing antibody. Nature, 376, 92-4.
Boudikova, B., Szumlanski, C., Maidak, B. and Weinshilboum, R. (1990) Human liver catechol-O-methyltransferase pharmacogenetics. Clin Pharmacol Ther, 48, 381-9.
Brockmoller, J., Kerb, R., Drakoulis, N., Nitz, M. and Roots, I. (1993) Genotype and phenotype of glutathione S-transferase class mu isoenzymes mu and psi in lung cancer patients and controls. Cancer Res, 53, 1004-11.
Bulun, S.E., Zeitoun KM, Takayama K, Sasano H. (2000a) Estrogen biosynthesis in endometriosis: molecular basis and clinical relevance. J Mol Endocrinol , 25, 35-42.
Bulun, S.E., Zeitoun, K.M. and Kilic, G. (2000b) Expression of dioxin-related transactivating factors and target genes in human eutopic endometrial and endometriotic tissues. Am J Obstet Gynecol, 182, 767-75.
Burdon, R.H. (1995) Superoxide and hydrogen peroxide in relation to mammalian cell proliferation. Free Radic Biol Med, 18, 775-94.
Cavalieri, E.L., Stack, D.E., Devanesan, P.D., Todorovic, R., Dwivedy, I., Higginbotham, S., Johansson, S.L., Patil, K.D., Gross, M.L., Gooden, J.K. et al. (1997) Molecular origin of cancer: catechol estrogen-3,4-quinones as endogenous tumor initiators. Proc. Natl Acad. Sci., 94, 10937-10942.
Carter, J.E. (1994) Combined hysteroscopic and laparoscopic findings in patients with chronic pelvic pain. J Am Assoc Gynecol Laparosc, 2, 43-7.
Chakraborty, C., Huet-Hudson, Y.M. and Dey, S.K. (1990) Catecholoestrogen synthesis and metabolism in the rabbit uterus during the periimplantation period. J Steroid Biochem, 35, 39-46.
Chance, B., Sies, H. and Boveris, A. (1979) Hydroperoxide metabolism in mammalian organs. Physiol Rev, 59, 527-605.
Chen, S.S., Chang, L.S., Chen, H.W. and Wei, Y.H. (2002) Polymorphisms of glutathione S-transferase M1 and male infertility in Taiwanese patients with varicocele. Hum Reprod, 17, 718-25.
Cullen, T.S., (1896) Adenomyoma of the round ligament Bull Johns Hopkins Hosp 7, 112
Cushman, M., He, H.M., Katzenellenbogen, J.A., Lin, C.M. and Hamel, E. (1995) Synthesis, antitubulin and antimitotic activity, and cytotoxicity of analogs of 2-methoxyestradiol, an endogenous mammalian metabolite of estradiol that inhibits tubulin polymerization by binding to the colchicine binding site. J Med Chem, 38, 2041-9.
Dawling, S., Roodi, N., Mernaugh, R.L., Wang, X. and Parl, F.F. (2001) Catechol-O-methyltransferase (COMT)-mediated metabolism of catechol estrogens: comparison of wild-type and variant COMT isoforms. Cancer Res, 61, 6716-22.
De Leon FD, Vijayakumar R, Brown M, Rao CV, Yussman MA, Schultz G. (1986) Peritoneal fluid volume, estrogen, progesterone, prostaglandin, and epidermal growth factor concentrations in patients with and without endometriosis. Obstet Gynecol. 68, 189-94
Doty, D.W., Gruber, J.S., Wolf, G.C. and Winslow, R.C. (1980) 46,XY pure gonadal dysgenesis: report of 2 unusual cases. Obstet Gynecol, 55, 61S-65S.
El Mahgoud, S.; Yaseen, S., (1980) A positive proof for the theory of coelomic metaplasia Am J Obstet Gynecol 137. 137-140
Espey, L.L. (1980) Ovulation as an inflammatory reaction--a hypothesis. Biol Reprod, 22, 73-106.
Gonzalez, F.J. and Nebert, D.W. (1990) Evolution of the P450 gene superfamily: animal-plant ''warfare'', molecular drive and human genetic differences in drug oxidation. Trends Genet, 6, 182-6.
Halme, J., Hammond, M.G., Hulka, J.F., Raj, S.G. and Talbert, L.M. (1984) Retrograde menstruation in healthy women and in patients with endometriosis. Obstet Gynecol, 64, 151-4.
Harada T, Enatsu A, Mitsunari M, Nagano Y, Ito M, Tsudo T, Taniguchi F, Iwabe T, Tanikawa M, Terakawa N. (1999) Role of cytokines in progression of endometriosis. Gynecol Obstet Invest, 47 Suppl 1, 34-40.
Hattori, K., Tanaka, M., Sugiyama, S., Obayashi, T., Ito, T., Satake, T., Hanaki, Y., Asai, J., Nagano, M. and Ozawa, T. (1991) Age-dependent increase in deleted mitochondrial DNA in the human heart: possible contributory factor to presbycardia. Am Heart J, 121, 1735-42.
Hippeli, S. and Elstner, E.F. (1999) Transition metal ion-catalyzed oxygen activation during pathogenic processes. FEBS Lett, 443, 1-7.
Hoffman, E.C., Reyes, H., Chu, F.F., Sander, F., Conley, L.H., Brooks, B.A. and Hankinson, O. (1991) Cloning of a factor required for activity of the Ah (dioxin) receptor. Science, 252, 954-8.
Holt, I.J., Harding, A.E., Cooper, J.M., Schapira, A.H., Toscano, A., Clark, J.B. and Morgan-Hughes, J.A. (1989) Mitochondrial myopathies: clinical and biochemical features of 30 patients with major deletions of muscle mitochondrial DNA. Ann Neurol, 26, 699-708.
Holt, I.J., Harding, A.E. and Morgan-Hughes, J.A. (1988) Deletions of muscle mitochondrial DNA in patients with mitochondrial myopathies. Nature, 331, 717-9.
Hoshiai, H., Ishikawa, M., Sawatari, Y., Noda, K. and Fukaya, T. (1993) Laparoscopic evaluation of the onset and progression of endometriosis. Am J Obstet Gynecol, 169, 714-9.
Huh K, Shin US, Choi JW, Lee SI. (1994) Effect of sex hormones on lipid peroxidation in rat liver. Arch Pharm Res.17, 109-14.
Iwabe, T., Harada, T., Tsudo, T., Nagano, Y., Yoshida, S., Tanikawa, M. and Terakawa, N. (2000) Tumor necrosis factor-alpha promotes proliferation of endometriotic stromal cells by inducing interleukin-8 gene and protein expression. J Clin Endocrinol Metab, 85, 824-9.
Kao, S.H., Chao, H.T. and Wei, Y.H. (1998) Multiple deletions of mitochondrial DNA are associated with the decline of motility and fertility of human spermatozoa. Mol Hum Reprod, 4, 657-66.
Kelly, R.W. and Abel, M.H. (1981) A comparison of the effects of 4-catechol oestrogens and 2-pyrogallol oestrogens on prostaglandin synthesis by the rat and human uterus. J Steroid Biochem, 14, 787-91.
Kirshon, B. and Poindexter, A.N., 3rd. (1988) Contraception: a risk factor for endometriosis. Obstet Gynecol, 71, 829-31.
Kitawaki J, Kado N, Ishihara H, Koshiba H, Kitaoka Y, Honjo H. (2002) Endometriosis: the pathophysiology as an estrogen-dependent disease J Steroid Biochem Mol Biol. 83,149-55.
Klauber, N., Parangi, S., Flynn, E., Hamel, E. and D''Amato, R.J. (1997) Inhibition of angiogenesis and breast cancer in mice by the microtubule inhibitors 2-methoxyestradiol and taxol. Cancer Res, 57, 81-6.
Kogelnik, A.M., Lott, M.T., Brown, M.D., Navathe, S.B. and Wallace, D.C. (1998) MITOMAP: a human mitochondrial genome database--1998 update. Nucleic Acids Res, 26, 112-5.
Lavigne, J.A., Helzlsouer, K.J., Huang, H.Y., Strickland, P.T., Bell, D.A., Selmin, O., Watson, M.A., Hoffman, S., Comstock, G.W. and Yager, J.D. (1997) An association between the allele coding for a low activity variant of catechol-O-methyltransferase and the risk for breast cancer. Cancer Res, 57, 5493-7.
Lavigne, J.A., Goodman, J.E., Fonong, T., Odwin, S., He, P., Roberts, D.W. and Yager, J.D. (2001) The effects of catechol-O-methyltransferase inhibition on estrogen metabolite and oxidative DNA damage levels in estradiol-treated MCF-7 cells. Cancer Res., 61, 7488-7494.
Lee, H.C. and Wei, Y.H. (1997) Mutation and oxidative damage of mitochondrial DNA and defective turnover of mitochondria in human aging. J Formos Med Assoc, 96, 770-8.
Lestienne, P., Bataille, N. and Lucas-Heron, B. (1995) Role of the mitochondrial DNA and calmitine in myopathies. Biochim Biophys Acta, 1271, 159-63.
Mannervik, B., Awasthi, Y.C., Board, P.G., Hayes, J.D., Di Ilio, C., Ketterer, B., Listowsky, I., Morgenstern, R., Muramatsu, M., Pearson, W.R. and et al. (1992) Nomenclature for human glutathione transferases. Biochem J, 282, 305-6.
Mannisto, P.T. and Kaakkola, S. (1999) Catechol-O-methyltransferase (COMT): biochemistry, molecular biology, pharmacology, and clinical efficacy of the new selective COMT inhibitors. Pharmacol Rev, 51, 593-628.
Martin, J.D., Jr. and Hauck, A.E. (1985) Endometriosis in the male. Am Surg, 51, 426-30.
Martucci, C.P. and Fishman, J. (1993) P450 enzymes of estrogen metabolism. Pharmacol. Ther., 57, 237-257.
Merriam, G.R., MacLusky, N.J., Johnson, L.A. and Naftolin, F. (1980) 2-hydroxyestradiol-17 alpha and 4-hydroxyestradiol-17 alpha, catechol estrogen analogs with reduced estrogen receptor affinity. Steroids, 36, 13-20.
Merrill, J.A. (1966) Endometrial induction of endometriosis across Millipore filters. Am J Obstet Gynecol, 94, 780-90.
Meyer, R., (1903) Uber eine adenomatose Wuchenrung der Serosa in einer Bauchnarbe Z Geburtsh Gynakol 49. 32-41
Mita, S., Rizzuto, R., Moraes, C.T., Shanske, S., Arnaudo, E., Fabrizi, G.M., Koga, Y., DiMauro, S. and Schon, E.A. (1990) Recombination via flanking direct repeats is a major cause of large- scale deletions of human mitochondrial DNA. Nucleic Acids Res, 18, 561-7.
Mitrunen, K., Kataja, V., Eskelinen, M., Kosma, V.M., Kang, D., Benhamou, S., Vainio, H., Uusitupa, M. and Hirvonen, A. (2002) Combined COMT and GST genotypes and hormone replacement therapy associated breast cancer risk. Pharmacogenetics, 12, 67-72.
Murphy, A.A., Palinski, W., Rankin, S., Morales, A.J. and Parthasarathy, S. (1998a) Evidence for oxidatively modified lipid-protein complexes in endometrium and endometriosis. Fertil Steril, 69, 1092-4.
Murphy, A.A., Santanam, N. and Parthasarathy, S. (1998b) Endometriosis: a disease of oxidative stress? Semin Reprod Endocrinol, 16, 263-73.
Ota, H., Igarashi, S., Hatazawa, J. and Tanaka, T. (1998) Endothelial nitric oxide synthase in the endometrium during the menstrual cycle in patients with endometriosis and adenomyosis. Fertil Steril, 69, 303-8.
Ota, H., Igarashi, S., Hatazawa, J. and Tanaka, T. (1999) Immunohistochemical assessment of superoxide dismutase expression in the endometrium in endometriosis and adenomyosis. Fertil Steril, 72, 129-34.
Ota, H., Igarashi, S., Kato, N. and Tanaka, T. (2000) Aberrant expression of glutathione peroxidase in eutopic and ectopic endometrium in endometriosis and adenomyosis. Fertil Steril, 74, 313-8.
Ota, H., Igarashi, S. and Tanaka, T. (2001) Xanthine oxidase in eutopic and ectopic endometrium in endometriosis and adenomyosis. Fertil Steril, 75, 785-90.
Paria, B.C., Lim, H., Wang, X.N., Liehr, J., Das, S.K. and Dey, S.K. (1998) Coordination of differential effects of primary estrogen and catecholestrogen on two distinct targets mediates embryo implantation in the mouse. Endocrinology, 139, 5235-46.
Peng, D.X., He, Y.L., Qiu, L.W., Yang, F. and Lin, J.M. (2003) Association between glutathione S-transferase M1 gene deletion and genetic susceptibility to endometriosis. Di Yi Jun Yi Da Xue Xue Bao, 23, 458-9.
Portz, D.M., Elkins, T.E., White, R., Warren, J., Adadevoh, S. and Randolph, J. (1991) Oxygen free radicals and pelvic adhesion formation: I. Blocking oxygen free radical toxicity to prevent adhesion formation in an endometriosis model. Int J Fertil, 36, 39-42.
Poulton, J., Deadman, M.E., Bindoff, L., Morten, K., Land, J. and Brown, G. (1993) Families of mtDNA re-arrangements can be detected in patients with mtDNA deletions: duplications may be a transient intermediate form. Hum Mol Genet, 2, 23-30.
Poyton, R.O. and McEwen, J.E. (1996) Crosstalk between nuclear and mitochondrial genomes. Annu Rev Biochem, 65, 563-607.
Prentice, A. (2001) Regular review: Endometriosis. Bmj, 323, 93-5.
Rier, S. and Foster, W.G. (2002) Environmental dioxins and endometriosis. Toxicol Sci, 70, 161-70.
Rier, S.E., Martin, D.C., Bowman, R.E. and Becker, J.L. (1995) Immunoresponsiveness in endometriosis: implications of estrogenic toxicants. Environ Health Perspect, 103 Suppl 7, 151-6.
Sampson, J.A., (1927) Peritoneal endometriosis due to menstrual dissemination of endometrial tissue into the peritoneal cavity Am J Obstet Gynecol 14, 422-469
Sampson JA., The development of the the implantation theory for the origin of peritoneal endometriosis. Am J Obstet Gynecol, 1940. 40:. 549.
Santanam, N., Murphy, A.A. and Parthasarathy, S. (2002) Macrophages, oxidation, and endometriosis. Ann N Y Acad Sci, 955, 183-98; discussion 19-200, 396-406.
Sastre, J., Pallardo, F.V., Garcia de la Asuncion, J. and Vina, J. (2000) Mitochondria, oxidative stress and aging. Free Radic Res, 32, 189-98.
Sawada, M. and Carlson, J.C. (1987) Changes in superoxide radical and lipid peroxide formation in the brain, heart and liver during the lifetime of the rat. Mech Ageing Dev, 41, 125-37.
Seli E, Berkkanoglu M, Arici A. (2003) Pathogenesis of endometriosis. Obstet Gynecol Clin North Am., 30, 41-61. Review.
Shanti, A., Santanam, N., Morales, A.J., Parthasarathy, S. and Murphy, A.A. (1999) Autoantibodies to markers of oxidative stress are elevated in women with endometriosis. Fertil Steril, 71, 1115-8.
Shearman, C.W. and Kalf, G.F. (1977) DNA replication by a membrane-DNA complex from rat liver mitochondria. Arch Biochem Biophys, 182, 573-86.
Shoffner, J.M., Lott, M.T., Voljavec, A.S., Soueidan, S.A., Costigan, D.A. and Wallace, D.C. (1989) Spontaneous Kearns-Sayre/chronic external ophthalmoplegia plus syndrome associated with a mitochondrial DNA deletion: a slip-replication model and metabolic therapy. Proc Natl Acad Sci U S A, 86, 7952-6.
Smith, G., Stanley, L.A., Sim, E., Strange, R.C. and Wolf, C.R. (1995) Metabolic polymorphisms and cancer susceptibility. Cancer Surv, 25, 27-65.
Strange RC, Spiteri MA, Ramachandran S, Fryer AA. (2001) Glutathione-S-transferase family of enzymes. Mutat Res. 482, 21-6.
Starzinski-Powitz, A., Handrow-Metzmacher, H. and Kotzian, S. (1999) The putative role of cell adhesion molecules in endometriosis: can we learn from tumour metastasis? Mol Med Today, 5, 304-9.
Tabibzadeh, S., (1992) Patterns of expression of integrin molecules in human endometrium throughout the menstrual cycle Hum Reprod 7. 876-882
Thompson, P.A., Shields, P.G., Freudenheim, J.L., Stone, A., Vena, J.E., Marshall, J.R., Graham, S., Laughlin, R., Nemoto, T., Kadlubar, F.F. and Ambrosone, C.B. (1998) Genetic polymorphisms in catechol-O-methyltransferase, menopausal status, and breast cancer risk. Cancer Res, 58, 2107-10.
Van Langendonckt, A., Casanas-Roux, F. and Donnez, J. (2002) Oxidative stress and peritoneal endometriosis. Fertil Steril, 77, 861-70.
Vinatier, D., Cosson, M. and Dufour, P. (2000) Is endometriosis an endometrial disease? Eur J Obstet Gynecol Reprod Biol, 91, 113-25.
Wang, Y., Sharma, R.K., Falcone, T., Goldberg, J. and Agarwal, A. (1997) Importance of reactive oxygen species in the peritoneal fluid of women with endometriosis or idiopathic infertility. Fertil Steril, 68, 826-30.
Wei, Q., Cheng, L., Hong, W.K. and Spitz, M.R. (1996) Reduced DNA repair capacity in lung cancer patients. Cancer Res, 56, 4103-7.
Wei, Y.H. (1998) Oxidative stress and mitochondrial DNA mutations in human aging. Proc Soc Exp Biol Med, 217, 53-63.
Weinshilboum, R.M. and Raymond, F.A. (1977) Inheritance of low erythrocyte catechol-o-methyltransferase activity in man. Am J Hum Genet, 29, 125-35.
Wheeler, J.M. (1989) Epidemiology of endometriosis-associated infertility. J Reprod Med, 34, 41-6.
Wieser F, Wenzl R, Tempfer C, Worda C, Huber J, Schneeberger C. (2002) Catechol-O-Methyltransferase Polymorphism and Endometriosis, J Assist Reprod Gene., 19, 343-8
Wong SH, Knight JA, Hopfer SM, Zaharia O, Leach CN Jr, Sunderman FW Jr. (1987) Lipoperoxides in plasma as measured by liquid-chromatographic separation of malondialdehyde-thiobarbituric acid adduct. Clin Chem. 32, 214-20
Worda, C., Sator, M.O., Schneeberger, C., Jantschev, T., Ferlitsch, K. and Huber, J.C. (2003) Influence of the catechol-O-methyltransferase (COMT) codon 158 polymorphism on estrogen levels in women. Hum Reprod, 18, 262-6.
Yager JD, Liehr JG. (1996) Molecular mechanisms of estrogen carcinogenesis. : Annu Rev Pharmacol Toxicol, 36, 203-32
Yen, T.C., Su, J.H., King, K.L. and Wei, Y.H. (1991) Ageing-associated 5 kb deletion in human liver mitochondrial DNA. Biochem Biophys Res Commun, 178, 124-31.
Zeitoun K, Takayama K, Sasano H, Suzuki T, Moghrabi N, Andersson S, Johns A, Meng L, Putman M, Carr B, Bulun SE. (1998) Deficient 17beta-hydroxysteroid dehydrogenase type 2 expression in endometriosis: failure to metabolize 17beta-estradiol J Clin Endocrinol Metab, 83, 4474-80
Zeller, J.M., Henig, I., Radwanska, E. and Dmowski, W.P. (1987) Enhancement of human monocyte and peritoneal macrophage chemiluminescence activities in women with endometriosis. Am J Reprod Immunol Microbiol, 13, 78-82.
Zeviani, M., Moraes, C.T., DiMauro, S., Nakase, H., Bonilla, E., Schon, E.A. and Rowland, L.P. (1988) Deletions of mitochondrial DNA in Kearns-Sayre syndrome. Neurology, 38, 1339-46.
Zhu, X.D., Bonet, B. and Knopp, R.H. (1997) 17beta-Estradiol, progesterone, and testosterone inversely modulate low- density lipoprotein oxidation and cytotoxicity in cultured placental trophoblast and macrophages. Am J Obstet Gynecol, 177, 196-209.
QRCODE
 
 
 
 
 
                                                                                                                                                                                                                                                                                                                                                                                                               
第一頁 上一頁 下一頁 最後一頁 top
系統版面圖檔 系統版面圖檔