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    Title: Effects of tannic acid and its related compounds on food mutagens or hydrogen peroxide-induced DNA strands breaks in human lymphocytes
    Authors: Wu, LT;Chu, CC;Chung, JG;Chen, CH;Hsu, LS;Liu, JK;Chen, SC
    Contributors: 醫學院醫研所;China Med Univ, Inst Med, Taichung, Taiwan;Natl Sun Yat Sen Univ, Dept Biol Sci, Kaohsiung 80424, Taiwan;Fooyin Univ, Dept Med Technol, Kaohsiung, Taiwan;Chung Shan Med Univ, Inst Biochem, Taichung, Taiwan
    Date: 2004
    Issue Date: 2010-09-24 14:52:40 (UTC+8)
    Publisher: ELSEVIER SCIENCE BV
    Abstract: Estrogen plays a role in the pathogenesis of endometriosis. The CYP17 gene codes for the cytochrome P450cl7alpha enzyme that is involved in the estrogen biosynthesis. We aimed to investigate if CYP 17 polymorphism could be used as marker to predict the susceptibility of endometriosis. Women were divided into two groups: (1) severe endometriosis (n= 119); (2) non-endometriosis groups (n=1 28). A 169-bp fragment encompassing the T/C polymorphic site in 5'-untranslated promoter region (5'-UTR) of the CYP17 was amplified by the polymerase chain reaction, treated with restriction enzyme MspA1I, and electrophoresis. The polymorphism was divided into restriction- enzyme indigestible (T homozygote), T/C heterozygote, and digestible (C homozygote). Genotypes and allelic frequencies for this polymorphism in both groups were compared. We observed a higher but non-significant percentage of T homozygote in the endometriosis women compared with the non-endometriosis women. Proportions of T homozygote/heterozygote/C homozygote for CYP17 in both groups were: (1) 26.1/46.2/27.7% and (2) 17.2/45.3/37.5% (p- value=0.13 1). T allele was related with higher susceptibility of endometriosis. T and C allele frequencies in both groups were: (1) 49.2/50.8%; (2) 39.8/60.2% (p- value=0.046). Despite the CYP17* T allele Appearing to be asscoiated with a trend of increased risk of endometriosis, CYP17 5'-UTR gene polymorphism might not be a useful marker for prediction of endometriosis susceptibility.
    Relation: MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS 556(1月2日):75-82
    Appears in Collections:[Graduate Institute of Medical Science] Journal articles

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