膳食补充剂表没食子儿茶素没食子酸酯或维生素e会引起体内肿瘤的放射调节反应吗?小鼠乳腺癌的初步研究。

Brian D Lawenda, Donald E Smith, Lei Xu, Andrzej Niemierko, Joshua R Silverstein, Yves Boucher, Satoshi Kashiwagi, Kathryn D Held, Rakesh K Jain, Jay S Loeffler, David M Eisenberg, Jeffrey B Blumberg
{"title":"膳食补充剂表没食子儿茶素没食子酸酯或维生素e会引起体内肿瘤的放射调节反应吗?小鼠乳腺癌的初步研究。","authors":"Brian D Lawenda, Donald E Smith, Lei Xu, Andrzej Niemierko, Joshua R Silverstein, Yves Boucher, Satoshi Kashiwagi, Kathryn D Held, Rakesh K Jain, Jay S Loeffler, David M Eisenberg, Jeffrey B Blumberg","doi":"10.2310/7200.2006.033","DOIUrl":null,"url":null,"abstract":"<p><p>The primary aim of this study was to evaluate a systematic and reproducible assay to examine the potential radiomodifying effects of vitamin E (VE) or epigallocatechin gallate (EGCG), antioxidants commonly consumed by cancer patients as dietary supplements, on tumor control. C3H mice were randomized to a control diet or to the control diet supplemented with VE or EGCG. A tumor control dose 50% (TCD(50)) assay was used to evaluate for a radiomodifying response in stage IV murine cancer (MCa-IV) tumors, implanted in the hindleg of mice, and allowed to grow to 8 mm before receiving a single dose of radiation. The effects of VE and EGCG on intratumoral angiogenesis and apoptosis were evaluated in a group of nonirradiated mice using immunohistochemical staining. Cell proliferation assays were conducted on MCa-IV tumors in vitro. EGCG slowed tumor growth rate by 10%. EGCG and VE slowed tumor regrowth by 24 to 25%. There were no significant differences in TCD(50) values between the groups (control = 73.9 Gy, VE = 77.2 Gy, EGCG = 76.4 Gy); however, normal tissues were protected from late radiation effects (autoamputations) in the VE group. VE and EGCG increased tumor cell apoptosis and decreased tumor cell proliferation but had no effect on microvessel density. In this pilot study, neither VE nor EGCG exerted a significant radiomodifying effect on the MCa-IV tumor. Nonetheless, the suggestion of a small degree of tumor radioprotection by these antioxidant compounds warrants further research. As supplementation with VE radioprotected normal tissue, additional studies on this putative benefit are recommended.</p>","PeriodicalId":87409,"journal":{"name":"Journal of the Society for Integrative Oncology","volume":"5 1","pages":"11-7"},"PeriodicalIF":0.0000,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Do the dietary supplements epigallocatechin gallate or vitamin e cause a radiomodifying response on tumors in vivo? A pilot study with murine breast carcinoma.\",\"authors\":\"Brian D Lawenda, Donald E Smith, Lei Xu, Andrzej Niemierko, Joshua R Silverstein, Yves Boucher, Satoshi Kashiwagi, Kathryn D Held, Rakesh K Jain, Jay S Loeffler, David M Eisenberg, Jeffrey B Blumberg\",\"doi\":\"10.2310/7200.2006.033\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The primary aim of this study was to evaluate a systematic and reproducible assay to examine the potential radiomodifying effects of vitamin E (VE) or epigallocatechin gallate (EGCG), antioxidants commonly consumed by cancer patients as dietary supplements, on tumor control. C3H mice were randomized to a control diet or to the control diet supplemented with VE or EGCG. A tumor control dose 50% (TCD(50)) assay was used to evaluate for a radiomodifying response in stage IV murine cancer (MCa-IV) tumors, implanted in the hindleg of mice, and allowed to grow to 8 mm before receiving a single dose of radiation. The effects of VE and EGCG on intratumoral angiogenesis and apoptosis were evaluated in a group of nonirradiated mice using immunohistochemical staining. Cell proliferation assays were conducted on MCa-IV tumors in vitro. EGCG slowed tumor growth rate by 10%. EGCG and VE slowed tumor regrowth by 24 to 25%. There were no significant differences in TCD(50) values between the groups (control = 73.9 Gy, VE = 77.2 Gy, EGCG = 76.4 Gy); however, normal tissues were protected from late radiation effects (autoamputations) in the VE group. VE and EGCG increased tumor cell apoptosis and decreased tumor cell proliferation but had no effect on microvessel density. In this pilot study, neither VE nor EGCG exerted a significant radiomodifying effect on the MCa-IV tumor. Nonetheless, the suggestion of a small degree of tumor radioprotection by these antioxidant compounds warrants further research. As supplementation with VE radioprotected normal tissue, additional studies on this putative benefit are recommended.</p>\",\"PeriodicalId\":87409,\"journal\":{\"name\":\"Journal of the Society for Integrative Oncology\",\"volume\":\"5 1\",\"pages\":\"11-7\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2007-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of the Society for Integrative Oncology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2310/7200.2006.033\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of the Society for Integrative Oncology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2310/7200.2006.033","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

本研究的主要目的是评估一种系统的、可重复的试验,以检查维生素E (VE)或表没食子儿茶素没食子酸酯(EGCG)的潜在辐射调节作用,这些抗氧化剂通常被癌症患者作为膳食补充剂食用,对肿瘤的控制。将C3H小鼠随机分为对照组和添加VE或EGCG的对照组。肿瘤控制剂量50% (TCD(50))试验用于评估IV期小鼠癌(MCa-IV)肿瘤的放射修饰反应,将其植入小鼠后腿,并在接受单剂量辐射之前允许其生长至8毫米。免疫组化染色法观察VE和EGCG对未辐照小鼠瘤内血管生成和细胞凋亡的影响。体外对MCa-IV肿瘤进行细胞增殖试验。EGCG使肿瘤生长速度减慢10%。EGCG和VE延缓肿瘤再生24 - 25%。TCD(50)值各组间差异无统计学意义(对照组= 73.9 Gy, VE = 77.2 Gy, EGCG = 76.4 Gy);然而,在VE组中,正常组织受到保护,免受后期辐射效应(自动截肢)。VE和EGCG增加肿瘤细胞凋亡,降低肿瘤细胞增殖,但对微血管密度无影响。在这项初步研究中,VE和EGCG对MCa-IV肿瘤都没有明显的放射调节作用。尽管如此,这些抗氧化化合物有一定程度的肿瘤放射防护的建议值得进一步研究。作为VE放射保护正常组织的补充,建议对这种假定的益处进行进一步的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Do the dietary supplements epigallocatechin gallate or vitamin e cause a radiomodifying response on tumors in vivo? A pilot study with murine breast carcinoma.

The primary aim of this study was to evaluate a systematic and reproducible assay to examine the potential radiomodifying effects of vitamin E (VE) or epigallocatechin gallate (EGCG), antioxidants commonly consumed by cancer patients as dietary supplements, on tumor control. C3H mice were randomized to a control diet or to the control diet supplemented with VE or EGCG. A tumor control dose 50% (TCD(50)) assay was used to evaluate for a radiomodifying response in stage IV murine cancer (MCa-IV) tumors, implanted in the hindleg of mice, and allowed to grow to 8 mm before receiving a single dose of radiation. The effects of VE and EGCG on intratumoral angiogenesis and apoptosis were evaluated in a group of nonirradiated mice using immunohistochemical staining. Cell proliferation assays were conducted on MCa-IV tumors in vitro. EGCG slowed tumor growth rate by 10%. EGCG and VE slowed tumor regrowth by 24 to 25%. There were no significant differences in TCD(50) values between the groups (control = 73.9 Gy, VE = 77.2 Gy, EGCG = 76.4 Gy); however, normal tissues were protected from late radiation effects (autoamputations) in the VE group. VE and EGCG increased tumor cell apoptosis and decreased tumor cell proliferation but had no effect on microvessel density. In this pilot study, neither VE nor EGCG exerted a significant radiomodifying effect on the MCa-IV tumor. Nonetheless, the suggestion of a small degree of tumor radioprotection by these antioxidant compounds warrants further research. As supplementation with VE radioprotected normal tissue, additional studies on this putative benefit are recommended.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信