美國研究人員8月4日在新一期美國《國家科學(xué)院院刊》（PNAS）上發(fā)表論文指出,，給患有癌癥的實(shí)驗(yàn)鼠注射大劑量的維生素C,，可以明顯減緩腫瘤生長。
來自美國國家衛(wèi)生研究所的一個(gè)科研小組介紹說,，肌體內(nèi)很多關(guān)鍵酶都需要維生素C才能正常工作,，長期缺乏維生素C可能導(dǎo)致壞血病。維生素C還起到抗氧化劑的作用,，能保護(hù)細(xì)胞免受自由基的危害,。但是他們發(fā)現(xiàn)，當(dāng)維生素C被大劑量注入實(shí)驗(yàn)鼠體內(nèi)時(shí),，反而會(huì)起到“促氧化劑”的作用,，導(dǎo)致形成過氧化氫，它可以殺死癌細(xì)胞,。
研究小組負(fù)責(zé)人馬克·萊文等人最初對43種癌癥細(xì)胞系和5種正常細(xì)胞系進(jìn)行的實(shí)驗(yàn)顯示,，高濃度的維生素C對75%的癌細(xì)胞系都有抑制效果，并且不會(huì)影響正常的細(xì)胞系,。他們隨后用患癌實(shí)驗(yàn)鼠進(jìn)行實(shí)驗(yàn)并發(fā)現(xiàn),，大劑量注射維生素C可使腫瘤重量和生長速度分別降低41%和53%。
研究人員分析認(rèn)為,，維生素C之所以有抗癌功效,，是由于它能在圍繞癌細(xì)胞的細(xì)胞外液中促使形成過氧化氫，正是過氧化氫殺死了一些癌細(xì)胞,。
研究小組稱,，這些動(dòng)物實(shí)驗(yàn)數(shù)據(jù)表明，應(yīng)該繼續(xù)推進(jìn)維生素C在人類癌癥治療領(lǐng)域的應(yīng)用,。醫(yī)學(xué)界早年曾一度掀起研究用維生素C治療癌癥的熱潮,，后來由于有些臨床試驗(yàn)得出結(jié)論認(rèn)為，口服高劑量維生素C對于癌癥患者沒有明顯益處,，研究熱潮逐漸降溫,。而萊文等人指出，只有通過注射,，人體內(nèi)的維生素C才能達(dá)到可發(fā)揮抗癌效果的水平,。他們已經(jīng)在設(shè)計(jì)新的人體臨床試驗(yàn)，以進(jìn)一步研究維生素C在人體中的抗癌功效,。（生物谷Bioon.com）
生物谷推薦原始出處：
PNAS,，doi: 10.1073/pnas.0804226105，Qi Chen, Mark Levine
Pharmacologic doses of ascorbate act as a prooxidant and decrease growth of aggressive tumor xenografts in mice
Qi Chen*,†, Michael Graham Espey*,†,‡, Andrew Y. Sun*, Chaya Pooput§, Kenneth L. Kirk§, Murali C. Krishna¶, Deena Beneda Khosh‖, Jeanne Drisko‖, and Mark Levine*,‡
+Author Affiliations
*Molecular and Clinical Nutrition Section and
§Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, and
¶Radiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; and
‖Program in Integrative Medicine, University of Kansas Medical Center, Kansas City, KS 66160
↵ †Q.C. and M.G.E. contributed equally to this work.
Edited by Bruce N. Ames, Children's Hospital Oakland Research Institute, Oakland, CA, and approved June 6, 2008 (received for review May 1, 2008)
Abstract
Ascorbic acid is an essential nutrient commonly regarded as an antioxidant. In this study, we showed that ascorbate at pharmacologic concentrations was a prooxidant, generating hydrogen-peroxide-dependent cytotoxicity toward a variety of cancer cells in vitro without adversely affecting normal cells. To test this action in vivo, normal oral tight control was bypassed by parenteral ascorbate administration. Real-time microdialysis sampling in mice bearing glioblastoma xenografts showed that a single pharmacologic dose of ascorbate produced sustained ascorbate radical and hydrogen peroxide formation selectively within interstitial fluids of tumors but not in blood. Moreover, a regimen of daily pharmacologic ascorbate treatment significantly decreased growth rates of ovarian (P < 0.005), pancreatic (P < 0.05), and glioblastoma (P < 0.001) tumors established in mice. Similar pharmacologic concentrations were readily achieved in humans given ascorbate intravenously. These data suggest that ascorbate as a prodrug may have benefits in cancers with poor prognosis and limited therapeutic options.
