根據(jù)最近發(fā)表在刊物《內(nèi)臟》（Gut）上的結(jié)果,，胃部的脂肪將使得維生素C促進(jìn)而非抑制特定致癌物質(zhì)的形成。
科學(xué)家們同時(shí)分析了脂肪（油脂）和維生素C（抗壞血酸）對(duì)胃下部亞硝酸鹽化學(xué)物質(zhì)的作用,，胃下部是最容易發(fā)生癌變和腫瘤生長的區(qū)域,。
亞硝酸鹽存在于人類的唾液和某些特定食物保護(hù)劑中，它們能轉(zhuǎn)化為致癌物質(zhì)亞硝胺,。亞硝胺主要在酸性環(huán)境中形成,，例如胃酸條件下。但是維生素C可以通過將亞硝酸鹽轉(zhuǎn)化為一氧化氮而阻礙以上過程的發(fā)生,。當(dāng)脂肪不存在時(shí),，維生素C將抑制兩種亞硝胺的生成，抑制因子達(dá)到5－1000之間,；而對(duì)于另外兩種亞硝胺,，維生素C則將起到完全消除的作用。
但是當(dāng)環(huán)境中存在10%的脂肪時(shí),，維生素C將起到促進(jìn)亞硝酸鹽生成的作用,，促進(jìn)的效率在8－140倍之間。
文章作者表示,，脂肪在進(jìn)食之后將在胃的下部存在一段時(shí)間,，并且它們也是構(gòu)成胃內(nèi)表面細(xì)胞的組成成分之一。當(dāng)維生素C在酸性環(huán)境下和亞硝酸鹽反應(yīng)時(shí)就將生成一氧化氮,。但是生成的一氧化氮能擴(kuò)散到脂肪中,，然后通過和氧氣反應(yīng)而形成能產(chǎn)生亞硝胺的化學(xué)物質(zhì)。
因此作者認(rèn)為,，以上發(fā)現(xiàn)或許能說明為什么最近一些研究觀察到攝入維生素C并不能降低癌癥風(fēng)險(xiǎn),。
原文鏈接：http://www.physorg.com/news108094911.html
原始出處:
Gut. Published Online First: 4 September 2007. doi:10.1136/gut.2007.128587
Fat transforms ascorbic acid from inhibiting to promoting acid catalysed n-nitrosation
Emilie Combet 1, Stuart Paterson 2, Katsunori Iijima 2, Jack Winter 2, William Mullen 1, Alan Crozier 1, Tom Preston 3 and Kenneth E. L. McColl 1*
1 The University of Glasgow, United Kingdom
2 Western Infirmary, Glasgow, United Kingdom
3 Stable Isotope Biochemistry Laboratory, SUERC, United Kingdom
* To whom correspondence should be addressed. E-mail: [email protected] .
Background: The major potential site of acid nitrosation is the proximal stomach, an anatomical site prone to a rising incidence of metaplasia and adenocarcinoma. Nitrite, a pre-carcinogen present in saliva, can be converted to nitrosating species and N-nitroso compounds by acidification at low gastric pH in the presence of thiocyanate.
Aims: To assess the effect of lipid and ascorbic acid on the nitrosative chemistry under conditions simulating the human proximal stomach.
Methods: The nitrosative chemistry was modelled in vitro by measuring the nitrosation of four secondary amines under conditions simulating the proximal stomach. The N-nitrosamines formed were measured by gas chromatography - ion-trap tandem mass spectrometry, while nitric oxide and oxygen levels were measured amperometrically.
Results: In absence of lipid, nitrosative stress was inhibited by ascorbic acid through conversion of nitrosating species to nitric oxide. Addition of ascorbic acid reduced the amount of N-nitrosodimethylamine formed by 5-fold, N-nitrosomorpholine by >1000-fold and totally prevented the formation of N-nitrosodiethylamine and N-nitrosopiperidine. In contrast, when 10% lipid was present, ascorbic acid increased the amount of N-nitrosodimethylamine, N-nitrosodiethylamine and N-nitrosopiperidine formed by approximately 8, 60 and 140-fold respectively compared to absence of ascorbic acid.
Conclusion: The presence of lipid converts ascorbic acid from inhibiting to promoting acid nitrosation. This may be explained by nitric oxide, formed by ascorbic acid in the aqueous phase, being able to regenerate nitrosating species by reacting with O2 in the lipid phase.
