Rocha Bárbara S, Gago Bruno, Barbosa Rui M, Cavaleiro Carlos, Laranjinha João
Faculty of Pharmacy and Center for Neurosciences and Cell Biology, University of Coimbra, 3000-548 Coimbra, Portugal.
Department of Health Sciences, University of Aveiro, Aveiro, Portugal.
Free Radic Biol Med. 2015 May;82:160-6. doi: 10.1016/j.freeradbiomed.2015.01.021. Epub 2015 Jan 30.
Nitric oxide ((∙)NO), a ubiquitous molecule involved in a plethora of signaling pathways, is produced from dietary nitrate in the gut through the so-called nitrate-nitrite-NO pathway. In the stomach, nitrite derived from dietary nitrate triggers a network of chemical reactions targeting endogenous and exogenous biomolecules, thereby producing new compounds with physiological activity.
The aim of this study was to ascertain whether compounds with physiological relevance are produced in the stomach upon consumption of nitrate- and ethanol-rich foods.
Human volunteers consumed a serving of lettuce (source of nitrate) and alcoholic beverages (source of ethanol). After 15 min, samples of the gastric headspace were collected and ethyl nitrite was identified by GC-MS. Wistar rats were used to study the impact of ethyl nitrite on gastric smooth muscle relaxation at physiological pH.
Nitrogen oxides, produced from nitrite in the stomach, induce nitrosation of ethanol from alcoholic beverages in the human stomach yielding ethyl nitrite. Ethyl nitrite, a potent vasodilator, is produced in vivo upon the consumption of lettuce with either red wine or whisky. Moreover, at physiological pH, ethyl nitrite induces gastric smooth muscle relaxation through a cGMP-dependent pathway. Overall, these results suggest that ethyl nitrite is produced in the gastric lumen and releases (∙)NO at physiological pH, which ultimately may have an impact on gastric motility. Systemic effects may also be expected if ethyl nitrite diffuses through the gastric mucosa reaching blood vessels, therefore operating as a (∙)NO carrier throughout the body.
These data pinpoint posttranslational modifications as an underappreciated mechanism for the production of novel molecules with physiological impact locally in the gut and highlight the notion that diet may fuel compounds with the potential to modulate gastrointestinal welfare.
一氧化氮（∙NO）是一种参与众多信号通路的普遍存在的分子，它通过所谓的硝酸盐-亚硝酸盐-NO途径在肠道中由膳食硝酸盐产生。在胃中，源自膳食硝酸盐的亚硝酸盐引发一系列针对内源性和外源性生物分子的化学反应，从而产生具有生理活性的新化合物。
本研究的目的是确定食用富含硝酸盐和乙醇的食物后胃中是否会产生具有生理相关性的化合物。
人类志愿者食用一份生菜（硝酸盐来源）和酒精饮料（乙醇来源）。15分钟后，收集胃顶空气体样本，并通过气相色谱-质谱联用仪鉴定亚硝酸乙酯。使用Wistar大鼠研究亚硝酸乙酯在生理pH值下对胃平滑肌舒张的影响。
胃中亚硝酸盐产生的氮氧化物促使人体胃中酒精饮料中的乙醇发生亚硝化反应，生成亚硝酸乙酯。亚硝酸乙酯是一种有效的血管扩张剂，在食用生菜搭配红酒或威士忌后在体内产生。此外，在生理pH值下，亚硝酸乙酯通过依赖环磷酸鸟苷（cGMP）的途径诱导胃平滑肌舒张。总体而言，这些结果表明亚硝酸乙酯在胃腔中产生，并在生理pH值下释放∙NO，这最终可能会影响胃动力。如果亚硝酸乙酯扩散穿过胃黏膜到达血管，进而作为全身的∙NO载体发挥作用，那么也可能会产生全身效应。
这些数据指出翻译后修饰是肠道局部产生具有生理影响的新分子但未得到充分认识的机制，并强调了饮食可能产生具有调节胃肠道健康潜力的化合物这一观点。
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