微量营养素对人体硫化氢代谢的调节作用,初步数据。

IF 4.7 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2022-01-07 eCollection Date: 2022-01-01 DOI:10.1177/11786388211065372
Maurizio Dattilo, Carolina Fontanarosa, Michele Spinelli, Vittorio Bini, Angela Amoresano
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引用次数: 0

摘要

背景:硫化氢(H2S)是一种重要的气体递质,与一氧化氮(NO)和一氧化碳(CO)共同调节人体的基本平衡功能。它通过胱硫醚β合成酶(CBS)和胱硫醚γ裂解酶(CSE)以及半胱氨酸氨基转移酶(CAT)/3-巯基丙酮酸硫转移酶(3MPST)的转硫化替代途径释放。此外,还有一种非酶性的血管内释放。我们回顾性地研究了通过补充微量营养素(L-胱氨酸、牛磺酸和 5-磷酸吡哆醛/P5P)来调节人体内源性 H2S 释放和信号传递的可能性:方法:对以抗衰老为目的的患者进行为期 10 天的补充。在基线和治疗后收集血液,并通过质谱法研究代谢组,以监测报告 H2S 代谢和相关途径的代谢物的变化:结果:6 名中年受试者(2 名女性)提供了数据。微量营养素增加了3-巯基丙酮酸(P = .03),报告了3MPST为线粒体内释放H2S提供底物的CAT的活性;减少了lanthionine(P = .024),报告了CBS释放H2S的情况;对CSE释放H2S没有显著影响。这与体内平衡是一致的。我们还记录到 H2S 诱导的途径的报告物显著增加,包括报告甲基化能力的 5-MethylTHF (P = .001) 和 SAME (P = .022),以及报告一氧化氮代谢的 BH4 (P = .021) 和 BH2 (P = .028)。这些激活作用可通过同时诱导 H2S 的非酶释放来解释:尽管目前的证据还很薄弱,还需要进一步证实,但微量营养素的作用与H2S内源性释放的增加以及在平衡机制控制下的信号传导是一致的,这进一步证实了喂养在健康和疾病中的作用。这些效应可能会在病理活动缺陷的情况下产生 H2S 增强效应,这应该在适当设计的临床试验中进行检验。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Modulation of Human Hydrogen Sulfide Metabolism by Micronutrients, Preliminary Data.

Background: Hydrogen sulfide (H2S) is a pivotal gasotransmitter networking with nitric oxide (NO) and carbon monoxide (CO) to regulate basic homeostatic functions. It is released by the alternative pathways of transulfuration by the enzymes Cystathionine Beta Synthase (CBS) and Cystathionine Gamma Lyase (CSE), and by Cysteine AminoTransferase (CAT)/ 3-Mercaptopyruvate Sulfur Transferase (3MPST). A non-enzymatic, intravascular release is also in place. We retrospectively investigated the possibility to modulate the endogenous H2S release and signaling in humans by a dietary manipulation with supplemented micronutrients (L-cystine, Taurine and pyridoxal 5-phopsphate/P5P).

Methods: Patients referring for antiaging purposes underwent a 10-day supplementation. Blood was collected at baseline and after treatment and the metabolome was investigated by mass spectrometry to monitor the changes in the metabolites reporting on H2S metabolism and related pathways.

Results: Data were available from 6 middle aged subjects (2 women). Micronutrients increased 3-mercaptopyruvate (P = .03), reporting on the activity of CAT that provides the substrate for H2S release within mitochondria by 3MPST, decreased lanthionine (P = .024), reporting the release of H2S from CBS, and had no significant effect of H2S release from CSE. This is compatible with a homeostatic balancing. We also recorded a strong increase of reporters of H2S-induced pathways including 5-MethylTHF (P = .001) and SAME (P = .022), reporting on methylation capacity, and of BH4 (P = .021) and BH2 (P = .028) reporting on nitric oxide metabolism. These activations may be explained by the concomitant induction of non-enzymatic release of H2S.

Conclusions: Although the current evidences are weak and will need to be confirmed, the effect of micronutrients was compatible with an increase of the H2S endogenous release and signaling within the control of homeostatic mechanisms, further endorsing the role of feeding in health and disease. These effects might result in a H2S boosting effect in case of defective activity of pathologic origin, which should be checked in duly designed clinical trials.

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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
期刊介绍: ACS Applied Bio Materials is an interdisciplinary journal publishing original research covering all aspects of biomaterials and biointerfaces including and beyond the traditional biosensing, biomedical and therapeutic applications. The journal is devoted to reports of new and original experimental and theoretical research of an applied nature that integrates knowledge in the areas of materials, engineering, physics, bioscience, and chemistry into important bio applications. The journal is specifically interested in work that addresses the relationship between structure and function and assesses the stability and degradation of materials under relevant environmental and biological conditions.
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