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活性碳原子对氘的捕获是降低生物水中氘含量的重要机制吗?

Is Deuterium Sequestering by Reactive Carbon Atoms an Important Mechanism to Reduce Deuterium Content in Biological Water?

作者信息

Seneff Stephanie, Nigh Greg, Kyriakopoulos Anthony M

机构信息

Computer Science and Artificial Intelligence Laboratory Massachusetts Institute of Technology Cambridge Massachusetts USA.

Greg Nigh LLC Westerly Rhode Island USA.

出版信息

FASEB Bioadv. 2025 May 14;7(6):e70019. doi: 10.1096/fba.2025-00032. eCollection 2025 Jun.

DOI:10.1096/fba.2025-00032
PMID:40496345
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12147506/
Abstract

Deuterium is a natural heavy isotope of hydrogen, having a neutron as well as a proton. Deuterium disrupts ATP synthesis in mitochondria, causing increased production of reactive oxygen species and reduced synthesis of ATP. Gut microbes likely play a significant role in providing deuterium depleted short chain fatty acids (SCFAs) to human colonocytes through hydrogen gas recycling. The production of deuterium depleted (deupleted) nutrients necessarily leaves behind deuterium enriched water, unless there is a process that can sequester deuterium in small molecules that are excreted through the feces. Here, we provide evidence that a small number of classes of uniquely structured carbon-nitrogen rings and bis-allylic carbon atoms in certain biologically active small molecules may play a crucial role in sequestering deuterium for export into feces or urine. Specifically, we have identified the imidazole ring present in histidine, histamine, and microbial derivatives of histidine, the tetraterpenoid lutein, bilirubin and the derivatives urobilinogen and stercobilinogen produced by gut microbes, and the bis-allylic carbons in polyunsaturated fatty acids as likely candidates for sequestering deuterium and thereby reducing the deuterium levels in the water-based medium. Normally, carbon atoms never exchange their bound protons with deuterons from the medium, but all the above classes of molecules are important exceptions to this rule, as has been shown experimentally.

摘要

氘是氢的一种天然重同位素,含有一个中子和一个质子。氘会破坏线粒体中的ATP合成,导致活性氧的产生增加以及ATP合成减少。肠道微生物可能在通过氢气循环为人类结肠细胞提供低氘短链脂肪酸(SCFAs)方面发挥重要作用。生产低氘营养物质必然会留下富含氘的水,除非有一个过程能够将氘隔离在通过粪便排出的小分子中。在此,我们提供证据表明,某些生物活性小分子中少量独特结构的碳氮环和双烯丙基碳原子可能在隔离氘以便将其排出到粪便或尿液中起着关键作用。具体而言,我们已确定组氨酸、组胺以及组氨酸的微生物衍生物中存在的咪唑环、肠道微生物产生的四萜类叶黄素、胆红素以及衍生物尿胆原和粪胆原,以及多不饱和脂肪酸中的双烯丙基碳是隔离氘从而降低水基介质中氘水平的可能候选物。通常情况下,碳原子不会与介质中的氘核交换其结合的质子,但如实验所示,上述所有类型的分子都是这一规则的重要例外情况。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4177/12147506/aa7a583dfa61/FBA2-7-e70019-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4177/12147506/626d11a7decd/FBA2-7-e70019-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4177/12147506/4018db28021b/FBA2-7-e70019-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4177/12147506/ae0ecaa33a96/FBA2-7-e70019-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4177/12147506/aa7a583dfa61/FBA2-7-e70019-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4177/12147506/626d11a7decd/FBA2-7-e70019-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4177/12147506/4018db28021b/FBA2-7-e70019-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4177/12147506/ae0ecaa33a96/FBA2-7-e70019-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4177/12147506/aa7a583dfa61/FBA2-7-e70019-g003.jpg

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