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Zinc protoporphyrin-trimethylamine-N-oxide complex involves cholesterol oxidation causing atherosclerosis.

Navendu Paul1, Rudra Sarkar1, Sabyasachi Sarkar2

  • 1Department of Chemistry, Indian Institute of Engineering Science and Technology, Shibpur, Botanic Garden, West Bengal, 711103, India.

Journal of Biological Inorganic Chemistry : JBIC : a Publication of the Society of Biological Inorganic Chemistry
|March 13, 2021
PubMed
Summary

Gut microbes produce trimethylamine-N-oxide (TMAO), a biomarker for atherosclerosis. TMAO binds with zinc protoporphyrin IX in plasma, forming a complex that oxidizes cholesterol, driving atherosclerosis progression.

Keywords:
AtherosclerosisCholesterol oxidationPhase transferPlaqueTMAOZinc protoporphyrin

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Gut microbial metabolism of dietary protein yields trimethylamine, oxidized to trimethylamine-N-oxide (TMAO) by hepatic enzymes.
  • TMAO is an emerging biomarker associated with atherosclerosis.
  • TMAO's hydrophilic nature necessitates phase transfer for interaction with lipid-soluble molecules involved in atherosclerosis.

Purpose of the Study:

  • To investigate the interaction between TMAO and zinc protoporphyrin IX (ZnPP) for phase transfer.
  • To elucidate the mechanism by which TMAO-ZnPP complexes may contribute to cholesterol oxidation and atherosclerosis.

Main Methods:

  • Phase transfer reactions to form TMAO-ZnPP complexes.
  • Structural analysis using model complexes like [TMAOZnTPP].
  • Chromatographic and circular dichroism (CD) studies to assess oxidation capabilities.

Main Results:

  • Free TMAO effectively binds to zinc protoporphyrin IX dimethyl ester (ZnPPDME) and potentially native ZnPP in plasma.
  • The resulting [TMAOZnPP] complex facilitates phase transfer from plasma to lipid sites.
  • Neither TMAO nor ZnPP alone oxidizes cholesterol; the complex is the active species.

Conclusions:

  • The formation of [TMAOZnPP] complexes is crucial for transporting TMAO to lipid sites.
  • These complexes act as oxo-transfer agents, oxidizing cholesterol and contributing to atherosclerosis.
  • This mechanism highlights a novel pathway in the development of atherosclerosis involving gut microbiota metabolites and metalloporphyrins.