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Open AccessEditor’s ChoiceArticle

TMA, A Forgotten Uremic Toxin, but Not TMAO, Is Involved in Cardiovascular Pathology

1
Department of Experimental Physiology and Pathophysiology, Laboratory of Centre for Preclinical Research, Medical University of Warsaw, 02-106 Warsaw, Poland
2
Department of Hypertension and Diabetology, Medical University of Gdansk, 80-211 Gdansk, Poland
3
Laboratory of Molecular Bases of Aging, Nencki Institute of Experimental Biology, Polish Academy of Sciences, 02-093 Warsaw, Poland
4
Department of Soft Condensed Matter, Institute of Physical Chemistry, Polish Academy of Sciences, 01-224 Warsaw, Poland
5
1st Chair and Department of Cardiology, Medical University of Warsaw, 02-106 Warsaw, Poland
*
Author to whom correspondence should be addressed.
Toxins 2019, 11(9), 490; https://doi.org/10.3390/toxins11090490
Received: 5 August 2019 / Revised: 16 August 2019 / Accepted: 23 August 2019 / Published: 26 August 2019
(This article belongs to the Section Uremic Toxins)
Trimethylamine-N-oxide (TMAO) has been suggested as a marker and mediator of cardiovascular diseases. However, data are contradictory, and the mechanisms are obscure. Strikingly, the role of the TMAO precursor trimethylamine (TMA) has not drawn attention in cardiovascular studies even though toxic effects of TMA were proposed several decades ago. We assessed plasma TMA and TMAO levels in healthy humans (HH) and cardiovascular patients qualified for aortic valve replacement (CP). The cytotoxicity of TMA and TMAO in rat cardiomyocytes was evaluated using an MTT test. The effects of TMA and TMAO on albumin and lactate dehydrogenase (LDH) were assessed using fluorescence correlation spectroscopy. In comparison to HH, CP had a two-fold higher plasma TMA (p < 0.001) and a trend towards higher plasma TMAO (p = 0.07). In CP plasma, TMA was inversely correlated with an estimated glomerular filtration rate (eGFR, p = 0.002). TMA but not TMAO reduced cardiomyocytes viability. Incubation with TMA but not TMAO resulted in the degradation of the protein structure of LDH and albumin. In conclusion, CP show increased plasma TMA, which is inversely correlated with eGFR. TMA but not TMAO exerts negative effects on cardiomyocytes, likely due to its disturbing effect on proteins. Therefore, TMA but not TMAO may be a toxin and a marker of cardiovascular risk. View Full-Text
Keywords: trimethylamine; TMAO; bacterial metabolites; biomarkers trimethylamine; TMAO; bacterial metabolites; biomarkers
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MDPI and ACS Style

Jaworska, K.; Hering, D.; Mosieniak, G.; Bielak-Zmijewska, A.; Pilz, M.; Konwerski, M.; Gasecka, A.; Kapłon-Cieślicka, A.; Filipiak, K.; Sikora, E.; Hołyst, R.; Ufnal, M. TMA, A Forgotten Uremic Toxin, but Not TMAO, Is Involved in Cardiovascular Pathology. Toxins 2019, 11, 490. https://doi.org/10.3390/toxins11090490

AMA Style

Jaworska K, Hering D, Mosieniak G, Bielak-Zmijewska A, Pilz M, Konwerski M, Gasecka A, Kapłon-Cieślicka A, Filipiak K, Sikora E, Hołyst R, Ufnal M. TMA, A Forgotten Uremic Toxin, but Not TMAO, Is Involved in Cardiovascular Pathology. Toxins. 2019; 11(9):490. https://doi.org/10.3390/toxins11090490

Chicago/Turabian Style

Jaworska, Kinga; Hering, Dagmara; Mosieniak, Grażyna; Bielak-Zmijewska, Anna; Pilz, Marta; Konwerski, Michał; Gasecka, Aleksandra; Kapłon-Cieślicka, Agnieszka; Filipiak, Krzysztof; Sikora, Ewa; Hołyst, Robert; Ufnal, Marcin. 2019. "TMA, A Forgotten Uremic Toxin, but Not TMAO, Is Involved in Cardiovascular Pathology" Toxins 11, no. 9: 490. https://doi.org/10.3390/toxins11090490

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