scholarly journals Choline Dehydrogenase, Mitochondrial

2020 ◽  
Author(s):  
1996 ◽  
Vol 377 (2) ◽  
pp. 129-138 ◽  
Author(s):  
Bernhard Miller ◽  
Heide Schmid ◽  
Tian Jun Chen ◽  
Michael Schmolke ◽  
Walter G. Guder

1995 ◽  
pp. 500-503
Author(s):  
Dietmar Schomburg ◽  
Dörte Stephan

Metabolomics ◽  
2020 ◽  
Vol 16 (12) ◽  
Author(s):  
Irena Roci ◽  
Jeramie D. Watrous ◽  
Kim A. Lagerborg ◽  
Mohit Jain ◽  
Roland Nilsson

Abstract Introduction Choline is an essential human nutrient that is particular important for proliferating cells, and altered choline metabolism has been associated with cancer transformation. Yet, the various metabolic fates of choline in proliferating cells have not been investigated systematically. Objectives This study aims to map the metabolic products of choline in normal and cancerous proliferating cells. Methods We performed 13C-choline tracing followed by liquid chromatography-high resolution mass spectrometry (LC-HRMS) analysis of metabolic products in normal and in vitro-transformed (tumor-forming) epithelial cells, and also in tumor-derived cancer cell lines. Selected metabolites were quantified by internal standards. Results Untargeted analysis revealed 121 LCMS peaks that were 13C-labeled from choline, including various phospholipid species, but also previously unknown products such as monomethyl- and dimethyl-ethanolamines. Interestingly, we observed formation of betaine from choline specifically in tumor-derived cells. Expression of choline dehydrogenase (CHDH), which catalyzes the first step of betaine synthesis, correlated with betaine synthesis across the cell lines studied. RNAi silencing of CHDH did not affect cell proliferation, although we observed an increased fraction of G2M phase cells with some RNAi sequences, suggesting that CHDH and its product betaine may play a role in cell cycle progression. Betaine cell concentration was around 10 µM, arguing against an osmotic function, and was not used as a methyl donor. The function of betaine in these tumor-derived cells is presently unknown. Conclusion This study identifies novel metabolites of choline in cancer and normal cell lines, and reveals altered choline metabolism in cancer cells.


1996 ◽  
Vol 14 (2) ◽  
pp. 177-180 ◽  
Author(s):  
Gösta Lilius ◽  
Niklas Holmberg ◽  
Leif Bülow

1975 ◽  
Vol 39 (7) ◽  
pp. 1513-1514
Author(s):  
Toru Nagasawa ◽  
Yoshiyasu Kawabata ◽  
Yoshiki Tani ◽  
Koichi Ogata

1989 ◽  
Vol 256 (1) ◽  
pp. F107-F112 ◽  
Author(s):  
E. B. Grossman ◽  
S. C. Hebert

Betaine belongs to the trimethylamine class of osmolytes (osmotically active substances believed to play an important role in cell volume homeostasis) and has recently been identified in the inner medulla of the mammalian kidney. Trimethylamines accumulate in the renal inner medulla during hypertonic stress, and betaine content in the inner medulla has been shown recently to increase during hypernatremia, yet the mechanisms governing the modulation of trimethylamine content and, in particular, of betaine content are not well understood. In this study, we demonstrate the presence of choline dehydrogenase activity in the renal inner medullas of three separate rat strains. Choline dehydrogenase is the enzyme that catalyzes the first of two successive oxidation steps in the biosynthetic conversion of choline to betaine. The presence of choline dehydrogenase activity in the inner medulla suggests that betaine accumulation in the inner medulla may result, at least in part, through in situ synthesis. The Km and Vmax of the reaction in the inner medullas of Long-Evans rats are 4.7 +/- 0.5 mM and 36.9 +/- 5.0 nmol.mg protein-1.min-1, respectively. These values are similar to the characteristics of choline dehydrogenase in mammalian liver. During hypernatremia, when betaine content of the inner medulla has been shown to increase 1.5-fold, choline dehydrogenase activity remains unchanged (or slightly increased), whereas enzyme activity in the cortex increases approximately 50%. Possible mechanisms of inner medullary betaine accumulation are discussed.


1976 ◽  
Vol 40 (10) ◽  
pp. 2077-2084 ◽  
Author(s):  
Toru NAGASAWA ◽  
Nobuhiro MORI ◽  
Yoshiki TANI ◽  
Koichi OGATA

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