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Cited by 42Cardiac Ischemia and ReperfusionCancer, Hypoxia, and MetabolismMitochondrial Function and Pathology

Pathways of succinate formation and their contribution to improvement of cardiac-function in the hypoxic rat-heart

Wiesner, R.J., Rösen, P., Grieshaber, M.K.·1988·Biochemical Medicine and Metabolic Biology
DOI 10.1016/0885-4505(88)90100-4
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Abstract

Hypoxia led to a dramatic acceleration of amino acid breakdown together with succinate synthesis in the rat heart. Our data do not confirm the simultaneous conversion of aspartate and glutamate to succinate, which has been repeatedly assumed in the literature (7, 8, 21, 28-30), but rather suggest that different pathways are involved during developing hypoxia and that glutamate is the sole source for anaerobic succinate production from endogenous sources in the glucose-perfused heart. Perfusion of hypoxic rat hearts with 2-oxoglutarate, malate, and fumarate (5 mM each) increased succinate formation three- to fourfold. The beneficial effects of these substances on left ventricular systolic pressure, end diastolic pressure, and time of recovery may be due to the elevated content of ATP in these hearts compared to hypoxic controls with glucose as the sole substrate. However, the maintenance of a high rate of anaerobic glycolysis in hearts perfused with 2-oxoglutarate, malate, and fumarate and not the small stimulation of succinate synthesis is considered to be the most important mechanism of cardiac protection. A proposed pathway assumes that malate, after dehydration to fumarate, may serve as an alternative electron acceptor for cytosolic NADH during conditions of oxygen deficiency, thereby cancelling glycolytic inhibition.

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Crossref · 10.1016/0885-4505(88)90100-4

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  • The increased succinate pool under hypoxia may come from glutamate via alpha-ketoglutarate by transamination or from partial reversal of the TCA cycle from malate through fumarate, which would require complex II to act as a fumarate reductase.

    “This increased succinate pool under hypoxia might be supplied either from glutamate through α-ketoglutarate by transamination [76,77] or by a partial reversal of the TCA cycle from malate through fumarate, which requires that complex II would become a fumarate reductase under hypoxia [36,79].”

    From Differential effects of complex II on mitochondrial ROS production and their relation to cardioprotective pre- and postconditioning (2013) · cites this paper as [76]

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Authors
Wiesner, R. J., Rösen, P., & Grieshaber, M. K.
Affiliations
Heinrich Heine University Düsseldorf (DE)
ORCID
Wiesner, R.J.
Venue
Biochemical Medicine and Metabolic Biology
Publisher
Elsevier BV
Published
1988-08
Volume
40
Issue
1
Pages
19-34
ISSN
0885-4505 (ISSN-L)
DOI
10.1016/0885-4505(88)90100-4
OpenAlex
W2007425036
Cited by
42
References
25
Citations by year
2024: 2 · 2021: 1 · 2019: 2 · 2018: 1 · 2017: 2 · 2016: 2 · 2015: 1 · 2014: 1 · 2013: 5 · 2012: 2
FWCI
1.06
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Biochemical Medicine and Metabolic Biology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
myocardial hypoxia, aspartic acid, alpha-ketoglutarate, malate, fumarate, anaerobic glycolysis, alternative electron acceptors, left ventricular function, cardioprotection, amino acid catabolism
MeSH terms
Amino Acids, Animals, Blood Pressure, Citric Acid Cycle, Coronary Disease, Dicarboxylic Acids, Energy Metabolism, Heart, Heart Rate, Male, Rats, Inbred Strains, Reference Values, Succinates, Rats

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