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Acute Coronary Syndrome III: Diagnostic Studies

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Diagnosing acute coronary syndrome or ACS begins with a thorough patient history. Notable symptoms include central, crushing chest pain radiating to the left arm, neck, jaw, or back, along with shortness of breath, sweating (diaphoresis), nausea, vomiting, dizziness, and palpitations.It is crucial to note any history of cardiac illnesses and assess risk factors, including age, gender, smoking, hypertension, diabetes, hyperlipidemia, and a sedentary lifestyle.During physical examination, vital...
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Related Experiment Videos

Succinate in ischemia: Where does it come from?

Christos Chinopoulos1

  • 1Department of Medical Biochemistry, Semmelweis University, Tuzolto st. 37-47, Budapest, 1094, Hungary.

The International Journal of Biochemistry & Cell Biology
|August 9, 2019
PubMed
Summary

During tissue ischemia, succinate accumulates primarily via the Krebs cycle, not reverse succinate dehydrogenase. Mammalian mitochondria lack the necessary components for fumarate reduction to succinate.

Keywords:
AnoxiaFumarateHypoxiaSubstrate-level phosphorylationSuccinate dehydrogenaseTCA cycle

Related Experiment Videos

Area of Science:

  • Biochemistry
  • Cellular Metabolism
  • Mitochondrial Function

Background:

  • Succinate accumulation occurs during tissue ischemia.
  • The precise metabolic pathways responsible for succinate buildup are debated.

Purpose of the Study:

  • To review the literature on succinate production during ischemia.
  • To clarify the role of Krebs cycle activity versus succinate dehydrogenase reversal.
  • To discuss the biochemical feasibility of fumarate reduction in mammalian mitochondria.

Main Methods:

  • Comprehensive literature review spanning nine decades.
  • Analysis of biochemical pathways and enzyme kinetics.
  • Evaluation of mitochondrial redox potentials.

Main Results:

  • Canonical Krebs cycle activity is the predominant source of succinate, even in hypoxia.
  • Succinate dehydrogenase exhibits a diode-like property, hindering reversal.
  • Mammalian mitochondria lack quinones with the required redox potential for fumarate reduction.

Conclusions:

  • The standard Krebs cycle pathway is the primary mechanism for succinate accumulation during ischemia in mammals.
  • A distinct "fumarate reductase" enzyme, as seen in other organisms, has not been identified in mammalian mitochondria.