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Related Experiment Videos

Mitochondrial calcium release induced by prooxidants

C Richter1, J Schlegel

  • 1Laboratorium für BIochemie I, ETH Zürich Schweiz.

Toxicology Letters
|April 1, 1993
PubMed
Summary

Prooxidants induce mitochondrial calcium release via NAD+ hydrolysis, causing cell damage. Inhibiting this pathway may lead to calcium overload and toxicity.

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Area of Science:

  • Mitochondrial biochemistry
  • Cellular redox signaling
  • Calcium homeostasis

Background:

  • Mitochondria are key regulators of cellular calcium (Ca2+) and are sensitive to oxidative stress.
  • Prooxidants, such as hydrogen peroxide, can alter mitochondrial function by oxidizing pyridine nucleotides like NAD(P)H.
  • NAD+ hydrolysis in Ca2+-loaded mitochondria is linked to Ca2+ release pathways.

Purpose of the Study:

  • To investigate the mechanism of prooxidant-induced Ca2+ release from mitochondria.
  • To elucidate the role of NAD+ hydrolysis and peptidyl-prolyl cis-trans isomerase in this process.
  • To understand the consequences of Ca2+ cycling on mitochondrial integrity and cell toxicity.

Main Methods:

  • Oxidation of pyridine nucleotides (NAD(P)H to NAD(P)+) in isolated mitochondria.
  • Measurement of Ca2+ release from mitochondria using specific indicators.
  • Assessment of mitochondrial membrane potential and cell viability.
  • Utilizing inhibitors like cyclosporine A to probe the Ca2+ release pathway.

Main Results:

  • Prooxidants oxidize NAD(P)H to NAD(P)+, leading to NAD+ hydrolysis in Ca2+-loaded mitochondria.
  • Hydrolyzed NAD+ triggers Ca2+ release via a pathway sensitive to cyclosporine A and potentially regulated by peptidyl-prolyl cis-trans isomerase.
  • Prolonged Ca2+ cycling results in mitochondrial membrane potential collapse and cell damage.
  • Inhibitors of this pathway may cause toxicity through sustained mitochondrial Ca2+ overload.

Conclusions:

  • Prooxidant-induced mitochondrial Ca2+ release is mediated by NAD+ hydrolysis and involves a specific, cyclosporine A-sensitive pathway.
  • Excessive Ca2+ cycling is a significant mechanism of prooxidant toxicity.
  • Conversely, blocking this pathway can lead to detrimental Ca2+ accumulation within mitochondria.

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