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Opening of the mitochondrial permeability transition pore causes depletion of mitochondrial and cytosolic NAD+ and is a causative event in the death of myocytes in postischemic reperfusion of the heart
Open accessAbstract
The opening of the mitochondrial permeability transition pore (PTP) has been suggested to play a key role in various forms of cell death, but direct evidence in intact tissues is still lacking. We found that in the rat heart, 92% of NAD(+) glycohydrolase activity is associated with mitochondria. This activity was not modified by the addition of Triton X-100, although it was abolished by mild treatment with the protease Nagarse, a condition that did not affect the energy-linked properties of mitochondria. The addition of Ca(2+) to isolated rat heart mitochondria resulted in a profound decrease in their NAD(+) content, which followed mitochondrial swelling. Cyclosporin A(CsA), a PTP inhibitor, completely prevented NAD(+) depletion but had no effect on the glycohydrolase activity. Thus, in isolated mitochondria PTP opening makes NAD(+) available for its enzymatic hydrolysis. Perfused rat hearts subjected to global ischemia for 30 min displayed a 30% decrease in tissue NAD(+) content, which was not modified by extending the duration of ischemia. Reperfusion resulted in a more severe reduction of both total and mitochondrial contents of NAD(+), which could be measured in the coronary effluent together with lactate dehydrogenase. The addition of 0.2 microm CsA or of its analogue MeVal-4-Cs (which does not inhibit calcineurin) maintained higher NAD(+) contents, especially in mitochondria, and significantly protected the heart from reperfusion damage, as shown by the reduction in lactate dehydrogenase release. Thus, upon reperfusion after prolonged ischemia, PTP opening in the heart can be documented as a CsA-sensitive release of NAD(+), which is then partly degraded by glycohydrolase and partly released when sarcolemmal integrity is compromised. These results demonstrate that PTP opening is a causative event in reperfusion damage of the heart.
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“but low concentrations of ONOO− (0.1 mM) were found to protect neurons against NO•-mediated apoptosis by activating the phosphoinositide-3-kinase (PI3K)/Akt antiapoptotic signaling pathway (106).”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [106]
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“An additional deleterious outcome of extended mPTP opening is the loss of NAD+.”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [3]
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“Oxidative stress-dependent cell death largely depends on the activation of mPTP.”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [3]
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Metadata
- Authors
- Di Lisa, F., Menabò, R., Canton, M., Barile, M., & Bernardi, P.
- Affiliations
- University of Padua (IT)
- National Research Council (IT)
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2001-01
- Volume
- 276
- Issue
- 4
- Pages
- 2571-2575
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2147640676
- Cited by
- 678
- References
- 46
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 16 · 2023: 16 · 2022: 12 · 2021: 26 · 2020: 20 · 2019: 27 · 2018: 34 · 2017: 24 · 2016: 25 · 2015: 24 · 2014: 33 · 2013: 23 · 2012: 33
- FWCI
- 15.49
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion)
- Padua Research Archive (University of Padova) (submittedVersion)
- INFM-OAR (INFN Catania) (submittedVersion, cc-by)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- mitochondrial permeability transition pore, NAD+ depletion, NAD glycohydrolase, cyclosporine, myocyte death, myocardial ischemia, mitochondrial swelling, calcineurin, cardioprotection, lactate dehydrogenase release
- MeSH terms
- Mitochondrial Permeability Transition Pore, Animals, Cytosol, Ion Channels, Male, Membrane Proteins, Mitochondria, Heart, Myocardium, NAD, NAD+ Nucleosidase, Myocardial Reperfusion Injury, Cyclosporine, Cell Death, Myocardial Ischemia, Rats, Wistar, Mitochondrial Membrane Transport Proteins, Rats, In Vitro Techniques
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