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Ischemia In Vivo Induces Cardiolipin Oxidation in Rat Kidney Mitochondria
SIMPLE SUMMARY: Mitochondrial cardiolipin is a unique phospholipid that plays a vital role in ATP synthesis. It has been observed that ischemia/reperfusion causes damage to cardiolipins in the heart or brain tissues; however, very little data has been found regarding kidney cardiolipins and related...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9026122/ https://www.ncbi.nlm.nih.gov/pubmed/35453739 http://dx.doi.org/10.3390/biology11040541 |
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author | Strazdauskas, Arvydas Trumbeckaite, Sonata Jakstas, Valdas Kamarauskaite, Justina Ivanauskas, Liudas Baniene, Rasa |
author_facet | Strazdauskas, Arvydas Trumbeckaite, Sonata Jakstas, Valdas Kamarauskaite, Justina Ivanauskas, Liudas Baniene, Rasa |
author_sort | Strazdauskas, Arvydas |
collection | PubMed |
description | SIMPLE SUMMARY: Mitochondrial cardiolipin is a unique phospholipid that plays a vital role in ATP synthesis. It has been observed that ischemia/reperfusion causes damage to cardiolipins in the heart or brain tissues; however, very little data has been found regarding kidney cardiolipins and related damage after ischemia/reperfusion. Oxidative stress plays a key role during reperfusion. However, even during ischemia, cardiolipins may be oxidized. Therefore, our aim was to evaluate cardiolipin oxidation during renal ischemia in vivo. Renal ischemia in vivo was induced in male Wistar rats for a 30–60-min period; we then isolated kidney mitochondria, extracted the lipids and analyzed cardiolipin by applying chromatographic and mass spectrometric methods. The results showed that after even 30 min of in vivo ischemia, the amounts of the dominant species of cardiolipin decreased almost in half, and it further decreased when extending the ischemia time. Cardiolipin was oxidized with up to eight additional oxygen atoms, yielding eight different species with multiple isomeric forms. This shows that even after ischemia, cardiolipin levels are altered, and many cardiolipin oxidation products are produced, which may also potentially be modified into more harmful lipid signaling molecules that may induce more damage to mitochondria. ABSTRACT: Cardiolipin is a mitochondrial phospholipid that plays a significant role in mitochondrial bioenergetics. Cardiolipin is oxidized under conditions like oxidative stress that occurs during ischemia/reperfusion; however, it is known that even during ischemia, many reactive oxygen species are generated. Our aim was to analyze the effect of in vivo ischemia on cardiolipin oxidation. Adult male Wistar rats were anesthetized; then, their abdomens were opened, and microvascular clips were placed on renal arteries for 30, 40 or 60 min, causing ischemia. After ischemia, kidneys were harvested, mitochondria were isolated, and lipids were extracted for chromatographic and mass spectrometric analysis of tetralinoleoyl cardiolipin and its oxidation products. Chromatographic and mass spectrometric analysis revealed a 47%, 68% and 74% decrease in tetralinoleoyl cardiolipin after 30 min, 40 min and 60 min of renal ischemia, respectively (p < 0.05). Eight different cardiolipin oxidation products with up to eight additional oxygens were identified in rat kidney mitochondria. A total of 40 min of ischemia caused an average of a 6.9-fold increase in all oxidized cardiolipin forms. We present evidence that renal ischemia in vivo alone induces tetralinoleoyl cardiolipin oxidation and depletion in rat kidney mitochondria. |
format | Online Article Text |
id | pubmed-9026122 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-90261222022-04-23 Ischemia In Vivo Induces Cardiolipin Oxidation in Rat Kidney Mitochondria Strazdauskas, Arvydas Trumbeckaite, Sonata Jakstas, Valdas Kamarauskaite, Justina Ivanauskas, Liudas Baniene, Rasa Biology (Basel) Article SIMPLE SUMMARY: Mitochondrial cardiolipin is a unique phospholipid that plays a vital role in ATP synthesis. It has been observed that ischemia/reperfusion causes damage to cardiolipins in the heart or brain tissues; however, very little data has been found regarding kidney cardiolipins and related damage after ischemia/reperfusion. Oxidative stress plays a key role during reperfusion. However, even during ischemia, cardiolipins may be oxidized. Therefore, our aim was to evaluate cardiolipin oxidation during renal ischemia in vivo. Renal ischemia in vivo was induced in male Wistar rats for a 30–60-min period; we then isolated kidney mitochondria, extracted the lipids and analyzed cardiolipin by applying chromatographic and mass spectrometric methods. The results showed that after even 30 min of in vivo ischemia, the amounts of the dominant species of cardiolipin decreased almost in half, and it further decreased when extending the ischemia time. Cardiolipin was oxidized with up to eight additional oxygen atoms, yielding eight different species with multiple isomeric forms. This shows that even after ischemia, cardiolipin levels are altered, and many cardiolipin oxidation products are produced, which may also potentially be modified into more harmful lipid signaling molecules that may induce more damage to mitochondria. ABSTRACT: Cardiolipin is a mitochondrial phospholipid that plays a significant role in mitochondrial bioenergetics. Cardiolipin is oxidized under conditions like oxidative stress that occurs during ischemia/reperfusion; however, it is known that even during ischemia, many reactive oxygen species are generated. Our aim was to analyze the effect of in vivo ischemia on cardiolipin oxidation. Adult male Wistar rats were anesthetized; then, their abdomens were opened, and microvascular clips were placed on renal arteries for 30, 40 or 60 min, causing ischemia. After ischemia, kidneys were harvested, mitochondria were isolated, and lipids were extracted for chromatographic and mass spectrometric analysis of tetralinoleoyl cardiolipin and its oxidation products. Chromatographic and mass spectrometric analysis revealed a 47%, 68% and 74% decrease in tetralinoleoyl cardiolipin after 30 min, 40 min and 60 min of renal ischemia, respectively (p < 0.05). Eight different cardiolipin oxidation products with up to eight additional oxygens were identified in rat kidney mitochondria. A total of 40 min of ischemia caused an average of a 6.9-fold increase in all oxidized cardiolipin forms. We present evidence that renal ischemia in vivo alone induces tetralinoleoyl cardiolipin oxidation and depletion in rat kidney mitochondria. MDPI 2022-03-31 /pmc/articles/PMC9026122/ /pubmed/35453739 http://dx.doi.org/10.3390/biology11040541 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Strazdauskas, Arvydas Trumbeckaite, Sonata Jakstas, Valdas Kamarauskaite, Justina Ivanauskas, Liudas Baniene, Rasa Ischemia In Vivo Induces Cardiolipin Oxidation in Rat Kidney Mitochondria |
title | Ischemia In Vivo Induces Cardiolipin Oxidation in Rat Kidney Mitochondria |
title_full | Ischemia In Vivo Induces Cardiolipin Oxidation in Rat Kidney Mitochondria |
title_fullStr | Ischemia In Vivo Induces Cardiolipin Oxidation in Rat Kidney Mitochondria |
title_full_unstemmed | Ischemia In Vivo Induces Cardiolipin Oxidation in Rat Kidney Mitochondria |
title_short | Ischemia In Vivo Induces Cardiolipin Oxidation in Rat Kidney Mitochondria |
title_sort | ischemia in vivo induces cardiolipin oxidation in rat kidney mitochondria |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9026122/ https://www.ncbi.nlm.nih.gov/pubmed/35453739 http://dx.doi.org/10.3390/biology11040541 |
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