Non-thermal atmospheric pressure plasma-irradiated cysteine protects cardiac ischemia/reperfusion injury by preserving supersulfides
Ischemic heart disease is the main global cause of death in the world. Abnormal sulfide catabolism, especially hydrogen sulfide accumulation, impedes mitochondrial respiration and worsens the prognosis after ischemic insults, but the substantial therapeutic strategy has not been established. Non-the...
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Elsevier
2025-02-01
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| Series: | Redox Biology |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2213231724004233 |
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| author | Akiyuki Nishimura Tomohiro Tanaka Kakeru Shimoda Tomoaki Ida Shota Sasaki Keitaro Umezawa Hiromi Imamura Yasuteru Urano Fumito Ichinose Toshiro Kaneko Takaaki Akaike Motohiro Nishida |
| author_facet | Akiyuki Nishimura Tomohiro Tanaka Kakeru Shimoda Tomoaki Ida Shota Sasaki Keitaro Umezawa Hiromi Imamura Yasuteru Urano Fumito Ichinose Toshiro Kaneko Takaaki Akaike Motohiro Nishida |
| author_sort | Akiyuki Nishimura |
| collection | DOAJ |
| description | Ischemic heart disease is the main global cause of death in the world. Abnormal sulfide catabolism, especially hydrogen sulfide accumulation, impedes mitochondrial respiration and worsens the prognosis after ischemic insults, but the substantial therapeutic strategy has not been established. Non-thermal atmospheric pressure plasma irradiation therapy is attracted attention as it exerts beneficial effects by producing various reactive molecular species. Growing evidence has suggested that supersulfides, formed by catenation of sulfur atoms, contribute to various biological processes involving electron transfer in cells. Here, we report that non-thermal plasma-irradiated cysteine (Cys∗) protects mouse hearts against ischemia/reperfusion (I/R) injury by preventing supersulfide catabolism. Cys∗ has a weak but long-lasting supersulfide activity, and the treatment of rat cardiomyocytes with Cys∗ prevents mitochondrial dysfunction after hypoxic stress. Cys∗ increases sulfide-quinone oxidoreductase (SQOR), and silencing SQOR abolishes Cys∗-induced supersulfide formation and cytoprotection. Local administration of mouse hearts with Cys∗ significantly reduces infarct size with preserving supersulfide levels after I/R. These results suggest that maintaining supersulfide formation through SQOR underlies cardioprotection by Cys∗ against I/R injury. |
| format | Article |
| id | doaj-art-331751f6da0e4dc194cde4085037029a |
| institution | Kabale University |
| issn | 2213-2317 |
| language | English |
| publishDate | 2025-02-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Redox Biology |
| spelling | doaj-art-331751f6da0e4dc194cde4085037029a2025-01-14T04:12:05ZengElsevierRedox Biology2213-23172025-02-0179103445Non-thermal atmospheric pressure plasma-irradiated cysteine protects cardiac ischemia/reperfusion injury by preserving supersulfidesAkiyuki Nishimura0Tomohiro Tanaka1Kakeru Shimoda2Tomoaki Ida3Shota Sasaki4Keitaro Umezawa5Hiromi Imamura6Yasuteru Urano7Fumito Ichinose8Toshiro Kaneko9Takaaki Akaike10Motohiro Nishida11National Institute for Physiological Sciences (NIPS), National Institutes of Natural Sciences, Okazaki, 444-8787, Japan; Exploratory Research Center on Life and Living Systems (ExCELLS), National Institutes of Natural Sciences, Okazaki, 444-8787, Japan; SOKENDAI, Department of Physiological Sciences, Okazaki, 444-8787, JapanNational Institute for Physiological Sciences (NIPS), National Institutes of Natural Sciences, Okazaki, 444-8787, Japan; Exploratory Research Center on Life and Living Systems (ExCELLS), National Institutes of Natural Sciences, Okazaki, 444-8787, Japan; Center for Novel Science Initiatives (CNSI), National Institutes of Natural Sciences, Tokyo, 105-0001, JapanNational Institute for Physiological Sciences (NIPS), National Institutes of Natural Sciences, Okazaki, 444-8787, Japan; Exploratory Research Center on Life and Living Systems (ExCELLS), National Institutes of Natural Sciences, Okazaki, 444-8787, Japan; SOKENDAI, Department of Physiological Sciences, Okazaki, 444-8787, Japan; Anesthesia Center for Critical Care Research of the Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USAOrganization for Research Promotion, Osaka Metropolitan University, Sakai, 599-8531, Japan; Graduate School of Medicine, Tohoku University, Sendai, 980-8575, JapanGraduate School of Engineering, Tohoku University, Sendai, 980-8579, JapanTokyo Metropolitan Institute for Geriatrics and Gerontology, Tokyo, 173-0015, JapanOrganization of Research Initiatives, Yamaguchi University, Yamaguchi, 753-8515, JapanGraduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan; Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, JapanAnesthesia Center for Critical Care Research of the Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USAGraduate School of Engineering, Tohoku University, Sendai, 980-8579, JapanGraduate School of Medicine, Tohoku University, Sendai, 980-8575, JapanNational Institute for Physiological Sciences (NIPS), National Institutes of Natural Sciences, Okazaki, 444-8787, Japan; Exploratory Research Center on Life and Living Systems (ExCELLS), National Institutes of Natural Sciences, Okazaki, 444-8787, Japan; SOKENDAI, Department of Physiological Sciences, Okazaki, 444-8787, Japan; Center for Novel Science Initiatives (CNSI), National Institutes of Natural Sciences, Tokyo, 105-0001, Japan; Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, 812-8582, Japan; Corresponding author. Department of Physiology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.Ischemic heart disease is the main global cause of death in the world. Abnormal sulfide catabolism, especially hydrogen sulfide accumulation, impedes mitochondrial respiration and worsens the prognosis after ischemic insults, but the substantial therapeutic strategy has not been established. Non-thermal atmospheric pressure plasma irradiation therapy is attracted attention as it exerts beneficial effects by producing various reactive molecular species. Growing evidence has suggested that supersulfides, formed by catenation of sulfur atoms, contribute to various biological processes involving electron transfer in cells. Here, we report that non-thermal plasma-irradiated cysteine (Cys∗) protects mouse hearts against ischemia/reperfusion (I/R) injury by preventing supersulfide catabolism. Cys∗ has a weak but long-lasting supersulfide activity, and the treatment of rat cardiomyocytes with Cys∗ prevents mitochondrial dysfunction after hypoxic stress. Cys∗ increases sulfide-quinone oxidoreductase (SQOR), and silencing SQOR abolishes Cys∗-induced supersulfide formation and cytoprotection. Local administration of mouse hearts with Cys∗ significantly reduces infarct size with preserving supersulfide levels after I/R. These results suggest that maintaining supersulfide formation through SQOR underlies cardioprotection by Cys∗ against I/R injury.http://www.sciencedirect.com/science/article/pii/S2213231724004233Non-thermal plasmaSupersulfidesMitochondrial energy metabolismSQORIschemia/reperfusion |
| spellingShingle | Akiyuki Nishimura Tomohiro Tanaka Kakeru Shimoda Tomoaki Ida Shota Sasaki Keitaro Umezawa Hiromi Imamura Yasuteru Urano Fumito Ichinose Toshiro Kaneko Takaaki Akaike Motohiro Nishida Non-thermal atmospheric pressure plasma-irradiated cysteine protects cardiac ischemia/reperfusion injury by preserving supersulfides Redox Biology Non-thermal plasma Supersulfides Mitochondrial energy metabolism SQOR Ischemia/reperfusion |
| title | Non-thermal atmospheric pressure plasma-irradiated cysteine protects cardiac ischemia/reperfusion injury by preserving supersulfides |
| title_full | Non-thermal atmospheric pressure plasma-irradiated cysteine protects cardiac ischemia/reperfusion injury by preserving supersulfides |
| title_fullStr | Non-thermal atmospheric pressure plasma-irradiated cysteine protects cardiac ischemia/reperfusion injury by preserving supersulfides |
| title_full_unstemmed | Non-thermal atmospheric pressure plasma-irradiated cysteine protects cardiac ischemia/reperfusion injury by preserving supersulfides |
| title_short | Non-thermal atmospheric pressure plasma-irradiated cysteine protects cardiac ischemia/reperfusion injury by preserving supersulfides |
| title_sort | non thermal atmospheric pressure plasma irradiated cysteine protects cardiac ischemia reperfusion injury by preserving supersulfides |
| topic | Non-thermal plasma Supersulfides Mitochondrial energy metabolism SQOR Ischemia/reperfusion |
| url | http://www.sciencedirect.com/science/article/pii/S2213231724004233 |
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