Počet záznamů: 1
Potential of Mitochondria-Targeted Antioxidants to Prevent Oxidative Stress in Pancreatic beta-cells
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SYSNO ASEP 0506716 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název Potential of Mitochondria-Targeted Antioxidants to Prevent Oxidative Stress in Pancreatic beta-cells Tvůrce(i) Plecitá-Hlavatá, Lydie (FGU-C) RID, ORCID
Engstová, Hana (FGU-C) RID, ORCID
Ježek, Jan (FGU-C) RID, ORCID
Holendová, Blanka (FGU-C) RID, ORCID, SAI
Tauber, Jan (FGU-C) RID, ORCID
Petrásková, Lucie (MBU-M) ORCID
Křen, Vladimír (MBU-M) RID, ORCID
Ježek, Petr (FGU-C) RID, ORCIDČíslo článku 1826303 Zdroj.dok. Oxidative Medicine and Cellular Longevity. - : Hindawi - ISSN 1942-0900
Roč. 2019, č. 2019 (2019)Poč.str. 16 s. Jazyk dok. eng - angličtina Země vyd. US - Spojené státy americké Klíč. slova pancreatic beta cells ; pancreatic islets ; mitochondria- targeted antioxidants ; oxidative stress ; SkQ ; S3QEL ; S1QEL Vědní obor RIV EA - Morfologické obory a cytologie Obor OECD Cell biology Vědní obor RIV – spolupráce Mikrobiologický ústav - Fyziologie CEP GA16-06700S GA ČR - Grantová agentura ČR GA17-01813S GA ČR - Grantová agentura ČR GA18-00121S GA ČR - Grantová agentura ČR Způsob publikování Open access Institucionální podpora FGU-C - RVO:67985823 ; MBU-M - RVO:61388971 UT WOS 000470182900001 EID SCOPUS 85069196242 DOI 10.1155/2019/1826303 Anotace Pancreatic beta-cells are vulnerable to oxidative stress due to their low content of redox buffers, such as glutathione, but possess a rich content of thioredoxin, peroxiredoxin, and other proteins capable of redox relay, transferring redox signaling. Consequently, it may be predicted that cytosolic antioxidants could interfere with the cytosolic redox signaling and should not be recommended for any potential therapy. In contrast, mitochondrial matrix-targeted antioxidants could prevent the primary oxidative stress arising from the primary superoxide sources within the mitochondrial matrix, such as at the flavin (I-F) and ubiquinone (I-Q) sites of superoxide formation within respiratory chain complex I and the outer ubiquinone site (IIIQ) of complex III. Therefore, using time-resolved confocal fluorescence monitoring with MitoSOX Red, we investigated various effects of mitochondria-targeted antioxidants in model pancreatic beta-cells (insulinoma INS-1E cells) and pancreatic islets. Both SkQ1 (a mitochondria-targeted plastoquinone) and a suppressor of complex III site Q electron leak (S3QEL) prevented superoxide production released to the mitochondrial matrix in INS-1E cells with stimulatory glucose, where SkQ1 also exhibited an antioxidant role for UCP2-silenced cells. SkQ1 acted similarly at nonstimulatory glucose but not in UCP2-silenced cells. Thus, UCP2 can facilitate the antioxidant mechanism based on SkQ1(+) fatty acid anion(-) pairing. The elevated superoxide formation induced by antimycin A was largely prevented by S3QEL, and that induced by rotenone was decreased by SkQ1 and S3QEL and slightly by S1QEL, acting at complex I site Q. Similar results were obtained with the MitoB probe, for the LC-MS-based assessment of the 4 hr accumulation of reactive oxygen species within the mitochondrial matrix but for isolated pancreatic islets. For 2 hr INS-1E incubations, some samples were influenced by the cell death during the experiment. Due to the frequent dependency of antioxidant effects on metabolic modes, we suggest a potential use of mitochondria-targeted antioxidants for the treatment of prediabetic states after cautious nutrition-controlled tests. Their targeted delivery might eventually attenuate the vicious spiral leading to type 2 diabetes. Pracoviště Fyziologický ústav Kontakt Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Rok sběru 2020 Elektronická adresa https://doi.org/10.1155/2019/1826303
Počet záznamů: 1