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The effect of inactin on kidney mitochondrial function and production of reactive oxygen species
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.ORCID iD: 0000-0002-9077-2682
Aarhus Univ, Dept Clin Med, Aarhus, Denmark.
Linkoping Univ, Dept Med & Hlth Sci, Linkoping, Sweden.ORCID iD: 0000-0001-6148-1053
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology.
2018 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 13, no 11, article id e0207728Article in journal (Refereed) Published
Abstract [en]

Inactin is a long lasting anesthetic agent commonly used in rat studies, but is also shown to exert physiological effects such as reducing renal blood flow, glomerular filtration rate and depressing tubular transport capacity. The effect of inactin on isolated kidney mitochondria is unknown and may be important when studying related topics in anaesthetized animals. The aim of this study was to determine whether inactin exerts effects on mitochondrial function and production of reactive oxygen species. Kidney mitochondrial function and production of reactive oxygen after acutely (5 min) or longer (1.5 hour) anesthetizing rats with inactin was evaluated using high-resolution respirometry. The results demonstrate that inactin significantly improves respiratory control ratio, inhibits complex I in the mitochondrial respiratory chain, reduce both unregulated proton leak and time dependently reduce the regulated proton leak via uncoupling protein-2 and adenine nucleotide translocase. Inactin also contributes to increased mitochondrial hydrogen peroxide production. In conclusion, inactin exerts persistent effects on mitochondrial function and these profound effects on mitochondrial function should to be considered when studying mitochondria isolated from animals anesthesized with inactin.

Place, publisher, year, edition, pages
2018. Vol. 13, no 11, article id e0207728
National Category
Physiology
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URN: urn:nbn:se:uu:diva-372448DOI: 10.1371/journal.pone.0207728ISI: 000451325700060PubMedID: 30475856OAI: oai:DiVA.org:uu-372448DiVA, id: diva2:1275988
Funder
Swedish Research CouncilSwedish Diabetes AssociationÅke Wiberg FoundationNovo NordiskSwedish Society for Medical Research (SSMF)Available from: 2019-01-07 Created: 2019-01-07 Last updated: 2019-01-07Bibliographically approved

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Schiffer, Tomas A.Palm, Fredrik

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