A 2×2 factorial design was used to evaluate possible preservation of mitochondrial functions in two cardioprotective experimental models, remote ischemic preconditioning and streptozotocin-induced diabetes mellitus, and their interaction during ischemia/reperfusion injury (I/R) of the heart. Male Wistar rats were randomly allocated into four groups: control (C), streptozotocin-induced diabetic (DM), preconditioned (RPC) and preconditioned streptozotocin-induced diabetic (DM+RPC). RPC was conducted by 3 cycles of 5-min hind-limb ischemia and 5-min reperfusion. DM was induced by a single dose of 65 mg/kg streptozotocin. Isolated hearts were exposed to ischemia/reperfusion test according to Langendorff. Thereafter mitochondria were isolated and the mitochondrial respiration was measured. Additionally, the ATP synthase activity measurements on the same preparations were done. Animals of all groups subjected to I/R exhibited a decreased state 3 respiration with the least change noted in DM+RPC group associated with no significant changes in state 2 respiration. In RPC, DM and DM+RPC group, no significant changes in the activity of ATP synthase were observed after I/R injury. These results suggest that the endogenous protective mechanisms of RPC and DM do preserve the mitochondrial function in heart when they act in combination.
- MeSH
- experimentální diabetes mellitus metabolismus MeSH
- ischemické přivykání metody MeSH
- krysa rodu rattus MeSH
- myokard metabolismus MeSH
- náhodné rozdělení MeSH
- potkani Wistar MeSH
- reperfuzní poškození myokardu metabolismus prevence a kontrola MeSH
- spotřeba kyslíku fyziologie MeSH
- srdeční mitochondrie fyziologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Z histórie je známe, že hlad ľudstva bol výsledkom zlej úrody, vojen a rôznych ekologických katastrof. Hladomory boli sprevádzané masovými stratami na ľudských životoch. Veľký strach z hladu často viedol ku kanibalizmu, dokonca medzi rodičmi a deťmi(1). Iná situácia je pri cielenom dennom obmedzení príjmu kalórií – reštrikcia kalórií (RK) počas niekoľkých dní, s cieľom predĺžiť ľudský vek a zlepšiť kvalitu života. Pravdepodobne najstaršie správy o význame RK pochádzajú od talianskeho šľachtica Luigiho Cornara, ktorý sa narodil v roku 1464. Vo veku 83 a 95 rokov napísal knihy o účinku RK na vek, pričom sám sa dožil 102 rokov. Propagoval vyslovene „triezvy život“ a „umenie, ako dlho žiť“. George Washington (1732 – 1799) poukázal na význam obmedzenia denného prísunu kalórií na zdravie a predĺženie veku. RK má priaznivý vplyv na choroby, spojené s vyšším vekom, znižuje riziko rakoviny, neurodegeneratívnych a kardiovaskulárnych chorôb, ako aj diabetu 2. typu(2,3).
UNLABELLED: Remote ischemic preconditioning (RIP)-induced protection of myocardial energetics was well documented on the level of tissue, but data concerning the involvement of mitochondria were missing. We aimed at the identification of changes in membrane properties and respiratory functions induced in rat heart mitochondria by RIP. Experiments were performed on 46 male Wistar rats divided into control and RIP-treated groups of 21 animals each. Blood flow in the occluded area was recorded by MRI angiography in four animals. RIP protocol comprised of three successive 5-min occlusions each followed by 5-min reperfusions of descending branches of the right hind limb femoral artery. The efficacy of RIP was evaluated as the extent of RIP-induced protection against damage to the functions of mitochondria isolated by differential centrifugation after 30-min global ischemia followed by 40-min reperfusion of the hearts in Langendorff mode. ASSESSMENTS: mitochondrial membrane fluidity with a fluorescent probe DPH, CoQ(9) and CoQ(10) with HPLC, mitochondrial respiration with the Oxygraph-2k (Oroboros). Results revealed that RIP was affecting the mitochondria. The immediate protection conferred by RIP involves beneficial and prognostically significant effects: a total elimination of ischemia/reperfusion-induced depression of mitochondrial membrane fluidity and a trend for better preservation of mitochondrial state 3 respiration.
- MeSH
- buněčná membrána metabolismus MeSH
- ischemické přivykání * MeSH
- končetiny krevní zásobení MeSH
- oxidativní fosforylace MeSH
- potkani Wistar MeSH
- srdeční mitochondrie metabolismus MeSH
- transport elektronů MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Publikační typ
- abstrakt z konference MeSH
- MeSH
- elektronový transportní řetězec fyziologie metabolismus MeSH
- finanční podpora výzkumu jako téma MeSH
- hypertenze metabolismus MeSH
- kosterní svaly enzymologie fyziologie metabolismus MeSH
- modely genetické MeSH
- mozek fyziologie patofyziologie MeSH
- oxid dusnatý biosyntéza chemická syntéza MeSH
- potkani inbrední SHR genetika metabolismus MeSH
- potkani Wistar anatomie a histologie MeSH
- svalové mitochondrie fyziologie genetika metabolismus MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- srovnávací studie MeSH
- Klíčová slova
- Provinol,
- MeSH
- alfa-tokoferol chemie MeSH
- fenoly farmakologie MeSH
- finanční podpora výzkumu jako téma MeSH
- hypertenze farmakoterapie MeSH
- krevní tlak účinky záření MeSH
- mitochondrie chemie MeSH
- mozek MeSH
- potkani inbrední SHR MeSH
- synthasa oxidu dusnatého chemie MeSH
- ubichinon chemie MeSH
- víno MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
Adjuvant arthritis (AA) is a model of chronic inflammation induced by Mycobacterium butyricum and characterized by similar pathophysiological and pathobiochemical changes as rheumatoid arthritis (RA) in humans. In this study the antirheumatic activity of coenzyme Q(10) supplementation was tested not only as to its capability to suppress the inflammation edema of the hind paw and to improve the body weight of the arthritic animals, but also to improve so important biochemical parameters as markers of inflammation and oxidative stress, and of mitochondrial bioenergetics. Despite the unfavorable effects on the rheumatic processes observed by monitoring biometric parameters (hind paw volume, relative body weight, relative weight of spleen), a significant protective effect was observed on the level of mitochondrial energetic and antioxidant disbalance. This finding speaks in favor of CoQ(10) supplementation in rheumatic patients, presumably as combinatory therapy with classical antirheumatics, e.g. NSAIDs.
Creatine kinase (CK) plays a central role in energy transfer in cells with high-energy demands, and the enzyme is rather susceptible to oxidative inactivation. The aim of the present study was to investigate whether the rate constant of forward CK reaction (k(for)) is a suitable indicator of alterations in cerebral energy metabolism. We monitored k(for) in the rat brain non-invasively by in vivo phosphorus ((31)P) magnetic resonance spectroscopy (MRS). To alter energy metabolism, we applied following experimental models: Huntington's disease, diabetes mellitus, chronic alcohol intoxication and chronic cerebral hypoperfusion (vascular dementia model). Results of our (31)P MRS experiment confirm importance of creatine kinase/phosphocreatinine (CK/PCr) system in the regulation of brain energy metabolism in vivo because a kinetic parameter k(for) was significantly changed in all above animal models that simulate neurodegenerative diseases or commonly during oxidative stress. Using this method we distinguished vascular dementia (VD) and Huntington disease (HD), because in VD model a kinetic parameter k(for) decreased and in the case HD increased. Considering the importance of CK for the maintenance of energy homeostasis in the brain, it is conceivable that an alteration of this enzyme activity in the brain may be one of the mechanisms by which various neurodegenerative diseases might be monitored just by means saturation transfer method (31)P MRS.
- MeSH
- biologické markery analýza MeSH
- energetický metabolismus MeSH
- Huntingtonova nemoc MeSH
- kreatinkinasa analýza MeSH
- krysa rodu rattus MeSH
- magnetická rezonanční spektroskopie diagnostické užití MeSH
- modely nemocí na zvířatech MeSH
- mozek metabolismus MeSH
- neurodegenerativní nemoci diagnóza MeSH
- vaskulární demence diagnóza MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Klíčová slova
- PROVINOL,
- MeSH
- finanční podpora výzkumu jako téma MeSH
- hypertenze genetika MeSH
- krysa rodu rattus MeSH
- mitochondrie metabolismus MeSH
- ubichinon metabolismus MeSH
- víno využití MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- zvířata MeSH
