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000136212 0247_ $$2doi$$a10.1016/j.mito.2010.12.012
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000136212 0247_ $$2ISSN$$a1872-8278
000136212 037__ $$aDZNE-2020-02534
000136212 041__ $$aEnglish
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000136212 1001_ $$aGizatullina, Zemfira Z$$b0
000136212 245__ $$aEffects of cyclosporine A and its immunosuppressive or non-immunosuppressive derivatives [D-Ser]8-CsA and Cs9 on mitochondria from different brain regions.
000136212 260__ $$aAmsterdam [u.a.]$$bElsevier Science$$c2011
000136212 264_1 $$2Crossref$$3print$$bElsevier BV$$c2011-05-01
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000136212 520__ $$aWe studied the functional properties of isolated brain mitochondria (BM) prepared from total rat brain (BM(total)) or from cerebral subregions under basal and Ca(2+) overload conditions in order to evaluate the effects of cyclosporine A (CsA) in a regiospecific manner. CsA-induced effects were compared with those of two derivatives-the none-immunosuppressive [O-(NH(2)(CH2)(5)NHC(O)CH(2))-D-Ser](8)-CsA (Cs9) and its congener, the immunosuppressive [D-Ser](8)-CsA. The glutamate/malate-dependent state 3 respiration of mitochondria (state 3(glu/mal)) differed in region-specific manner (cortex > striatum = cerebellum > substantia nigra > hippocampus), but was significantly increased by 1μM CsA (+21±5%) in all regions. Ca(2+) overload induced by addition of 20μM Ca(2+) caused a significant decrease of state 3(glu/mal) (-45 to -55%) which was almost completely prevented in the presence of 1μM CsA, 1μM Cs9 or 1μM [D-Ser](8)-CsA. Mitochondrial Ca(2+) accumulation thresholds linked to permeability transition (PT) as well as the rate and completeness of mitochondrial Ca(2+) accumulation differed between different brain regions. For the first time, we provide a detailed, regiospecific analysis of Ca(2+)-dependent properties of brain mitochondria. Regardless of their immunosuppressive impact, CsA and its analogues improved mitochondrial functional properties under control conditions. They also preserved brain mitochondria against Ca(2+) overload-mediated PT and functional impairments. Since Cs9 does not mediate immunosuppression, it might be used as a more specific PT inhibitor than CsA.
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000136212 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x1
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000136212 650_7 $$2NLM Chemicals$$aEnzyme Inhibitors
000136212 650_7 $$083HN0GTJ6D$$2NLM Chemicals$$aCyclosporine
000136212 650_7 $$0SY7Q814VUP$$2NLM Chemicals$$aCalcium
000136212 650_2 $$2MeSH$$aAnimals
000136212 650_2 $$2MeSH$$aBrain: drug effects
000136212 650_2 $$2MeSH$$aCalcium: metabolism
000136212 650_2 $$2MeSH$$aCell Respiration: drug effects
000136212 650_2 $$2MeSH$$aCyclosporine: metabolism
000136212 650_2 $$2MeSH$$aEnergy Metabolism: drug effects
000136212 650_2 $$2MeSH$$aEnzyme Inhibitors: metabolism
000136212 650_2 $$2MeSH$$aMale
000136212 650_2 $$2MeSH$$aMitochondria: drug effects
000136212 650_2 $$2MeSH$$aRats
000136212 7001_ $$aGaynutdinov, Timur M$$b1
000136212 7001_ $$aSvoboda, Hanno$$b2
000136212 7001_ $$aJerzembek, Doreen$$b3
000136212 7001_ $$aKnabe, Annette$$b4
000136212 7001_ $$0P:(DE-HGF)0$$aVielhaber, Stefan$$b5
000136212 7001_ $$aMalesevic, Miroslav$$b6
000136212 7001_ $$0P:(DE-2719)2260426$$aHeinze, Hans-Jochen$$b7$$udzne
000136212 7001_ $$aFischer, Gunter$$b8
000136212 7001_ $$0P:(DE-2719)9000420$$aStriggow, Frank$$b9$$udzne
000136212 7001_ $$0P:(DE-HGF)0$$aGellerich, Frank N$$b10$$eCorresponding author
000136212 77318 $$2Crossref$$3journal-article$$a10.1016/j.mito.2010.12.012$$b : Elsevier BV, 2011-05-01$$n3$$p421-429$$tMitochondrion$$v11$$x1567-7249$$y2011
000136212 773__ $$0PERI:(DE-600)2056923-3$$a10.1016/j.mito.2010.12.012$$gVol. 11, no. 3, p. 421 - 429$$n3$$p421-429$$q11:3<421 - 429$$tMitochondrion$$v11$$x1567-7249$$y2011
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