title: [MITOCHONDRIA RESPIRATION AND OXIDATIVE PHOSPHORILATION OF RAT TISSUES AT TAURINE PER ORAL INJECTION].
abstract: Taurine--sulphur-containing amino acid is a necessary component of mitochondrial matrix, where it maintains pH and is included in mitochondrial transport RNA. But still it is unclear how taurine influences on ATP synthesis and mitochondrial respiration chain components activity. Thus, the aim of the work was to study the effect of long-term per oral taurine injection on mitochondrial respiration intensity in rat tissues: liver, brain, testes and thigh muscle. For this purpose male Wistar rats, that weighted 190-220 g, were divided in three groups, daily during 28 days they were injected drinking water (control group) or taurine solution 40 and 100 mg per kg of body weight (I and II research groups, correspondingly). Respiration intensity was measured polarogrifically with use of Clark electrode at endogenic substrates oxidation (V₁), with exogenic α-ketoglutarate (5 mmol/l) or succinate (1 mmol/l;V₄S) addition, at ADP addition to concentration 200 µmol/l (V₃), and after ADP depletion (V₄ATP). Phosphorylation time, oxidative phosphorilation efficacy (ADP/O), respiratory controls by Lardy (V₃/V₄S) and Chance (V₃/V₄ATP) were calculated. It was found that long term taurine injection increased V₁ in animal brain and liver of both research groups, but it decreased in testes and muscles of I research group. In liver of I research group animals, when both α-ketoglutarate and succinate were oxidated, V₄S, V₃ and V₄ATP were 4-7 times larger than in control. At the same time, Lardy respiratory control increased at succinate oxidation, this may indirectly point on increased coupling between respiration and oxidative phosphorylation. In liver of II research group animals V₄S, V₃ and V₄/ATP when α-ketoglutarate was oxidated were significantly higher than in control. In muscles of I research group V₄S, V₃ and V₄ATP when α-ketoglutarate and succinate was added were lower than in control. In thigh muscle of II research group animals at α-ketoglutarate oxidation V₃ was higher than in control. When succinate was added V₄S and V₄ATP increased in testes mitochondria of both research groups and in brain of I research group. But in II research group animals mitochondria V₄S brain was lower than in control. At the same time, coupling between respiration and oxidative phosphorytation in brain was on control level, in testes of I research group it was lower. In testes of II research group animals at α-ketoglutarate addition increased respiratory controls. Thus, the effect of long term per oral taurine injection on mitochondria respiration intensity is dose-dependent and tissue-specific and, obviously, has different significance and is implemented by different mechanisms.
authors.forename: R D
authors.initials: RD
authors.lastname: Ostapiv
authors.forename: V V
authors.initials: VV
authors.lastname: Manko
mesh_terms: D000244:Adenosine Diphosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000284:Administration, Oral; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D007656:Ketoglutaric Acids / Q000378:metabolism* / Q000494:pharmacology; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism; D009928:Organ Specificity; D010085:Oxidative Phosphorylation / Q000187:drug effects*; D010101:Oxygen Consumption / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D019802:Succinic Acid / Q000378:metabolism* / Q000494:pharmacology; D013654:Taurine / Q000378:metabolism / Q000494:pharmacology*; D013737:Testis / Q000187:drug effects / Q000378:metabolism
chemical_list: D007656:Ketoglutaric Acids; D013654:Taurine; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D019802:Succinic Acid