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JOURNAL ARTICLE
[A pH-dependent mechanism of energy transformation in joint fluid cells in osteoarthrosis of the knee joint and benefits of chondroitinsulfate].
AIM: To study bioenergetic processes in the synovial fluid (SF) in osteoarthrosis and to study relevant effects of chondroitinsulphate (structum).
MATERIAL AND METHODS: Changes in bioenergy parameters of SF were analysed in the course of 3-month structum treatment of 15 osteoarthrosis (OA) patients. Classic enzymatic tests and polarographic test of SF cells oxygen absorption rate were used. Physiological-biochemical indices were compared at the height of the disease and after therapy.
RESULTS: A significant shift of SF pH to the acid direction was found in OA patients. There was also transformation of bioenergetic processes with resultant loss of synovial cells energetics (low ATP and switch on of a reserve energetic mechanism of creatinephosphate consumption). Pharmacological correction of energy metabolism of SF cells was obtained due to action of chondroprotector structum.
CONCLUSION: OA provokes bioenergetic changes in SF with activation of glycolysis, employment of reserve bioenergetic mechanisms, enhancement of creatinephosphate degradation, discoordination of respiration with oxidant phosphorilation. The pH shift to acid direction (from 7.4 to 6.85 in OA) is a trigger mechanism of OA. Replacement therapy with polyanion drug structum corrects pH in 3 months and bioenergetic parameters.
MATERIAL AND METHODS: Changes in bioenergy parameters of SF were analysed in the course of 3-month structum treatment of 15 osteoarthrosis (OA) patients. Classic enzymatic tests and polarographic test of SF cells oxygen absorption rate were used. Physiological-biochemical indices were compared at the height of the disease and after therapy.
RESULTS: A significant shift of SF pH to the acid direction was found in OA patients. There was also transformation of bioenergetic processes with resultant loss of synovial cells energetics (low ATP and switch on of a reserve energetic mechanism of creatinephosphate consumption). Pharmacological correction of energy metabolism of SF cells was obtained due to action of chondroprotector structum.
CONCLUSION: OA provokes bioenergetic changes in SF with activation of glycolysis, employment of reserve bioenergetic mechanisms, enhancement of creatinephosphate degradation, discoordination of respiration with oxidant phosphorilation. The pH shift to acid direction (from 7.4 to 6.85 in OA) is a trigger mechanism of OA. Replacement therapy with polyanion drug structum corrects pH in 3 months and bioenergetic parameters.
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