[Participation of cytoplasmic mitochondrial function regulator in glycogen synthesis in the rat diaphragm].
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Biomedical subjects
Publications and source records attributed to I I Lavina.
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The insulin-dependent cytoplasmic factor-regulator (IDR) was shown to inhibit pyruvate and succinate oxidation by the rat liver mitochondria. In view of the fact that insulin increases and adrenaline decreases IDR activity in the liver cytoplasm it is suggested that oxidation of the substrate in mitochondria in vivo is regulated by changes in IDR content in cytoplasm. It was shown that adrenaline-activated oxidation apart from decreased activity of IDR in cytoplasm is induced by a different mechanism not related to IDR content.
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It was shown that a factor from the thyroxine-injured mitochondria caused inhibition of mitochondrial swelling in isotonic KNO3 and NH4NO3 solutions in the presence of rotenone. These data were interpreted as permeability inhibition for K+ and H+ ions.
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In ischemic impairment of liver tissue the activating effect of the cytoplasmic thermostable fraction on the transport of Ca2+ ions was decreased in liver mitochondria. Fast decrease in the cytoplasmic activity occurred also after preincubation of liver homogenate with salt solutions. Inactivation of the cytoplasmic regulator was prevented by addition of EGTA into the homogenate, but Ca2+ showed the opposite effect. The data obtained suggest that high concentration, of Ca2+ in cytosol under conditions of ischemia is responsible for decrease of the cytoplasmic regulator activity.