Mitochondrial structural and functional abnormalities in Parkinson's disease and experimental animal models of this pathology are described. Special attention is paid to the inactivation of mitochondrial enzymes, mutations in mitochondrial and nuclear DNA, and genomic and proteomic research of mitochondrial proteins in Parkinson's disease and experimental parkinsonism of animals.
Isatin-binding activity of mice liver proteins has been investigated in the samples from the control and flight groups by using the methods of biosensor and proteomic analysis. It was found the higher isatin-binding activity in mice of flight group. The content of a number of individual isatin-binding proteins in the samples of the flight groups differ slightly from the ground control. However, in samples from animals which have weekly post-flight adaptation, the level of certain proteins was significantly increased. The latter allows us to assume that the main events in the proteome of mice (at least in subproteome of isatin-binding proteins), occurs in early post-flight period.
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