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Strand asymmetry in human mitochondrial DNA mutations.
TLDR
Recurrence of nucleotide substitutions at 4-fold degenerate sites was distinctly asymmetric between the two strands: G-->A and T-->C transitions were 9- and 1.8-fold more frequent on the L strand than on the H strand, respectively. Expand
MITOCHONDRIAL DNA MUTATIONS AS AN IMPORTANT CONTRIBUTOR TO AGEING AND DEGENERATIVE DISEASES
TLDR
It is proposed that the accumulation of mitochondrial mutations and the subsequent cytoplasmic segregation of these mutations during life is an important contributor both to the ageing process and to several human degenerative diseases. Expand
Deficiencies in complex I subunits of the respiratory chain in Parkinson's disease.
TLDR
No clear difference was noted in immunoblotting studies on subunits of Complexes III and IV between the control and Parkinson's disease, but defects in Complex I subunits seem to be one of the most important clues to elucidate pathogenesis of Parkinson's Disease. Expand
Identification of two point mutations in the gene coding luteinizing hormone (LH) beta-subunit, associated with immunologically anomalous LH variants.
TLDR
Two nucleotide substitutions in the LH beta gene of the patients, which cause amino acid replacements from Trp8 (TGG) to Arg8 (CGG) and Ile15 (ATC) to Thr15 (ACC) are suggested to be responsible for this immunologically anomalous variant. Expand
Genetic and functional changes in mitochondria associated with aging.
  • T. Ozawa
  • Biology, Medicine
  • Physiological reviews
  • 1 April 1997
TLDR
The somatically acquired mutations and oxidative damage of the genome, which lead an individual to the fragmentation of mitochondrial DNA, cellular energy crisis, naturally occurring cell death (apoptosis), and tissue degeneration and atrophy, are reviewed. Expand
Mechanism of somatic mitochondrial DNA mutations associated with age and diseases.
  • T. Ozawa
  • Biology, Medicine
  • Biochimica et biophysica acta
  • 24 May 1995
TLDR
Comprehensive analyses of the entire mtDNA, including the total base-sequencing and the total deletion correlating with oxygen free-radical damage, has revealed a clear relationship between the genotype and its phenotype, such as the severity of clinical symptoms and the survival time of the patients. Expand
Age-associated oxygen damage and mutations in mitochondrial DNA in human hearts.
TLDR
The results indicate that accumulation of somatically acquired oxygen damage together with age-associated mutations in mtDNA which lead to bioenergetic deficiency and the heart muscle weakness are inevitable in human life. Expand
Age-associated damage in mitochondrial function in rat hearts
TLDR
From the results, age-associated decline in mitochondrial function might play an important role in cell aging, particularly in postmitotic cells such as heart muscle, and accumulation of oxidative damage to mtDNA might be involved in this mechanism. Expand
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