Abstract
Mitochondria is where the bulk of the cell's ATP is produced. Mutations occur to genes coding for members of the complexes involved in energy production. Some are a result of damages to nuclear coded genes and others to mitochondrial coded genes. This review describes approaches to bring small molecules, proteins and RNA/DNA into mitochondria. The purpose is to repair damaged genes as well as to interrupt mitochondrial function including energy production, oxygen radical formation and the apoptotic pathway.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Antioxidants / pharmacology
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Apoptosis / drug effects
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Apoptosis / physiology
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Carrier Proteins / metabolism
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DNA Repair / drug effects
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DNA Repair / genetics
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DNA, Mitochondrial / drug effects
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DNA, Mitochondrial / genetics
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Drug Delivery Systems / methods*
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Humans
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Macromolecular Substances / administration & dosage*
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Macromolecular Substances / metabolism
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Mitochondria / metabolism*
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Mitochondrial Diseases / drug therapy
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Mitochondrial Diseases / metabolism
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Mitochondrial Membrane Transport Proteins / metabolism*
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Mitochondrial Membranes / metabolism
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Mitochondrial Precursor Protein Import Complex Proteins
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Onium Compounds / metabolism
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Oxidative Stress
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Peptide Nucleic Acids / metabolism
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Peptide Nucleic Acids / pharmacokinetics*
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Protein Sorting Signals / genetics
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Reactive Oxygen Species / metabolism
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Saccharomyces cerevisiae
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Trityl Compounds / metabolism
Substances
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Antioxidants
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Carrier Proteins
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DNA, Mitochondrial
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Macromolecular Substances
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Mitochondrial Membrane Transport Proteins
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Mitochondrial Precursor Protein Import Complex Proteins
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Onium Compounds
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Peptide Nucleic Acids
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Protein Sorting Signals
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Reactive Oxygen Species
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TIMM23 protein, human
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Trityl Compounds
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triphenylmethylphosphonium