title: The mitochondrial F1-ATPase and the aging process.
abstract: A progressive dysfunction of the mitochondrion probably plays a decisive role in the aging process. In the present hypothesis it is suggested that the functional defect specifically concerns the catalytic subunit of the mitochondrial F1-ATPase. This proposal is based on observations concerning two classical models of the aging process. 1. The Werner syndrome of premature aging is autosomally recessive; meaning that this disorder--in analogy with other recessive inborn errors of metabolism--results from a single specific mutation, typically resulting in an enzyme defect. 2. The strong association between the ATPase activity of the SV40 T-antigen and the process of cellular immortalization in vitro, suggests that the putative enzyme dysfunction could concern an ATPase. The decrease with aging in the activity of the mitochondrial F1-ATPase--the main producer of ATP--could lay behind the progressive lack of homeostasis observed in senescence.
authors.affiliation: Department of Clinical Chemistry, Blekinge County Hospital, Karlskrona, Sweden.
authors.forename: J
authors.initials: J
authors.lastname: Kröll
mesh_terms: D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000375:Aging / Q000378:metabolism*; D000952:Antigens, Polyomavirus Transforming / Q000502:physiology; D002472:Cell Transformation, Viral; D005808:Genes, Recessive; D006706:Homeostasis; D006801:Humans; D008928:Mitochondria / Q000201:enzymology* / Q000502:physiology; D008954:Models, Biological; D010085:Oxidative Phosphorylation; D006180:Proton-Translocating ATPases / Q000172:deficiency* / Q000235:genetics / Q000502:physiology; D013539:Simian virus 40 / Q000201:enzymology; D014898:Werner Syndrome / Q000201:enzymology / Q000235:genetics
chemical_list: D000952:Antigens, Polyomavirus Transforming; D000255:Adenosine Triphosphate; D006180:Proton-Translocating ATPases