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aco-2  -  Protein ACO-2

Caenorhabditis elegans

 
 
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High impact information on aco-2

  • Utilizing an immunochemical probe for oxidatively modified proteins, we show that mitochondrial aconitase, an enzyme in the citric acid cycle, is a specific target during aging of the housefly [1].
  • The oxidative damage detected immunochemically was paralleled by a loss of catalytic activity of aconitase, an enzyme activity that is critical in energy metabolism [1].
  • This expected decrease was observed when flies were exposed to hyperoxia, which oxidizes aconitase, and when they were given fluoroacetate, an inhibitor of aconitase [1].
  • We have investigated physiological changes associated with long-term diapause survival, and found that dauer larvae slowly develop senescence-like symptoms, including decrease of metabolic capacity, aconitase enzyme activity, and ATP stores, and increase of lipofuscin- and oxidised flavin-specific fluorescence [2].

References

  1. Oxidative damage during aging targets mitochondrial aconitase. Yan, L.J., Levine, R.L., Sohal, R.S. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  2. Ageing is reversed, and metabolism is reset to young levels in recovering dauer larvae of C. elegans. Houthoofd, K., Braeckman, B.P., Lenaerts, I., Brys, K., De Vreese, A., Van Eygen, S., Vanfleteren, J.R. Exp. Gerontol. (2002) [Pubmed]
 
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