CGC Bibliography Paper 5449

Life span extensions associated with upregulation of gene expression of antioxidant enzymes in Caenorhabditis elegans: studies of mutation in the age-1, PI3 kinase homologue and short-term exposure to

Honda Y, Honda S

Medline:

Citation:

Journal of the American Aging Association 24: 179-186 2001

Type:

ARTICLE

Genes:

age-1 ctl-1 daf-2 daf-16 daf-18 fer-15 sod-1 sod-2 sod-3

Abstract:

To explain trends emerging from the study of longevity mutants, a modification of the reactive oxygen species (ROS) model of aging is suggested. ROS do not appear to be produced in greater quantities during cellular activity unless specific factors are also present. These include raised cytosolic calcium and sodium ions, nitric oxide (NO) or dopamine. Metabolically active cells that are repeatedly exposed to these factors, especially in combination, show the most ROS damage and may contribute most to aging. This explains the importance of neurons, which is highlighted by genetic studies, and points to which cells are the most aging-sensitive. Control pathways disrupted in long-lived mutants are those which control one or more of these ROS promoting factors. The daf-2/daf-16 pathway may interact with these factors in several ways. Changes in control networks may be propagated from a relatively small number of cells/junctions by neural connectivity and hormonal