title: Laboratory markers as an index of aging.
abstract: At the cellular level, mutations in deoxyribonucleic acid (DNA) can lead to synthesis of altered proteins which are unable to sustain specific cell functions, eventually leading to its death. Veritably apoptosis, or programmed cell death, is a device to eliminate heavily mutated cells. Cell membranes with altered proteins can be recognized as foreign by the immune system, thus triggering autoimmunity. Molecular biology techniques allow us to examine changes that occur in DNA, reflected by polymorphisms and variable numbers of tandem repeats (VNTR). A general decline in organ function is associated with aging. However, these changes may also be precipitated by disease processes. Homeostatic control by the hypothalamus-pituitary-adrenal axis is also compromised with aging, leading to an increase in plasma adrenocorticotrophic hormone (ACTH) and corticosteroid levels. Derangement of the immune system with aging results in dysregulation of cytokine production. The ability of the cell to survive the onslaught of oxygen-free radicals with enzymatic and nonenzymatic antioxidants, and to repair DNA by activation of nuclear enzymes such as poly (ADP-ribose) polymerase (PAD-PRP), are some of determinants of aging.
authors.affiliation: Department of Pathology, New York Medical College, Metropolitan Hospital Center, New York, NY 10029.
authors.forename: S
authors.initials: S
authors.lastname: Narayanan
mesh_terms: D000375:Aging; D000818:Animals; D017209:Apoptosis; D004260:DNA Repair; D004314:Down Syndrome / Q000276:immunology; D005609:Free Radicals; D005979:Glutathione Peroxidase / Q000502:physiology; D006801:Humans; D015850:Interleukin-6 / Q000096:biosynthesis; D015032:Zinc / Q000502:physiology
chemical_list: D005609:Free Radicals; D015850:Interleukin-6; D005979:Glutathione Peroxidase; D015032:Zinc