Aging: Alteration of DNA-Protein Information

Abstract

The techniques behind the investigation of freeradical, somatic mutation, and DNA-protein deterioration theories are no longer adequate to further our knowledge significantly on the role of DNA-protein complexes in aging dysfunction. Clearly, only the preliminaries were accomplished by studies based on the hypotheses of DNA-protein interactions for aging. As we see it, we urgently need to address ourselves to one simple question at a time, specifically to age changes in the DNA-protein complex, a potential site of primary changes leading to aging dysfunction.

Brain Poly(A)RNA During Aging: Stability of Yield and Sequence Complexity in Two Rat Strains

“…However, the mechanisms by which the genome controls aging processes remain controversial. According t o a long-standing view, 336 P. D. COLMAN ET AL. the genome becomes impaired in most cells during aging, owing t o the accumulation of somatic mutations (Szilard, 1959;Burnet, 1974) or the crosslinking of chromatin complexes (reviewed in Price and Makinodan, 1973). Impaired transcription during aging in the brain is suggested by reports of major reductions (30-50%) in the hybridization of nonrepetitive DNA t o nuclear R N A from aging mice (Cutler, 1975) and by decreased RNA content measured in whole brain or in specific neuronal types in aging rodents and humans (reviewed in Chaconas and Finch, 1973;Mann et al, 1978).…”

Introduction

“…(3) The level of the ultimate cause of aging. Here one might consider spontaneous somatic mutation, genetic programming, cross-linking, error catastrophe, free radical effects, and deterioration of the nuclear DNAprotein complex [1],…”