Download Free Relationship Between Dna Repair Capacity And Cellular Aging Book in PDF and EPUB Free Download. You can read online Relationship Between Dna Repair Capacity And Cellular Aging and write the review.

Aging occurs at the level of individual cells, a complex interplay between intrinsic "programming" and exogenous "wear and tear", with genetically-determined cellular capacity to repair environmentally-induced DNA damage playing a central role in the rate of aging and its specific manifestations. In 12 chapters, "The Role of DNA Damage and Repair in Cell Aging" provides an intellectual framework for aging of mitotic and post-mitotic cells, describes a variety of model systems for further studies, and reviews current concepts of DNA responses and their relationship to the phenomenon of aging. As part of a series entitled "Advances in Cell Aging and Gerontology," this volume also summarizes seminal recent discoveries such as the molecular basis for Werner syndrome (a mutant DNA helicase), the complementary roles of telomere shortening and telomerase activity in cell senescence versus immortalization, the role of apoptosis in the homeostasis of aging tissue, and the existence of an inducible SOS-like response in mammalian cells that minimizes DNA damage from repeatedly encountered injurious environmental agents. Insights into the relationship between cellular aging and age-associated diseases, particularly malignancies, are also provided in several chapters. This book is an excellent single source of information for anyone interested in DNA repair, mechanisms of aging, or certainly their intersection. Students will gain a general appreciation of these fields, but even the most senior investigators will benefit from the detailed coverage of rapidly advancing areas.
Why organisms age and why sexual reproduction exists are major unsolved problems in biology. This book provides an integrated explanation of aging and sex based on current knowledge of DNA damage and repair. Discusses the universality of the problem of DNA damage Describes aging as a consequence of accumulated DNA damage Considers meiosis as an adaptation for DNA repair Discusses mating in eukaryotes as an adaptation for masking mutation
This book investigates the various processes that are affected by the age of an organism. Several new tools for the analysis of biological aging have been introduced recently, and this volume provides methods and protocols for these new techniques in addition to its coverage of established procedures. Researchers seeking new technology and techniques will find this volume of tremendous benefit as they move towards new directions.
"How long can humans live? Is immortality possible? Just what is the aging process? The aging and inevitable death of the human body have inspired more myths and outrageous quackery than anything else subject to scientific inquiry. . . . Now comes a most fascinating book, insightful and scholarly, to provide what answers have emerged so far." --San Francisco Chronicle Here, at last, preeminent cell biologist Leonard Hayflick presents the truth about human aging. Based on more than thirty years of pioneering research in the field, How and Why We Age explores not only how our major biological systems change as we grow older, but also examines the intangible alterations in our modes of thinking and feeling, our moods and sexual desires, our personality traits and our memories. With the immediacy of the latest scientific discoveries, Dr. Hayflick explains how aging affects every part of the body, and dispels many of the most persistent aging myths, to show that: * Hearts do not naturally get weaker with age. * Regular exercise and a low-fat diet won't slow aging. * Curing cancer would only add two years to the average sixty-five-year-old American life. Curing heart disease, however would add fourteen years. * Only five percent of people over the age of sixty-five are in nursing homes * No human has lived--or probably can live--past 120 years. Gracefully written, clearly organized, and packed with essential facts and statistics, How and Why We Age is a landmark study of the aging process for readers of all ages. "Written in clear, nontechnical language, it is an excellent introduction to the scientific and demographic literature on this multifacetedsubject." --Nature
This text examines the relationship between DNA damage and repair, cellular senescence, genomic instability, and aging. The authors provide in-depth discussions of various types of DNA damage, the DNA repair network, and cellular responses to genetic damage to assess their impact on the modulation of aging processes and age-related diseases, including cancer development. Chromosomal Instability and Aging describes cloning genes for human chromosomal instability disorders, the causal factors and consequences of chromosomal injury, the telomere hypothesis of aging, and age-dependant mitochondrial genetic instability. It includes more than 2200 references to facilitate further research, making it an informative and timely guide.
Cutting edge reviews by leading researchers illuminate key aspects of DNA repair in mammalian systems and its relationship to human genetic disease and cancer. Major topics include UV and X-Ray repair, repair of chemical damage, recombinational repair, mismatch repair, transcription-repair coupling, and the role of DNA repair in disease prevention. Extensive up-to-date references and rigorous peer-review of each chapter make this volume definitive and bring it to the active frontiers of research.
The covalent attachment to deoxyribonucleic acid in vivo of a large number of different types of chemical compounds (both normal cellular constituents such as proteins and amino acids, and also exogenous compounds such as drugs, carcinogens, etc. ) have been shown to exert profound effects upon cells. Four research activi ties, formerly considered to be totally independent, relate to this problem of nucleic acid adducts--(1) normal covalent attachment of DNA to membranes, protein linkers in chromosomes, etc. ; (2) the roles of radiation and chemical enhancement of DNA adduct formation in cell killing and mutagenesis. (A related field is the use of known cross-linking reactions to gain information on structural associations in macromolecular complexes. ); (3) the relevance of DNA adducts to chemical and radiation carcinogenesis; (4) the rele vance of DNA adducts to the cross-linking theory of cellular aging. (1) There are numerous examples of normal linkages between DNA and protein, e. g. , DNA-membrane attachment sites, protein linkers in chromosomes, amino acids covalently linked to DNA as a function of growth conditions, and gene regulation by non-covalently bound proteins. A summary of data on natural adducts to DNA thus serves to introduce the subject of the radiation and chemical enhancement of DNA adduct formation. (2) In the past, radiation biology has been concerned mainly with trying to understand the radiation chemistry of purified DNA, and the biological effects and repair of these radiation-induced alterations when produced in cellular DNA.
The ?eld of cellular responses to DNA damage has attained widespread recognition and interest in recent years commensurate with its fundamental role in the ma- tenance of genomic stability. These responses, which are essential to preventing cellular death or malignant transformation, are organized into a sophisticated s- tem designated the “DNA damage response”. This system operates in all living organisms to maintain genomic stability in the face of constant attacks on the DNA from a variety of endogenous by-products of normal metabolism, as well as exogenous agents such as radiation and toxic chemicals in the environment. The response repairs DNA damage via an intricate cellular signal transduction network that coordinates with various processes such as regulation of DNA replication, tr- scriptional responses, and temporary cell cycle arrest to allow the repair to take place. Defects in this system result in severe genetic disorders involving tissue degeneration, sensitivity to speci?c damaging agents, immunode?ciency, genomic instability, cancer predisposition and premature aging. The ?nding that many of the crucial players involved in DNA damage response are structurally and functionally conserved in different species spurred discoveries of new players through similar analyses in yeast and mammals. We now understand the chain of events that leads to instantaneous activation of the massive cellular responses to DNA lesions. This book summarizes several new concepts in this rapidly evolving ?eld, and the advances in our understanding of the complex network of processes that respond to DNA damage.