Molecular Mechanisms Of Dna Photodamage

Written in an accessible and comprehensive manner, DNA Photodamage will appeal to all scientists working in the area whether specialists in the discipline or not and provides a complete coverage of the field, from ultrafast spectroscopy to biomedical research.

An "age" has passed in the 40 years since we first observed recovery from radiation damage in irradiated bacteria. During the early 1930s, we had been discussing the possibility of rapid changes after radiation exposure with Farring ton Daniels, Benjamin Duggar, John Curtis, and others at the University of Wisconsin. After working with living cells, we had concluded that organisms receiving massive insults must have a wide variety of repair mechanisms available for restoration of at least some of the essential properties of the cell. The problem was how to fmd and identify these recovery phenomena. At that time I was working on a problem considered to be of great importance-the existence of the so-called mitogenetic rays. Several hundred articles and a score of books had already appeared dealing with mitogenetic rays, a type of radiation that was thought to exist in the shorter ultraviolet region. Our search for mitogenetic rays necessitated the design of experiments of greatest sensitivity for the detection of ultraviolet. It was vital that conditions be kept as constant as possible during exposure. All the work was done at icewater temperature (3-5°C) during and after exposure. We knew that light was an important factor for cell recovery, so all our experiments were done in dim light, with the plated-out cells being covered with dark cloth. Our statements on the effect of visible light stimulated Kelner to search for "photoreactivation' (as it was later called).

Mechanisms of DNA Repair.

DNA Repair Mechanisms is an account of the proceedings at a major international conference on DNA Repair Mechanisms held at Keystone, Colorado on February 1978. The conference discusses through plenary sessions the overall standpoint of DNA repair. The papers presented and other important documents, such as short summaries by the workshop session conveners, comprise this book. The compilation describes the opposing views, those that agree and dispute about certain topic areas. This book, divided into 15 parts, is arranged according to the proceedings in the conference. The plenary sessions are grouped with the related workshop and poster manuscripts. The first two parts generally tackle repair in terms of its identification and quantification, as well as the models, systems, and perspectives it utilizes. The following parts discuss the various types of repair including base excision, nucleotide excision repair in bacteria, excision repair in mammalian cells, inducible/error-prone repair in prokaryotes, and strand break repair in mammalian cells among others. This reference material looks into the replicative bypass mechanisms in mammalian cells, viral probes, and hereditary repair defects. It explains repair deficiency and human disease, as well as mutagenesis and carcinogenesis. The last part of this book deals with the consequences and effects of DNA repair. This volume is a helpful source of reference for students, teachers, scientists, and researchers in the different fields of genetics, radiology, biochemistry, and environmental biology.

This book is based on the papers presented at the conference on "Mecha nisms of DNA Damage and Repair: Implications for Carcinogenesis and Risk Assessment," held at the National Bureau of Standards on June 2-7, 1985, This volume deals with mechanisms of DNA damage and repair at the molecular level; consequences of unrepaired or misrepaired damage, with major emphasis on carcinogenesis; drugs which bind selectively to altered and potentially damaging DNA sequences; and potential utilization of DNA damage as an endpoint for assessing risks of UV light, ionizing radiations, chemicals, drugs, and hazardous agents in foods. Because the induction of mutations by radiation and genotoxic chemicals has been observed to follow one-hit kinetics in some instances, it is generally assumed that any level of exposure to a DNA-damaging agent may increase the risk of genetic disease or cancer in an exposed population. At the same time, however, there is evidence that although the DNA of living cells is continually damaged by natural background radiation, free radicals, and other naturally occurring processes, most of the damage is normally repaired.

Stands as the most comprehensive guide to the subject-covering every essential topic related to DNA damage identification and repair. Covering a wide array of topics from bacteria to human cells, this book summarizes recent developments in DNA damage repair and recognition while providing timely reviews on the molecular mechanisms employe

DNA is the most important biomolecule ever discovered. Indeed, this molecule bears genetic information from one generation to another. In this regard, DNA bases have a key role in transferring genetic information and data safely. However, there are cellular, genetic, and environmental factors that may damage the different parts of DNA molecules. These damages may result in mutations and cell death. As such, several DNA repair mechanisms have evolved. Over three sections, this book examines many of these mechanisms.

The objectives of this work are to elucidate the molecular mechanisms that are responsible for radiation-induced DNA damage. The overall goal is to understand the relationship between the chemical and structural changes produced by ionizing radiation in DNA and the resulting impairment of biological function expressed as carcinogenesis or cell death. The studies are based on theoretical explorations of possible mechanisms that link initial radiation damage in the form of base and sugar damage to conformational changes in DNA. These mechanistic explorations should lead to the formulation of testable hypothesis regarding the processes of impairment of regulation of gene expression, alternation in DNA repair, and damage to DNA structure involved in cell death or cancer.