Advances in radiation biology 

About: Advances in radiation biology is an academic journal. The journal publishes majorly in the area(s): Radiobiology & DNA repair. It has an ISSN identifier of 0065-3292. Over the lifetime, 133 publications have been published receiving 6184 citations.

Four R's of radiotherapy

Abstract: Publisher Summary Radiotherapy given as multiple doses are effective in sterilizing cancers, but the processes whereby the neoplasm is eradicated and the normal tissues are preserved are not fully understood. The differential between normal tissue and tumor response is enhanced by dose fractionation, single doses resulting in severe normal tissue injury when the dose is sufficient to control a proportion of treated tumors. This chapter focuses on the four Rs that influence the outcome of fractionated-dose radiotherapy, one or more of which may account for the relative sparing of normal tissues. These are repair of sublethal injury in normal and neoplastic cells, reoxygenation of the tumor, redistribution through the division cycle, and regeneration of surviving normal and malignant cells between dose fractions. These have been called the four Rs of fractionated radiotherapy. Other factors are involved in the outcome of multifraction radiotherapy—for example, the maintenance of the architectural integrity of the normal tissues, the volume of tissue irradiated, the tumor bed, and the immunocompetence of the host are some other factors that play a significant role in the differential response.

Mutation Induction in Mice

Abstract: Publisher Summary This chapter reviews gene or point mutations. It also discusses the fine structure of mutation-induced point mutations in mice. The work on mutation induction in mice has lead to an accurate assessment of human genetic hazards from radiation. Induced point mutations are detected and studied mainly by genetic methods, although biochemical techniques have also been used. Male germ cells take up a more central or medullary position whereas female germ cells take up a more peripheral or cortical one. It has been found that on the development and radiation response of germ cells in female mice that with postnatal irradiation at any age, the progeny will be derived from irradiated dictyate oocytes, unless fertilization of the eggs takes place within 12 hours of the irradiation. With neonatal and late fetal irradiation, exposed germ cells are normally in predictyate stages of meiotic prophase. Irradiations of younger embryos expose oogonia and their precursors. The specific locus method is the most efficient way of studying point mutations in mice. It is designed to detect mutations affecting a particular set of loci in the mouse that are chosen because their known mutant alleles have a clear-cut and easily visible effect.

Molecular mechanisms of radiation-induced damage to nucleic acids

Abstract: Publisher Summary The integrity of DNA is essential for the well-being of a cell. Damage to this molecule, whether caused by reaction with chemical mutagens, by irradiation with ultraviolet (UV) light, or by ionizing radiation, has dire consequences. Thus, much effort has been expended in attempting to understand the effects of these agents on DNA. This chapter describes some of the chemical mechanisms whereby DNA is damaged by ionizing radiation. The major advances in understanding of molecular mechanisms have come from the studies of simple model systems. The chapter explains the three basic model systems that have been designed to examine radiation-induced damage to DNA. Each type of system yields useful information, but the applicability of this information to the in vivo situation is limited in all cases. The chapter also discusses the indirect effects of the free radicals produced by the radiolysis of water, in terms of both initial species and final products.

Repair Processes for Photochemical Damage in Mammalian Cells

Abstract: Publisher Summary This chapter discusses different repair processes for photochemical damage in mammalian cells. Eukaryotic chromosomes respond to DNA and protein damage in different ways. Damage to DNA alone has minimal effect on overall chromosomal structure that is maintained by protein. Damage to protein results in disruption of the chromosome and breaks in DNA. Repair of damage to each chromosomal component is different. Protein damage does not initially involve loss of genetic information, so repair can be affected through normal protein synthesis pathways that are active at all stages of the cell cycle. Repair of DNA involves novel pathways, such as photo reactivation and excision repair that are distinct from normal DNA synthesis and insensitive to many inhibitors that block semi-conservative DNA replication. During normal replication, there is an additional recovery system, S-phase recovery, which enables DNA to be replicated on damaged templates.

ADP-Ribose in DNA Repair: A New Component of DNA Excision Repair

Abstract: Publisher Summary This chapter focuses on ADP-ribose in DNA repair. The fact that (ADP-ribose) n biosynthesis is required for efficient DNA repair rests on a large variety of observations. All DNA-damaging agents lower cellular NAD because they promote the biosynthesis of (ADP-ribose) n . DNA-damaging agents increase intracellular (ADP-ribose) n . Nuclear ADP-ribosyl transferase is activated by both single- and double-strand breaks in the DNA. All the inhibitors of nuclear ADP-ribosyl transferase prevent the drop in cellular NAD caused by DNA-damaging agents. All the enzyme inhibitors also inhibit DNA excision repair after both chemical and radiation damage. Alkylation damage increases DNA ligase activity, and it is predominantly DNA ligase II activity that is increased. One function of (ADP-ribose) n in DNA repair is in regulating DNA ligase II activity. Nuclear ADP-ribosyl transferase activity is activated by breaks in the DNA, and ADP-ribosylation, in turn, regulates DNA ligase II activity. Nuclear ADP-ribosyl transferase regulates DNA ligation in DNA repair and in other DNA rearrangements, such as DNA recombination, gene rearrangements, transpositions, sister chromatid exchanges, and chromosomal aberrations.