Book contents
- Frontmatter
- Contents
- Contributors
- Part I General Principles of Cell Death
- 1 Human Caspases – Apoptosis and Inflammation Signaling Proteases
- 2 Inhibitor of Apoptosis Proteins
- 3 Death Domain–Containing Receptors – Decisions between Suicide and Fire
- 4 Mitochondria and Cell Death
- 5 The Control of Mitochondrial Apoptosis by the BCL-2 Family
- 6 Endoplasmic Reticulum Stress Response in Cell Death and Cell Survival
- 7 Autophagy – The Liaison between the Lysosomal System and Cell Death
- 8 Cell Death in Response to Genotoxic Stress and DNA Damage
- 9 Ceramide and Lipid Mediators in Apoptosis
- 10 Cytotoxic Granules House Potent Proapoptotic Toxins Critical for Antiviral Responses and Immune Homeostasis
- Part II Cell Death in Tissues and Organs
- Part III Cell Death in Nonmammalian Organisms
- Plate section
- References
8 - Cell Death in Response to Genotoxic Stress and DNA Damage
from Part I - General Principles of Cell Death
Published online by Cambridge University Press: 07 September 2011
- Frontmatter
- Contents
- Contributors
- Part I General Principles of Cell Death
- 1 Human Caspases – Apoptosis and Inflammation Signaling Proteases
- 2 Inhibitor of Apoptosis Proteins
- 3 Death Domain–Containing Receptors – Decisions between Suicide and Fire
- 4 Mitochondria and Cell Death
- 5 The Control of Mitochondrial Apoptosis by the BCL-2 Family
- 6 Endoplasmic Reticulum Stress Response in Cell Death and Cell Survival
- 7 Autophagy – The Liaison between the Lysosomal System and Cell Death
- 8 Cell Death in Response to Genotoxic Stress and DNA Damage
- 9 Ceramide and Lipid Mediators in Apoptosis
- 10 Cytotoxic Granules House Potent Proapoptotic Toxins Critical for Antiviral Responses and Immune Homeostasis
- Part II Cell Death in Tissues and Organs
- Part III Cell Death in Nonmammalian Organisms
- Plate section
- References
Summary
Cells are subjected to multiple types of stress throughout their life cycle, including starvation, infection, and physical and chemical agents. Stressors cause transient and permanent damage. Transient damage is reflected at the level of the protein or RNA and is largely associated with the generation of reactive oxygen radicals, which directly or indirectly impact translation, folding, or conformation of proteins. In contrast to transient damage, which is expected to be cleared by existing cellular machinery that allows recognition and removal of damaged proteins, permanent damage is primarily reflected at the level of the DNA, although it could also result from damaged proteins that fail to support proper repair or cell duplication. DNA-damaging agents induce a variety of modifications that may result in improper chromosomal duplication, recombination between chromosomes, gene mutations, or gene amplification, which may result in malignant transformations if not properly repaired. Damage is generated by both endogenous and exogenous sources: endogenous (spontaneous) damage is caused by agents within the cell itself (i.e., the products of normal cellular metabolism, replication, mitosis), whereas exogenous sources include ultraviolet (UV) light, ionizing radiation (IR), and environmental genotoxins (e.g., alkylating compounds, polycyclic aromatic hydrocarbons, biphenyls, and heterocyclic amines). Most cytotoxic anticancer drugs react either directly or indirectly (through reactive metabolites) with DNA or by blocking DNA-metabolizing functions, such as DNA polymerases or topoisomerases.
- Type
- Chapter
- Information
- ApoptosisPhysiology and Pathology, pp. 74 - 87Publisher: Cambridge University PressPrint publication year: 2011
References
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