Ionizing radiation-induced metabolic oxidative stress and prolonged cell injury

By E. Azzam, J. Jay-Gerin, D. Pain. Cancer Letters, 2011

1,411 citations recorded by the source corpus.

Cellular exposure to ionizing radiation leads to oxidizing events that alter atomic structure through direct interactions of radiation with target macromolecules or via products of water radiolysis. Further, the oxidative damage may spread from the targeted to neighboring, non-targeted bystander cells through redox-modulated intercellular communication mechanisms. To cope with the induced stress and the changes in the redox environment, organisms elicit transient responses at the molecular, cellular and tissue levels to counteract toxic effects of radiation. Metabolic pathways are induced during and shortly after the exposure. Depending on radiation dose, dose-rate and quality, these protective mechanisms may or may not be sufficient to cope with the stress. When the harmful effects exceed those of homeostatic biochemical processes, induced biological changes persist and may be propagated to progeny cells. Physiological levels of reactive oxygen and nitrogen species play critical roles in many cellular functions. In irradiated cells, levels of these reactive species may be increased due to perturbations in oxidative metabolism and chronic inflammatory responses, thereby contributing to the long-term effects of exposure to ionizing radiation on genomic stability. Here, in addition to immediate biological effects of water radiolysis on DNA damage, we also discuss the role of mitochondria in the delayed outcomes of ionization radiation. Defects in mitochondrial functions lead to accelerated aging and numerous pathological conditions. Different types of radiation vary in their linear energy transfer (LET) properties, and we discuss their effects on various aspects of mitochondrial physiology. These include short and long-term in vitro and in vivo effects on mitochondrial DNA, mitochondrial protein import and metabolic and antioxidant enzymes.

Subfields: Molecular Biology, Radiology, Nuclear Medicine and Imaging

View Paper: https://www.semanticscholar.org/paper/c496bb3174743d21dc05c9aa75ff854905499939

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In Molecular Biology

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2. K. Aquilano
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Citations in the corpus

• Effects of Ionizing Radiation on Biological Molecules—Mechanisms of Damage and Emerging Methods of Detection (2014, background): “The overall amount of ROS generated from primary ionization events is further propagated via the intracellular activation of endogenous ROS-producing systems such as nicotinamide adenine dinucleotide phosphate, reduced form (NADPH) oxidase, and the mitochondrial electron transport chain (ETC) (12, 1”
• Efficacy of Dietary Antioxidants on Broiler Oxidative Stress, Performance and Meat Quality: Science and Market (2015, background): “Exposure to ionising radiation is another important environmental cause that extensively increases the production of free radicals in biological organisms by altering the atomic structure of cell macromolecules thereby triggering oxidation reactions (Azzam et al., 2012).”
• Glutathione: new roles in redox signaling for an old antioxidant (2014, background): “…in several pathological conditions (e.g., inflammation, endotoxic shock, diabetes, ischemia/reperfusion injury; Wong and Billiar, 1995; Iadecola, 1997; Szabo, 1998; Friederich et al., 2009) or upon exposure to pharmacological drugs (Scatena et al., 2010) or ionizing radiation (Azzam et al., 2012).”