Drug-Induced Oxidative Stress and Toxicity
By D. Deavall, E. A. Martin, Judith Horner, R. Roberts. Journal of Toxicology, 2012
667 citations recorded by the source corpus.
Reactive oxygen species (ROS) are a byproduct of normal metabolism and have roles in cell signaling and homeostasis. Species include oxygen radicals and reactive nonradicals. Mechanisms exist that regulate cellular levels of ROS, as their reactive nature may otherwise cause damage to key cellular components including DNA, protein, and lipid. When the cellular antioxidant capacity is exceeded, oxidative stress can result. Pleiotropic deleterious effects of oxidative stress are observed in numerous disease states and are also implicated in a variety of drug-induced toxicities. In this paper, we examine the nature of ROS-induced damage on key cellular targets of oxidative stress. We also review evidence implicating ROS in clinically relevant, drug-related side effects including doxorubicin-induced cardiac damage, azidothymidine-induced myopathy, and cisplatin-induced ototoxicity.
Subfields: Cardiology and Cardiovascular Medicine, Pathology and Forensic Medicine, Plant Science
View Paper: https://www.semanticscholar.org/paper/73b969e1077c62ba76bcf7f8d5b47d9aaef7abee
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Citations in the corpus
- Oxidative stress: an essential factor in the pathogenesis of gastrointestinal mucosal diseases. (2014, background): “Anticancer drugs such as anthracyclines and analogs, mitoxantrone and other quinones, actinomycin D, enediynes such as bleomycin, chartreusins, elasmin A and related compounds can cause oxidative stress (76).”
- Several lines of antioxidant defense against oxidative stress: antioxidant enzymes, nanomaterials with multiple enzyme-mimicking activities, and low-molecular-weight antioxidants (2024, background): “Various drugs, such as non-steroidal anti-inflammatory (NSAID) drugs, anticancer therapy agents, painkillers, and antiviral drugs, are known to be toxic and produce ROS (Deavall et al. 2012).”