Chemotherapy-Associated Oxidative Stress: Impact on Chemotherapeutic Effectiveness

By K. Conklin. Integrative Cancer Therapies, 2004

736 citations recorded by the source corpus.

Antineoplastic agents induce oxidative stress in biological systems. During cancer chemotherapy, oxidative stress-induced lipid peroxidation generates numerous electrophilic aldehydes that can attack many cellular targets. These products of oxidative stress can slow cell cycle progression of cancer cells and cause cell cycle checkpoint arrest, effects that may interfere with the ability of anticancer drugs to kill cancer cells. The aldehydes may also inhibit drug-induced apoptosis (programmed cell death) by inactivating death receptors and inhibiting caspase activity. These effects would also diminish the efficacy of the treatment. The use of anti-oxidants during chemotherapy may enhance therapy by reducing the generation of oxidative stress-induced aldehydes.

Subfields: Biochemistry, Molecular Biology, Organic Chemistry

View Paper: https://www.semanticscholar.org/paper/431cf66f8deff61a4b92fa359bdd915083ce6c6d

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Citations in the corpus

Immunogenic cell death and DAMPs in cancer therapy (2012, background): “These authors showed that a recombinant N-terminal fragment of CRT (39-272) is a potent inducer of activation and maturation of B cells and macrophages and can trigger Ig class switching in B cells without T cell help in vitro and in vivo72.”
The importance of antioxidants which play the role in cellular response against oxidative/nitrosative stress: current state (2015, background): “Unfortunately, these ROS/RNS often are the source of serious side effects, as well [184].”
Mitochondrial reactive oxygen species and cancer (2014, background): “Increasing ROS production specifically in cancer cells is likely difficult to accomplish, although it is one proposed mechanism for how many current chemotherapeutics function [108].”
CERAMIDE SYNTHASE 1 IS REGULATED BY PROTEASOMAL MEDIATED TURNOVER (2009, background): “It is important to note in this context that all of these diverse cellular stresses have been associated with eliciting an increase in reactive oxygen species (ROS; [32], and future work should test whether ROS are mediators of CerS1 turnover.”
Targeting Free Radicals in Oxidative Stress-Related Human Diseases. (2017, background): “In addition to drugs that act via DNA-intercalation mechanisms, various currently marketed anticancer drugs are characterized by the induction of severe oxidative stress causing cellular and DNA damage [28].”
Oxidative stress: an essential factor in the pathogenesis of gastrointestinal mucosal diseases. (2014, background): “, etoposide and teniposide), and the camptothecins (60).”