Elizabeth A. Martin

TL;DR: The nature of ROS-induced damage on key cellular targets of oxidative stress is examined and evidence implicating ROS in clinically relevant, drug-related side effects including doxorubicin-induced cardiac damage, azidothymidine-induced myopathy, and cisplatin-induced ototoxicity is reviewed.

TL;DR: Data indicate that all three endonucleases recognize oxidative DNA damage and, in addition, FPG and ENDOIII also recognize alkylation damage.

TL;DR: This effort supports the HESI Committee goal of developing a framework for use of DNA adduct data in risk assessment by reviewing available methods for identification of DNA damage and quantification of adducts.

TL;DR: These results provide convincing evidence that pharmacologically increasing muscle CHO oxidation reduces simvastatin‐induced myopathy by dampening the upregulation of genes known to increase proteasomal and lysosomal protein breakdown and inhibit CHO oxidation.

TL;DR: A perspective on approaches to safety evaluations by reviewing and applying general concepts and integrating key steps in the toxicological evaluation of individual extractables or leachables is provided.