Journal of Drug Metabolism & Toxicology
Open Access
ISSN: 2157-7609
+44-77-2385-9429
ISSN: 2157-7609
+44-77-2385-9429
Hyung-Jin Kim, Sei-Hoon Yang, Kang-Beom Kwon and Hong-Seob So
School of Korean Medicine, Korea
Posters-Accepted Abstracts: J Drug Metab Toxicol
Ototoxicity is an important issue in patients receiving cisplatin chemotherapy. Numerous studies have demonstrated that several mechanisms, including oxidative stress, DNA damage, and inflammatory responses, are closely associated with cisplatin-induced ototoxicity. Although much attention has been directed at identifying ways to protect the inner ear from cisplatin-induced damage, the precise underlying mechanisms have not yet been elucidated. The cofactor nicotinamide adenine dinucleotide (NAD+) has emerged as an important regulator of cellular energy metabolism and homeostasis. NAD+ acts as a cofactor for various enzymes including sirtuins (SIRTs) and poly (ADP-ribose) polymerases (PARPs), and therefore, maintaining adequate NAD+ levels has therapeutic benefits because of its effect on NAD+-dependent enzymes. Recent studies demonstrated that disturbance in intracellular NAD+ levels is critically involved in cisplatin-induced cochlear damage associated withoxidative stress, DNA damage, and inflammatory responses. In this review, we describe the importance of NAD+ in cisplatin-induced ototoxicity and discuss potential strategies for the prevention or treatment of cisplatin-induced ototoxicity with a particular focus on NAD+-dependent cellular pathways.