Cellular and molecular mechanisms involved in age-related hearing loss with focusing on oxidative stress

Age-related hearing loss (ARHL) is a type of bilateral hearing loss that progresses from low frequencies to high frequencies with age. This disorder is classified as a multifactorial disease. Factors involved in ARHL pathology are divided into two categories of genetic and non-genetic factors. The genes involved in this disorder include three categories of genes involved in cochlear structure and function, genes correlated with oxidative stress, and mitochondrial-dependent genes. Oxidative stress, apoptosis, and inflammation are the three main causes of ARHL. Damage to hair cells induces intrinsic and extrinsic apoptosis and can therefore accelerate ARHL. Some process in cells leads to the production of high amounts of reactive oxygen species including hydrogen peroxide (H۲O۲), anion superoxide (O۲-), and hydroxyl radical (OH). Reactive oxygen species or ROS can generally have several sources including nitric oxide synthase, NADPH oxidase, microsomal, mitochondrial, and proxisomal pathways. In typical conditions, ROS is produced and neutralized by antioxidant enzymes such as superoxide dismutase, catalase, and glutathione, balancing cell homeostasis. Though, the process of aging, drug treatment, and some other factors upset this homeostasis, and this causes oxidative stress and induction of ARHL in the cells of the auditory system. The aim of this study was to describe the cellular and molecular mechanisms involved in ARHL with a focus on oxidative stress.

Keywords:

Age-related hearing loss , Cellular mechanism , Inflammation , Apoptosis , oxidative stress