Ototoxicity is based on inner ear dysfunction creating hearing loss, balance disorder or both symptoms depending on the drug or chemical agent.
Genetic and nongenetic risk factors, in addition to dose and time, play important roles in cisplatin ototoxicity.Although the changes firstly begin from first line of outer hairy cells on the Corti organ in the inner ear and then progress. Though the effect on the spiral ganglion and stria vascularis in addition to the Corti organ are well-defined, the molecular mechanisms that cause hearing loss are not fully understood. Cellular and molecular mechanisms and particularly apoptotic mechanisms explain cisplatin cytotoxicity leading to cochlea damage. DNA damage induced by cisplatin and ROS production seem to be mainly responsible for cisplatin toxicity.
Children treated with cisplatin are at risk of early or late hearing loss which could affect learning, communication, school performance, social communication and general quality of life. For this reason, many protective agents are used with cisplatin without changing its antitumoral efficiency. Studies of compounds to prevent ototoxicity may provide compounds for use in routine clinical practice and prevent one of the major dose-limiting side effects of cisplatin therapy, which will increase treatment efficacy and improve patient quality of life.
When the article is accepted for publication in the HSQ authors transfer all copyright in the article to the Holistence Academy Ar-Ge Yazılım Yayıncılık Eğitim Danışmanlık ve Organizasyon Ticaret Ltd. Şti.The authors reserve all proprietary right other than copyright, such as patent rights.
Everyone who is listed as an author in this article should have made a substantial, direct, intellectual contribution to the work and should take public responsibility for it.
This paper contains works that have not previously published or not under consideration for publication in other journals.