TY - JOUR
T1 - Potential use of n-3 PUFAs to prevent oxidative stress-derived ototoxicity caused by platinum-based chemotherapy
AU - Cortés Fuentes, Ignacio A.
AU - Burotto, Mauricio
AU - Retamal, Mauricio A.
AU - Frelinghuysen, Michael
AU - Caglevic, Christian
AU - Gormaz, Juan G.
N1 - Funding Information:
This work was supported by Fondo Nacional de Desarrollo Científico y Tecnológico (FONDECYT) grant number 11150999 .
Publisher Copyright:
© 2020 Elsevier Inc.
PY - 2020/11/20
Y1 - 2020/11/20
N2 - Platinum-based compounds are widely used for the treatment of different malignancies due to their high effectiveness. Unfortunately, platinum-based treatment may lead to ototoxicity, an often-irreversible side effect without a known effective treatment and prevention plan. Platinum-based compound-related ototoxicity results mainly from the production of toxic levels of reactive oxygen species (ROS) rather than DNA-adduct formation, which has led to test strategies based on direct ROS scavengers to ameliorate hearing loss. However, favorable clinical results have been associated with several complications, including potential interactions with chemotherapy efficacy. To understand the contribution of the different cytotoxic mechanisms of platinum analogues on malignant cells and auditory cells, the particular susceptibility and response of both kinds of cells to molecules that potentially interfere with these mechanisms, is fundamental to develop innovative strategies to prevent ototoxicity without affecting antineoplastic effects. The n-3 long-chain polyunsaturated fatty acids (n-3 PUFAs) have been tried in different clinical settings, including with cancer patients. Nevertheless, their use to decrease cisplatin-induced ototoxicity has not been explored to date. In this hypothesis paper, we address the mechanisms of platinum compounds-derived ototoxicity, focusing on the differences between the effects of these compounds in neoplastic versus auditory cells. We discuss the basis for a strategic use of n-3 PUFAs to potentially protect auditory cells from platinum-derived injury without affecting neoplastic cells and chemotherapy efficacy.
AB - Platinum-based compounds are widely used for the treatment of different malignancies due to their high effectiveness. Unfortunately, platinum-based treatment may lead to ototoxicity, an often-irreversible side effect without a known effective treatment and prevention plan. Platinum-based compound-related ototoxicity results mainly from the production of toxic levels of reactive oxygen species (ROS) rather than DNA-adduct formation, which has led to test strategies based on direct ROS scavengers to ameliorate hearing loss. However, favorable clinical results have been associated with several complications, including potential interactions with chemotherapy efficacy. To understand the contribution of the different cytotoxic mechanisms of platinum analogues on malignant cells and auditory cells, the particular susceptibility and response of both kinds of cells to molecules that potentially interfere with these mechanisms, is fundamental to develop innovative strategies to prevent ototoxicity without affecting antineoplastic effects. The n-3 long-chain polyunsaturated fatty acids (n-3 PUFAs) have been tried in different clinical settings, including with cancer patients. Nevertheless, their use to decrease cisplatin-induced ototoxicity has not been explored to date. In this hypothesis paper, we address the mechanisms of platinum compounds-derived ototoxicity, focusing on the differences between the effects of these compounds in neoplastic versus auditory cells. We discuss the basis for a strategic use of n-3 PUFAs to potentially protect auditory cells from platinum-derived injury without affecting neoplastic cells and chemotherapy efficacy.
KW - Antioxidants
KW - Cisplatin
KW - Hearing loss
KW - Omega-3
KW - Otoprotection
KW - Ototoxicity
KW - Platinum-analogue
KW - n-3 PUFAs
UR - http://www.scopus.com/inward/record.url?scp=85089837452&partnerID=8YFLogxK
U2 - 10.1016/j.freeradbiomed.2020.07.035
DO - 10.1016/j.freeradbiomed.2020.07.035
M3 - Article
C2 - 32827639
AN - SCOPUS:85089837452
SN - 0891-5849
VL - 160
SP - 263
EP - 276
JO - Free Radical Biology and Medicine
JF - Free Radical Biology and Medicine
ER -