Exploring Angiotensin II and Oxidative Stress in Radiation-Induced Cataract Formation: Potential for Therapeutic Intervention

Authors

Vidya P. Kumar, The Uniformed Services University of the Health Sciences
Yali Kong, Macon & Joan Brock Virginia Health Sciences at Old Dominion UniversityFollow
Riana Dolland, Trocar Pharma Inc.
Sandra R. Brown, LensCrafters
Kan Wang, Macon & Joan Brock Virginia Health Sciences at Old Dominion UniversityFollow
Damian Dolland, Trocar Pharma Inc.
David Mu, Macon & Joan Brock Virginia Health Sciences at Old Dominion UniversityFollow
Milton L. Brown, Macon & Joan Brock Virginia Health Sciences at Old Dominion UniversityFollow

ORCID

0000-0002-7762-0182 (Mu), 0009-0009-0489-8245 (Brown)

Document Type

Article

Publication Date

2024

DOI

10.3390/antiox13101207

Publication Title

Antioxidants

Volume

13

Issue

10

Pages

1207 (1-13)

Abstract

Radiation-induced cataracts (RICs) represent a significant public health challenge, particularly impacting individuals exposed to ionizing radiation (IR) through medical treatments, occupational settings, and environmental factors. Effective therapeutic strategies require a deep understanding of the mechanisms underlying RIC formation (RICF). This study investigates the roles of angiotensin II (Ang II) and oxidative stress in RIC development, with a focus on their combined effects on lens transparency and cellular function. Key mechanisms include the generation of reactive oxygen species (ROS) and oxidative damage to lens proteins and lipids, as well as the impact of Ang II on inflammatory responses and cellular apoptosis. While the generation of ROS from water radiolysis is well established, the impact of Ang II on RICs is less understood. Ang II intensifies oxidative stress by activating type 1 receptors (AT1Rs) on lens epithelial cells, resulting in increased ROS production and inflammatory responses. This oxidative damage leads to protein aggregation, lipid peroxidation, and apoptosis, ultimately compromising lens transparency and contributing to cataract formation. Recent studies highlight Ang II's dual role in promoting both oxidative stress and inflammation, which accelerates cataract development. RICs pose a substantial public health concern due to their widespread prevalence and impact on quality of life. Targeting Ang II signaling and oxidative stress simultaneously could represent a promising therapeutic approach. Continued research is necessary to validate these strategies and explore their efficacy in preventing or reversing RIC development.

Rights

© 2024 by the authors.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International (CC BY 4.0) License.

Original Publication Citation

Kumar, V. P., Kong, Y., Dolland, R., Brown, S. R., Wang, K., Dolland, D., Mu, D., & Brown, M. L. (2024). Exploring angiotensin II and oxidative stress in radiation-induced cataract formation: Potential for therapeutic intervention. Antioxidants, 13(10), 1-13, Article 1207. https://doi.org/10.3390/antiox13101207

Repository Citation

Kumar, V. P., Kong, Y., Dolland, R., Brown, S. R., Wang, K., Dolland, D., Mu, D., & Brown, M. L. (2024). Exploring angiotensin II and oxidative stress in radiation-induced cataract formation: Potential for therapeutic intervention. Antioxidants, 13(10), 1-13, Article 1207. https://doi.org/10.3390/antiox13101207