Date of Award
Spring 2023
Degree Name
Bachelor of Arts
Department
Biology; College of Arts & Sciences
First Advisor
Megan Wright, PhD
Abstract
Blue light (BL) is a high energy, short wavelength spanning 400 to 500 nm. Found in technological and environmental forms, BL has been shown to induce photochemical damage of the retina by reactive oxygen species (ROS) production. Excess ROS leads to oxidative stress, which disrupts retinal mitochondrial structure and function. As mitochondria amply occupy photoreceptors, they also contribute to oxidative stress due to their selectively significant absorption of BL at 400 to 500 nm. ROS generation that induces oxidative stress subsequently promotes retinal mitochondrial apoptosis. BL filtering and preventative mechanisms have been suggested to improve or repair BL-induced retinal damage, including BL blocking lenses and the low light therapy called photobiomodulation (PBM). The mechanism behind ROS leading to apoptosis when stimulated by red light (RL) and near-infrared light (NIRL), or PBM, remains poorly understood. However, previous studies have shown PBM to improve mitochondrial apoptotic conditions and respiration, while also decreasing ROS production and protecting photoreceptor gene expression. This thesis evaluates the ameliorative effect of PBM on BL-induced retinal mitochondrial apoptosis, oxidative stress, and metabolism instability. A study conducted by Heinig et al. (2020) observed that PBM increased oxidative phosphorylation complex activity, improved apoptotic conditions, and regulated mRNA gene expression following BL exposure. Additionally, Heinig et al. determined that complexes I and II are also PBM targets besides complex IV in the mitochondrial respiratory chain. A study by Kaynezhad et al. (2022) found that environmental BL significantly disrupts retinal cell hemodynamics and mitochondrial metabolism. PBM has illustrated the ability to improve retinal damage caused by BL, solidifying its revolutionary application in effective treatments against BL exposure.
Recommended Citation
Malinsky, Jessica, "High energy blue light induces oxidative stress and retinal cell apoptosis" (2023). Capstone Showcase. 6.
https://scholarworks.arcadia.edu/showcase/2023/bio/6
Included in
Amino Acids, Peptides, and Proteins Commons, Atomic, Molecular and Optical Physics Commons, Cells Commons, Electrical and Electronics Commons, Electronic Devices and Semiconductor Manufacturing Commons, Enzymes and Coenzymes Commons, Eye Diseases Commons, Musculoskeletal, Neural, and Ocular Physiology Commons, Nervous System Commons, Optometry Commons, Semiconductor and Optical Materials Commons
High energy blue light induces oxidative stress and retinal cell apoptosis
Blue light (BL) is a high energy, short wavelength spanning 400 to 500 nm. Found in technological and environmental forms, BL has been shown to induce photochemical damage of the retina by reactive oxygen species (ROS) production. Excess ROS leads to oxidative stress, which disrupts retinal mitochondrial structure and function. As mitochondria amply occupy photoreceptors, they also contribute to oxidative stress due to their selectively significant absorption of BL at 400 to 500 nm. ROS generation that induces oxidative stress subsequently promotes retinal mitochondrial apoptosis. BL filtering and preventative mechanisms have been suggested to improve or repair BL-induced retinal damage, including BL blocking lenses and the low light therapy called photobiomodulation (PBM). The mechanism behind ROS leading to apoptosis when stimulated by red light (RL) and near-infrared light (NIRL), or PBM, remains poorly understood. However, previous studies have shown PBM to improve mitochondrial apoptotic conditions and respiration, while also decreasing ROS production and protecting photoreceptor gene expression. This thesis evaluates the ameliorative effect of PBM on BL-induced retinal mitochondrial apoptosis, oxidative stress, and metabolism instability. A study conducted by Heinig et al. (2020) observed that PBM increased oxidative phosphorylation complex activity, improved apoptotic conditions, and regulated mRNA gene expression following BL exposure. Additionally, Heinig et al. determined that complexes I and II are also PBM targets besides complex IV in the mitochondrial respiratory chain. A study by Kaynezhad et al. (2022) found that environmental BL significantly disrupts retinal cell hemodynamics and mitochondrial metabolism. PBM has illustrated the ability to improve retinal damage caused by BL, solidifying its revolutionary application in effective treatments against BL exposure.