Abstract
Reactive oxygen species (ROS) are important secondary metabolites that play major roles in signaling pathways, with their levels often used as analytical tools to investigate various cellular scenarios. They potentially damage genetic material and facilitate tumorigenesis by inhibiting certain tumor suppressors. In diabetic conditions, substantial levels of ROS stimulate oxidative stress through specialized precursors and enzymatic activity, while minimum levels are required for proper wound healing. Photobiomodulation (PBM) uses light to stimulate cellular mechanisms and facilitate the removal of oxidative stress. Photodynamic therapy (PDT) generates ROS to induce selective tumor destruction. The regulatory roles of PBM via crosstalk between ROS and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-кB) are substantial for the appropriate management of various conditions.
Highlights
Reactive oxygen species (ROS) are formed by the fractional reduction of molecular oxygen and include, but are not limited to, superoxide anions, hydrogen peroxide, and hydroxyl radicals, all obtained from sequential oxidation–reduction processes involving nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, lipoxygenases, or cyclooxygenases [1]
This review focuses on the effect of ROS on NF-кB activity, how ROS are affected by PBM/Photodynamic therapy (PDT), and its role in diabetes, wound healing, and cancer, respectively
Both superoxide anions and hydrogen peroxides are constantly produced by complex III, with 80% released into the intermembrane space and the rest into the mitochondrial matrix
Summary
Reactive oxygen species (ROS) are formed by the fractional reduction of molecular oxygen and include, but are not limited to, superoxide anions, hydrogen peroxide, and hydroxyl radicals, all obtained from sequential oxidation–reduction processes involving nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, lipoxygenases, or cyclooxygenases [1]. The down-regulation of ROS production and targeting factors resulting in their increased generation may have a significant role in controlling diabetic complications [6,7]. Under chronic conditions, increased production of free radicals was observed, thereby inhibiting the proliferation and migration of key cell types and leading to delayed wound healing [8,9]. Photodynamic therapy (PDT) uses a specific wavelength light to activate the photosensitizer to induce cell death in conjunction with molecular oxygen. PBM treatment parameters vary, such as the wavelength, fluence, power density, pulse structure, and irradiation time These are factors that preclude efficient clinical transition of PBM [21,22,23,24]. This review focuses on the effect of ROS on NF-кB activity, how ROS are affected by PBM/PDT, and its role in diabetes, wound healing, and cancer, respectively
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