Abstract

The aging process is induced by numerous exogenous and endogenous stressors that can cause genetic modifications, epigenetic changes, and alteration in protein homeostasis, speeding up the aging process. Another critical factor that also plays a significant role during cellular senescence is the production of reactive oxygen species (ROS), showing benefits at optimal levels, but harmful effects when in excess [1]. In organisms that use oxygen in their respiratory 114chain, the mitochondria generate oxygen radicals, and efficient electron transport decreases over time [2]. The malfunction of mitochondria increases ROS production and induces cell damage and aging [3]. ROS production can alter proteins, lipids, carbohydrates, and nucleic acids, changing cellular function [4]. ROS accumulation activates inflammation and oxidative stress, and the chronic production of ROS leads to the induction of age-related diseases [5]. Increased oxidative stress levels increase the susceptibility to pathologies associated with age due to damages in essential intracellular components that alter the cell’s overall redox, metabolic, and protein homeostasis [4]. Oxidative stress has been reported as associated with the aging process and numerous chronic-aged diseases such as neurodegeneration and cancer [6].

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