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Subsequently, the second GSH molecule can bind to the H-site and the H-site bound GSH is deprotonated into the GS form

TMAO levels rise with age-related cognitive dysfunction, inducing mitochondrial dysfunction, oxidative stress, neuronal senescence, and synaptic damage

The main sources of ROS under physiological conditions include the mitochondrial respiratory chain, peroxisomes, NADPH oxidase (NOX), and lipoxygenase (ALOX), and additional ROS-producing enzymes, such as cyclooxygenases (COXs) and cytochrome p450s (CYPs) [12, 13]