Pathologically, dysregulated ferroptosis contributes to diverse pathological processes and represents a promising therapeutic target for acute and chronic CNS disorders, including traumatic brain injury (TBI) [12], Alzheimers disease (AD) [13, 14], and amyotrophic lateral sclerosis (ALS) [15], as well as TSCI [16]
Kang I, Chu CT, Kaufman BA
Olaparib treatment also replenished NAD + levels, enhanced mitochondrial function, and promoted fatty acid oxidation, thereby reversing non-alcoholic fatty liver disease (NAFLD) in mice fed a high-fat, high-sucrose diet 164 (Fig
It appears that an active transport mechanism concentrates OTA in the kidney, which results in the toxicity of OTA [77,78]
However, it is essential to note that GSH levels in both dose groups generally returned to baseline levels after a one-month washout period, suggesting that continuous supplementation is necessary to maintain elevated GSH levels
3.2 Alleviating mitochondrial oxidative stress Mitochondrial respiration is the main source of cellular ATP