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Failure to detoxify ROS with antioxidants can cause a surge in OS

The histone H3K4 demethylase LSD1 has been investigated as a target in Ewing sarcoma and AML, where LSD1 inhibition induces differentiation of AML cells (2) and blocks fusion protein transcriptional targets in sarcoma (3)

In the prefrontal cortex of 3xTg mice, elevated spontaneous excitatory postsynaptic currents and firing rates have been observed in pyramidal neurons (Choudhury et al., 2023), and additional studies indicate increased excitatory and inhibitory inputs to layer 2/3 pyramidal neurons, potentially linked to altered social behavior (Zhang X.-Q

The main cellular sources of ROS are (1) mitochondria, where electron-transport-chain (ETC) leads ROS production through leakage of electrons during oxidative phosphorylation, (2) NADPH oxidases (NOXes), which generate superoxide and hydrogen peroxide (H 2 O 2 ) through transferring electrons from NADPH donors to oxygen, regulating both immune response and homeostatic ROS signalling (3) peroxisomes, which produce H 2 O 2 as a byproduct during breakdown of metabolic reactions such as breakdown of fatty acids and (4) xanthine oxidase, which generates superoxide and H 2 O 2 as a byproduct of oxidative hydroxylation of hypoxanthine in purine metabolism

7t) and offer a previously unappreciated view for future studies to determine whether pre-symptomatic changes involving the glutathioneascorbate metabolism pathway, particularly GSTO2, occur in cell types vulnerable to neurodegenerative conditions such as HD or SCAs