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The mechanisms include reduction of excitotoxicity and oxidative stress, enhanced neurotrophic factor expression supporting neuronal survival, angiogenesis improving cerebral blood flow, and modulation of dopamine and serotonin systems

All included participants provided written informed consent and were recruited prospectively

193 These findings suggest that inhibiting ferroptosis may be a potential strategy for treating reproductive toxicity caused by drugs or stress

4.3.4 Organelle dysfunction CS also impairs the function of critical organelles central to ferroptosis regulation: (1) Mitochondrial Damage: CS stimulates DRP1-dependent mitochondrial fission, resulting in fragmented, dysfunctional mitochondria that overproduce reactive oxygen species (ROS)