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The present study showed that oxidative stress causes several changes, such as: (1) mitochondrial dysfunction, abnormal neuron formation, abnormal myelination, impaired neurotransmitter production, and impaired reorganization of synaptic connections, (2) impaired release of neurotransmitters, abnormal processes of neurogenesis, (3) a deficit of ATP and a disturbed energy balance of cells and their enzymatic activity, (4) lipid peroxidation, altered protein structure, mutations in protein coding, disturbed protein–protein interaction, (5) DNA mutations, impaired gene expression, and impaired activation of DNA repair pathways, (6) disrupted cell homeostasis as a toxic effect of high H 2 S concentration, (7) destruction of metabolic pathways and changes in substrate utilization, (8) increased apoptosis and increased inflammatory responses, (9) microdamage of dopaminergic endings and loss of neuronal connections, (10) impaired synthesis and transmission of neurotransmitters, (11) impaired synaptic signaling, (12) non-enzymatic oxidation of dopamine—an increase in hydrogen peroxide, (13) increased levels of nitric oxide (peroxynitrite)—neurotoxic effects

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