Advances of H2S in Regulating Neurodegenerative Diseases by Preserving Mitochondria Function

Neurotoxicity is induced by different toxic substances, including environmental chemicals, drugs, and pathogenic toxins, resulting in oxidative damage and neurodegeneration in mammals. The nervous system is extremely vulnerable to oxidative stress because of its high oxygen demand. Mitochondria are...

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Bibliographic Details
Published in:Antioxidants 2023-03, Vol.12 (3), p.652
Main Authors: Zhou, Lina, Wang, Qiang
Format: Article
Language:English
Subjects:
Alzheimer's disease
Animal cognition
Apoptosis
Brain
Cognitive ability
Cytochrome
Enzymes
Homeostasis
Homocysteine
Hydrogen sulfide
Inflammation
Laboratory animals
Metabolism
Mitochondria
mitochondria dysfunction
Nervous system
Neurodegeneration
Neurodegenerative diseases
Neurological diseases
Neuromodulation
Neurons
Neuroprotective agents
Neurotoxicity
Oxidative stress
Parkinson's disease
Phosphorylation
Physiology
Proteins
Review
sulfhydration
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Summary:Neurotoxicity is induced by different toxic substances, including environmental chemicals, drugs, and pathogenic toxins, resulting in oxidative damage and neurodegeneration in mammals. The nervous system is extremely vulnerable to oxidative stress because of its high oxygen demand. Mitochondria are the main source of ATP production in the brain neuron, and oxidative stress-caused mitochondrial dysfunction is implicated in neurodegenerative diseases. H2S was initially identified as a toxic gas; however, more recently, it has been recognized as a neuromodulator as well as a neuroprotectant. Specifically, it modulates mitochondrial activity, and H2S oxidation in mitochondria produces various reactive sulfur species, thus modifying proteins through sulfhydration. This review focused on highlighting the neuron modulation role of H2S in regulating neurodegenerative diseases through anti-oxidative, anti-inflammatory, anti-apoptotic and S-sulfhydration, and emphasized the importance of H2S as a therapeutic molecule for neurological diseases.
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox12030652