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Potential for therapeutic use of hydrogen sulfide in oxidative stress-induced neurodegenerative diseases.
Int J Med Sci. 2019; 16(10):1386-1396.IJ

Abstract

Oxidative phosphorylation is a source of energy production by which many cells satisfy their energy requirements. Endogenous reactive oxygen species (ROS) are by-products of oxidative phosphorylation. ROS are formed due to the inefficiency of oxidative phosphorylation, and lead to oxidative stress that affects mitochondrial metabolism. Chronic oxidative stress contributes to the onset of neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). The immediate consequences of oxidative stress include lipid peroxidation, protein oxidation, and mitochondrial deoxyribonucleic acid (mtDNA) mutation, which induce neuronal cell death. Mitochondrial binding of amyloid-β (Aβ) protein has been identified as a contributing factor in AD. In PD and HD, respectively, α-synuclein (α-syn) and huntingtin (Htt) gene mutations have been reported to exacerbate the effects of oxidative stress. Similarly, abnormalities in mitochondrial dynamics and the respiratory chain occur in ALS due to dysregulation of mitochondrial complexes II and IV. However, oxidative stress-induced dysfunctions in neurodegenerative diseases can be mitigated by the antioxidant function of hydrogen sulfide (H2S), which also acts through the potassium (KATP/K+) ion channel and calcium (Ca2+) ion channels to increase glutathione (GSH) levels. The pharmacological activity of H2S is exerted by both inorganic and organic compounds. GSH, glutathione peroxidase (Gpx), and superoxide dismutase (SOD) neutralize H2O2-induced oxidative damage in mitochondria. The main purpose of this review is to discuss specific causes and effects of mitochondrial oxidative stress in neurodegenerative diseases, and how these are impacted by the antioxidant functions of H2S to support the development of advancements in neurodegenerative disease treatment.

Authors+Show Affiliations

Department of Anatomy and Cell Biology, College of Medicine, Dong-A University, 32, Daesingongwon-ro, Seo-gu, Busan, 49201, Korea. Department of Medicine, Graduate School, Dong-A University, 32, Daesingongwon-ro, Seo-gu, Busan, 49201, Korea.Department of Anatomy and Cell Biology, College of Medicine, Dong-A University, 32, Daesingongwon-ro, Seo-gu, Busan, 49201, Korea. Department of Medicine, Graduate School, Dong-A University, 32, Daesingongwon-ro, Seo-gu, Busan, 49201, Korea.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

31692944

Citation

Tabassum, Rubaiya, and Na Young Jeong. "Potential for Therapeutic Use of Hydrogen Sulfide in Oxidative Stress-induced Neurodegenerative Diseases." International Journal of Medical Sciences, vol. 16, no. 10, 2019, pp. 1386-1396.
Tabassum R, Jeong NY. Potential for therapeutic use of hydrogen sulfide in oxidative stress-induced neurodegenerative diseases. Int J Med Sci. 2019;16(10):1386-1396.
Tabassum, R., & Jeong, N. Y. (2019). Potential for therapeutic use of hydrogen sulfide in oxidative stress-induced neurodegenerative diseases. International Journal of Medical Sciences, 16(10), 1386-1396. https://doi.org/10.7150/ijms.36516
Tabassum R, Jeong NY. Potential for Therapeutic Use of Hydrogen Sulfide in Oxidative Stress-induced Neurodegenerative Diseases. Int J Med Sci. 2019;16(10):1386-1396. PubMed PMID: 31692944.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Potential for therapeutic use of hydrogen sulfide in oxidative stress-induced neurodegenerative diseases. AU - Tabassum,Rubaiya, AU - Jeong,Na Young, Y1 - 2019/09/20/ PY - 2019/05/08/received PY - 2019/07/23/accepted PY - 2019/11/7/entrez PY - 2019/11/7/pubmed PY - 2020/4/3/medline KW - central nervous system KW - hydrogen sulphide KW - mitochondrial dysfunction KW - neurodegenerative diseases KW - oxidative stress SP - 1386 EP - 1396 JF - International journal of medical sciences JO - Int J Med Sci VL - 16 IS - 10 N2 - Oxidative phosphorylation is a source of energy production by which many cells satisfy their energy requirements. Endogenous reactive oxygen species (ROS) are by-products of oxidative phosphorylation. ROS are formed due to the inefficiency of oxidative phosphorylation, and lead to oxidative stress that affects mitochondrial metabolism. Chronic oxidative stress contributes to the onset of neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). The immediate consequences of oxidative stress include lipid peroxidation, protein oxidation, and mitochondrial deoxyribonucleic acid (mtDNA) mutation, which induce neuronal cell death. Mitochondrial binding of amyloid-β (Aβ) protein has been identified as a contributing factor in AD. In PD and HD, respectively, α-synuclein (α-syn) and huntingtin (Htt) gene mutations have been reported to exacerbate the effects of oxidative stress. Similarly, abnormalities in mitochondrial dynamics and the respiratory chain occur in ALS due to dysregulation of mitochondrial complexes II and IV. However, oxidative stress-induced dysfunctions in neurodegenerative diseases can be mitigated by the antioxidant function of hydrogen sulfide (H2S), which also acts through the potassium (KATP/K+) ion channel and calcium (Ca2+) ion channels to increase glutathione (GSH) levels. The pharmacological activity of H2S is exerted by both inorganic and organic compounds. GSH, glutathione peroxidase (Gpx), and superoxide dismutase (SOD) neutralize H2O2-induced oxidative damage in mitochondria. The main purpose of this review is to discuss specific causes and effects of mitochondrial oxidative stress in neurodegenerative diseases, and how these are impacted by the antioxidant functions of H2S to support the development of advancements in neurodegenerative disease treatment. SN - 1449-1907 UR - https://www.unboundmedicine.com/medline/citation/31692944/Potential_for_therapeutic_use_of_hydrogen_sulfide_in_oxidative_stress_induced_neurodegenerative_diseases_ DB - PRIME DP - Unbound Medicine ER -