Oxygen-dependent activation of Cu,Zn-superoxide dismutase-1

Metallomics ◽  
2017 ◽  
Vol 9 (8) ◽  
pp. 1047-1059 ◽  
Author(s):  
Morgan M. Fetherolf ◽  
Stefanie D. Boyd ◽  
Duane D. Winkler ◽  
Dennis R. Winge
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Reactive Oxygen ◽  
Intermembrane Space ◽  
Oxygen Species ◽  
Superoxide Dismutase 1 ◽  
Copper Zinc Superoxide Dismutase ◽  
Zinc Superoxide Dismutase ◽  
Copper Zinc ◽  
Mitochondrial Intermembrane Space

Copper zinc superoxide dismutase (Sod1) is a critical enzyme in limiting reactive oxygen species in both the cytosol and the mitochondrial intermembrane space.

scholarly journals The neuroprotective effects of activated α7 nicotinic acetylcholine receptor against mutant copper–zinc superoxide dismutase 1-mediated toxicity

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Taisei Ito ◽  
Masatoshi Inden ◽  
Tomoyuki Ueda ◽  
Yuta Asaka ◽  
Hisaka Kurita ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Motor Neurons ◽  
Superoxide Dismutase 1 ◽  
Α7 Nicotinic Acetylcholine Receptor ◽  
Neuroprotective Effects ◽  
Nicotinic Acetylcholine ◽  
Copper Zinc Superoxide Dismutase ◽  
Zinc Superoxide Dismutase ◽  
Α7 Nachr ◽  
Copper Zinc

AbstractAmyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the selective and progressive loss of motor neurons. Although many drugs have entered clinical trials, few have shown effectiveness in the treatment of ALS. Other studies have shown that the stimulation of α7 nicotinic acetylcholine receptor (nAChR) can have neuroprotective effects in some models of neurodegenerative disease, as well as prevent glutamate-induced motor neuronal death. However, the effect of α7 nAChR agonists on ALS-associated mutant copper–zinc superoxide dismutase 1 (SOD1) aggregates in motor neurons remains unclear. In the present study, we examined whether α7 nAChR activation had a neuroprotective effect against SOD1G85R-induced toxicity in a cellular model for ALS. We found that α7 nAChR activation by PNU282987, a selective agonist of α7 nAChR, exhibited significant neuroprotective effects against SOD1G85R-induced toxicity via the reduction of intracellular protein aggregates. This reduction also correlated with the activation of autophagy through the AMP-activated protein kinase (AMPK)–mammalian target of rapamycin (mTOR) signaling pathway. Furthermore, the activation of α7 nAChRs was found to increase the biogenesis of lysosomes by inducing translocation of the transcription factor EB (TFEB) into the nucleus. These results support the therapeutic potential of α7 nAChR activation in diseases that are characterized by SOD1G85R aggregates, such as ALS.

scholarly journals Pengaruh Lidokain Intravena Terhadap Kadar Superoxide Dismutase 1 (Sod-1) Paru Kelinci Dengan Lung Ischemic Reperfusion Injury Model

2015 ◽  
Vol 7 (3) ◽  
pp. 146
Author(s):  
Mohammad Arief Kurniawan ◽  
Johan Arifin ◽  
Taufik Eko Nugroho
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Reperfusion Injury ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Superoxide Dismutase 1 ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Injury Model

Latar belakang : Angka kejadian komplikasi paru paska operasi non jantung dibandingkan dengan komplikasi jantung yaitu 2,7% dan 2,5%. Penyebab hal ini adalah stres oksidatif, ketidakseimbangan radikal oksigen dan endogenous scavenging system.Lidokain  menghambat saluran natrium dan, mengurangi masukan kalsium intraseluler, mengurangi produksi Reactive Oxygen Species (ROS) dan modulasi bioenergetika mitokondria, sehingga diharapkan lidokain mampu meningkatkan kadar antioksidan alami di dalam sel.Superoxide Dismutase-1 (SOD-1) adalah salah satu antioksidan alami didalam sel yang berperan dalam melindungi organ dari anion superoksida yang berbahaya dengan mengubah anion yang dihasilkan dari cedera setelah ischaemia-reperfusion.Tujuan : Mengetahui efek lidokain intravena terhadap kadar Superoxide Dismutase 1 (SOD-1) paru kelinci dengan lung ischemic reperfusion injury model.Metode : Desain eksperimental laboratorik, 16 kelinci dibagi menjadi dua kelompok secara acak. Kelompok kontrol mendapat perlakuan lung ischemic reperfusion injury dan kelompok perlakuan dilakukan lung ischemic reperfusion injurydan mendapat injeksi lidokain 1,5mg/kgBB/jam intravena secara kontinyu kemudian diukur kadar SOD-1 jaringan paru kedua kelompok. Uji normalitas menggunakan uji Shapiro Wilk dilanjutkan uji beda Independent T-test.Hasil : Kadar SOD-1 paru kelinci dengan lung ischemic reperfusion injurydan mendapat lidokain lebih tinggi secara signifikan (p=0,01) dibandingkan dengan kadar SOD-1 paru kelinci dengan lung ischemic reperfusion injuryKesimpulan : Pemberian lidokain kontinyu intravena dapat meningkatkan kadar SOD-1 paru kelinci dengan lung ischemic reperfusion injury. 

Apoptosis: bombarding the mitochondria

2003 ◽  
Vol 39 ◽  
pp. 41-51 ◽  
Author(s):  
Philippe Parone ◽  
Muriel Priault ◽  
Dominic James ◽  
Steven F Nothwehr ◽  
Jean-Claude Martinou
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Membrane ◽  
Family Members ◽  
Reactive Oxygen ◽  
Intermembrane Space ◽  
Oxygen Species ◽  
Outer Mitochondrial Membrane ◽  
Caspase Activation ◽  
Mitochondrial Intermembrane Space ◽  
Death Signals

Mitochondria play a central role in apoptosis triggered by many stimuli. They integrate death signals through Bcl-2 family members and co-ordinate caspase activation through the release of apoptogenic factors that are normally sequestered in the mitochondrial intermembrane space. The release of these proteins is the result of the outer mitochondrial membrane becoming permeable. In addition, mitochondria can initiate apoptosis through the production of reactive oxygen species.

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