Long term stability of mitochondrial superoxide dismutase activity in NIST diets I?V

1990 ◽  
Vol 338 (4) ◽  
pp. 453-454 ◽  
Author(s):  
D. J. Scholfield ◽  
G. V. Iyengar ◽  
S. Reiser
Keyword(s):  
Superoxide Dismutase ◽  
Superoxide Dismutase Activity ◽  
Term Stability ◽  
Long Term Stability ◽  
Mitochondrial Superoxide ◽  
Mitochondrial Superoxide Dismutase

Diazoxide Modulates Cardiac Hypertrophy by Targeting H2O2 Generation and Mitochondrial Superoxide Dismutase Activity

2020 ◽  
Vol 13 (1) ◽  
pp. 76-83
Author(s):  
Aline Maria Brito Lucas ◽  
Joana Varlla de Lacerda Alexandre ◽  
Maria Thalyne Silva Araújo ◽  
Cicera Edna Barbosa David ◽  
Yuana Ivia Ponte Viana ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Cardiac Hypertrophy ◽  
Superoxide Dismutase Activity ◽  
Heart Weight ◽  
Pharmacological Intervention ◽  
Wall Thickening ◽  
H2o2 Production ◽  
Mitochondrial Superoxide ◽  
Mitochondrial Superoxide Dismutase

Background: Cardiac hypertrophy involves marked wall thickening or chamber enlargement. If sustained, this condition will lead to dysfunctional mitochondria and oxidative stress. Mitochondria have ATP-sensitive K+ channels (mitoKATP) in the inner membrane that modulate the redox status of the cell. Objective: We investigated the in vivo effects of mitoKATP opening on oxidative stress in isoproterenol- induced cardiac hypertrophy. Methods: Cardiac hypertrophy was induced in Swiss mice treated intraperitoneally with isoproterenol (ISO - 30 mg/kg/day) for 8 days. From day 4, diazoxide (DZX - 5 mg/kg/day) was used in order to open mitoKATP (a clinically relevant therapy scheme) and 5-hydroxydecanoate (5HD - 5 mg/kg/day) or glibenclamide (GLI - 3 mg/kg/day) were used as mitoKATP blockers. Results: Isoproterenol-treated mice had elevated heart weight/tibia length ratios (HW/TL). Additionally, hypertrophic hearts had elevated levels of carbonylated proteins and Thiobarbituric Acid Reactive Substances (TBARS), markers of protein and lipid oxidation. In contrast, mitoKATP opening with DZX avoided ISO effects on gross hypertrophic markers (HW/TL), carbonylated proteins and TBARS, in a manner reversed by 5HD and GLI. Moreover, DZX improved mitochondrial superoxide dismutase activity. This effect was also blocked by 5HD and GLI. Additionally, ex vivo treatment of isoproterenol- induced hypertrophic cardiac tissue with DZX decreased H2O2 production in a manner sensitive to 5HD, indicating that this drug also acutely avoids oxidative stress. Conclusion: Our results suggest that diazoxide blocks oxidative stress and reverses cardiac hypertrophy. This pharmacological intervention could be a potential therapeutic strategy to prevent oxidative stress associated with cardiac hypertrophy.

scholarly journals Mitochondrial Superoxide Dismutase in Cisplatin-Induced Kidney Injury

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1329
Author(s):  
Kranti A. Mapuskar ◽  
Emily J. Steinbach ◽  
Amira Zaher ◽  
Dennis P. Riley ◽  
Robert A. Beardsley ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Side Effects ◽  
Therapeutic Option ◽  
Kidney Injury ◽  
Long Term Effects ◽  
Mitochondrial Superoxide ◽  
Chemotherapy Agent ◽  
Ros Formation ◽  
Mitochondrial Superoxide Dismutase

Cisplatin is a chemotherapy agent commonly used to treat a wide variety of cancers. Despite the potential for both severe acute and chronic side effects, it remains a preferred therapeutic option for many malignancies due to its potent anti-tumor activity. Common cisplatin-associated side-effects include acute kidney injury (AKI) and chronic kidney disease (CKD). These renal injuries may cause delays and potentially cessation of cisplatin therapy and have long-term effects on renal function reserve. Thus, developing mechanism-based interventional strategies that minimize cisplatin-associated kidney injury without reducing efficacy would be of great benefit. In addition to its action of cross-linking DNA, cisplatin has been shown to affect mitochondrial metabolism, resulting in mitochondrially derived reactive oxygen species (ROS). Increased ROS formation in renal proximal convoluted tubule cells is associated with cisplatin-induced AKI and CKD. We review the mechanisms by which cisplatin may induce AKI and CKD and discuss the potential of mitochondrial superoxide dismutase mimetics to prevent platinum-associated nephrotoxicity.

scholarly journals Mitochondrial Superoxide Dismutase Activity in Amyotrophic Lateral Sclerosis

2009 ◽  
Vol 1 (1) ◽  
pp. 5-8
Author(s):  
Pilar Larrode ◽  
Pedro Inarrea ◽  
Jose L. Capablo ◽  
Cristina Iniguez ◽  
Jose R. Ara ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Superoxide Dismutase ◽  
Superoxide Dismutase Activity ◽  
Mitochondrial Superoxide ◽  
Mitochondrial Superoxide Dismutase ◽  
Lateral Sclerosis
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