Mitochondrial-Driven Ubiquinone Enhances Extracellular Calcium-Dependent Nitric Oxide Production and Reduces Glycochenodeoxycholic Acid-Induced Cell Death in Hepatocytes

2009 ◽  
Vol 22 (12) ◽  
pp. 1984-1991 ◽  
Author(s):  
Sandra González-Rubio ◽  
Ana B. Hidalgo ◽  
Gustavo Ferrín ◽  
Rosario I. Bello ◽  
Raul González ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Extracellular Calcium ◽  
Nitric Oxide Production ◽  
Calcium Dependent ◽  
Oxide Production

Calcium-dependent nitric oxide production is involved in the cytoprotective properties of n-acetylcysteine in glycochenodeoxycholic acid-induced cell death in hepatocytes

2010 ◽  
Vol 242 (2) ◽  
pp. 165-172 ◽  
Author(s):  
Sandra González-Rubio ◽  
Clara I. Linares ◽  
Rosario I. Bello ◽  
Raul González ◽  
Gustavo Ferrín ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Nitric Oxide Production ◽  
Calcium Dependent ◽  
Oxide Production

The influence of methylmercury on the nitric oxide production of alveolar macrophages

2008 ◽  
Vol 24 (8) ◽  
pp. 531-538 ◽  
Author(s):  
TC Kuo
Keyword(s):  
Nitric Oxide ◽  
Adenylate Cyclase ◽  
Alveolar Macrophages ◽  
Ion Concentration ◽  
Nitric Oxide Production ◽  
Calcium Dependent ◽  
Oxide Production ◽  
Extracellular Signal ◽  
Intracellular Calcium Ion ◽  
Living Organisms

Mercury is a global pollutant considered to be a persistent bioaccumulative and toxic chemical. Humans may be exposed to organic forms of mercury by either inhalation, oral, or dermal routes. Methylmercury is more toxic to living organisms than the inorganic forms. In this study, we attempted to elucidate the altered functions of alveolar macrophage including nitric oxide production after methylmercury exposure. Treatment of 7 μM methylmercury for 24 h inhibited lipopolysaccharide-induced nitric oxide and nitric oxide synthase production of alveolar macrophages. The addition of H-89 (PKA inhibitor) significantly decreased the methylmercury inhibition of lipopolysaccharide-mediated nitric oxide production. We found the cell had a calcium-dependent adenylate cyclase, and MeHg could inhibit the phosphorylation of extracellular-signal regulated kinase (ERK). Because methylmercury could increase the intracellular calcium ion concentration, it might activate the adenylate cyclase by increasing [Ca2+]i. Though the interaction of methylmercury with the immune system has been studied by several investigators, the actual mechanisms underlying these interactions are still poorly understood. We discovered that methylmercury could activate protein kinase A, which in turn would inhibit the activation of Raf-1-ERK and so inhibit the release of nitric oxide.

Nitric Oxide Production Correlates with Cell Death of Fibroblasts Treated by Bacillus pumilus Ribonuclease

2017 ◽  
Vol 8 (1) ◽  
pp. 319-322
Author(s):  
Pavel Zelenikhin ◽  
Andreas Koschinski ◽  
Olga Ilinskaya
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Bacillus Pumilus ◽  
Nitric Oxide Production ◽  
Oxide Production
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