Nitric oxide as a mediator of fructose 1,6-bisphosphate protection in galactosamine-induced hepatotoxicity in rats

Acetaminophen cytotoxicity is ameliorated in a human liver organotypic co-culture model

“…APAP toxicity in C3A:HUVEC co-cultures ( Fig. 5 ), was associated with increased levels of total NO which can also increase intracellular GSH 53 , inferring protection from oxidative stress 54 . This may have important implications for identifying redox-sensitive cell signaling pathways that can be activated by NO.…”

“…The observed complex effects may also be in part due to the fact that the reactivity of NO per se may be overestimated in vitro , because no drain is provided to remove NO. During APAP hepatotoxicity, peroxynitrite (superoxide + NO = peroxynitrite (ONOO−), a highly reactive, potent oxidant and nitrating species is generated in hepatocytes and sinusoidal endothelial cells, and can cause mitochondrial damage and oxidative cellular stress 54 . However, increased NO levels have been observed in AML-12 hepatocytes exposed to a NO donor with concomitant activation of antioxidant transcription factors 56 .…”

“…Given increased NO levels were seen in APAP-resistant co-cultures ( Fig. 5 ), we may also speculate that NO could induce an elevation of reduced glutathione (GSH) 54 . Moreover, NO production was dramatically increased in APAP-toxic mice 57 ; whereas inhibition of cytokine-mediated NO production potentiates APAP hepatotoxicity by modulation of hepatocyte glutathione stores - suggesting our organotypic model may mimic certain in vivo parameters of toxicity 58 .…”

Peripheral Oxidative Stress Blood Markers in Patients With Chronic Back or Neck Pain Treated With High-Velocity, Low-Amplitude Manipulation

“…24 Some authors have considered glutathione as an additional cofactor required for maximum activity of NO synthase, the enzyme responsible for synthesis of NO. 73 An increase in GPx activity induces greater consumption of glutathione. Thus, it can be hypothesized that the relationship between NO, glutathione, and GPx has some role in the lack of changes in NO after treatment by HVLA spinal manipulation.…”

SomeIn Vitro/In VivoChemically-Induced Experimental Models of Liver Oxidative Stress in Rats

“…Galactosamine metabolism depletes the uridine pool of hepatocytes, thus inducing transcriptional arrest and causing an increase in sensitization to cytokines such as TNF- α and an increase in oxidative stress and GSH depletion, which lead to mitochondrial dysfunction and cell death [59]. Both oxidative and nitrosative stress play a key role in the pathogenesis of GAL-induced hepatic injury [60].…”