scholarly journals Acute toxic liver injury. nicotinamide-adenine dinucleotide-pyrophosphorylase activity of nuclei isolated from rat liver in heliotrine and in dimethylnitrosamine poisoning

1962 ◽  
Vol 84 (2) ◽  
pp. 364-368 ◽  
Author(s):  
GS CHRISTIE ◽  
MJ BAILIE ◽  
RN LE PAGE
Keyword(s):  
Liver Injury ◽  
Rat Liver ◽  
Nicotinamide Adenine Dinucleotide ◽  
Nicotinamide Adenine ◽  
Toxic Liver Injury ◽  
Acute Toxic

The chemokine scavenging receptor D6 limits acute toxic liver injury in vivo

2009 ◽  
Vol 390 (10) ◽  
Author(s):  
Marie-Luise Berres ◽  
Christian Trautwein ◽  
Mirko Moreno Zaldivar ◽  
Petra Schmitz ◽  
Katrin Pauels ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Damage ◽  
Immune Modulation ◽  
Scavenger Receptor ◽  
Wild Type ◽  
Protein Levels ◽  
Inflammatory Chemokines ◽  
Toxic Liver Injury ◽  
Acute Toxic

Abstract The chemokine decoy receptor D6 is a promiscuous chemokine receptor lacking classical signaling functions. It negatively regulates inflammation by targeting CC chemokines to cellular internalization and degradation. Here we analyze the function of D6 in acute CCl4-induced liver damage in constitutive D6-/- and wild-type mice. The degree of liver injury was assessed by liver histology, serum transaminases, IL-6, and TNFα mRNA expression. Protein levels of D6 ligands (CCL2, CCL3, CCL5) and the non-D6-ligand CXCL9 within the livers were determined by ELISAs. The intrahepatic infiltration of immune cells was characterized by FACS. Genetic deletion of D6 led to prolonged liver damage after acute CCl4 administration. The augmented liver damage in D6-/- mice was associated with increased protein levels of intrahepatic inflammatory chemokines CCL2, CCL3, and CCL5 after 48 h, whereas CXCL9 was not different between knockout and wild-type mice. Functionally, increased intra-hepatic CC chemokine concentrations led to increased infiltration of CD45+ leukocytes, which were mainly identified as T and NK cells. In conclusion, the chemokine scavenger receptor D6 has a non-redundant role in acute toxic liver injury in vivo. These results support the importance of post-translational chemokine regulation and describe a new mechanism of immune modulation within the liver.

Nicotinamide adenine dinucleotide glycohydrolases and poly adenosine diphosphate ribose synthesis in rat liver

1968 ◽  
Vol 32 (2) ◽  
pp. 143-149 ◽  
Author(s):  
Kinya Nakazawa ◽  
Kunihiro Ueda ◽  
Tasuku Honjo ◽  
Koichiro Yoshihara ◽  
Yasutomi Nishizuka ◽  
...  
Keyword(s):  
Rat Liver ◽  
Nicotinamide Adenine Dinucleotide ◽  
Adenosine Diphosphate ◽  
Nicotinamide Adenine

scholarly journals The metabolism of nicotinamide-adenine dinucleotide in various classes of rat liver nuclei

1969 ◽  
Vol 115 (5) ◽  
pp. 56P-56P
Author(s):  
M E Haines ◽  
I R Johnston ◽  
A P Mathias ◽  
D Ridge
Keyword(s):  
Rat Liver ◽  
Nicotinamide Adenine Dinucleotide ◽  
Nicotinamide Adenine ◽  
Rat Liver Nuclei ◽  
Liver Nuclei

Endogenous glucocorticoids released during acute toxic liver injury enhance hepatic IL-10 synthesis and release

1999 ◽  
Vol 276 (1) ◽  
pp. G199-G205 ◽  
Author(s):  
Mark G. Swain ◽  
Caroline Appleyard ◽  
John Wallace ◽  
Howard Wong ◽  
Tai Le
Keyword(s):  
Liver Injury ◽  
Inflammatory Response ◽  
Glucocorticoid Receptor ◽  
Receptor Antagonist ◽  
Mrna Expression ◽  
Elevated Serum ◽  
Ru 486 ◽  
Tnf Α ◽  
Toxic Liver Injury ◽  
Acute Toxic

Endogenous glucocorticoids are known to play a role in the regulation of the inflammatory response possibly by modulating pro- and anti-inflammatory cytokine expression. We examined endogenous glucocorticoid secretion, hepatic damage, tumor necrosis factor-α (TNF-α), and interleukin-10 (IL-10) mRNA expression and release in rats treated with carbon tetrachloride (CCl4) after treatment with vehicle or a glucocorticoid receptor antagonist (RU-486). Rats treated with CCl4 demonstrated striking elevations of plasma corticosterone levels. Inhibition of endogenous glucocorticoid activity by pretreatment with the glucocorticoid receptor antagonist RU-486 resulted in augmented CCl4-mediated hepatotoxicity, as reflected by histology and serum transaminase levels, which were independent of alterations in serum TNF-α levels or hepatic mRNA expression. CCl4 treatment resulted in enhanced hepatic IL-10 mRNA expression and elevated serum IL-10 levels, which were markedly attenuated by glucocorticoid receptor blockade. In summary, significant endogenous glucocorticoid release occurs during acute toxic liver injury in the rat and suppresses the inflammatory response independent of effects on TNF-α but possibly by upregulating hepatic IL-10 production.

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