Alterations of Glucose Metabolism in Viral and Toxic Liver Injury

1964 ◽  
Vol 46 (4) ◽  
pp. 424-433 ◽  
Author(s):  
Kurt J. Isselbacher ◽  
Wallace A. Jones
Keyword(s):  
Glucose Metabolism ◽  
Liver Injury ◽  
Toxic Liver Injury

Four cases of toxic liver injury associated with Dictamnus dasycarpus

2008 ◽  
Vol 14 (2) ◽  
pp. 206 ◽  
Author(s):  
Jong Soon Jang ◽  
Eui Geun Seo ◽  
Cheol Han ◽  
Hee Bok Chae ◽  
Soon Je Kim ◽  
...  
Keyword(s):  
Liver Injury ◽  
Toxic Liver Injury

scholarly journals Decreased glutathione in patients with anorexia nervosa. Risk factor for toxic liver injury?

2004 ◽  
Vol 58 (2) ◽  
pp. 238-243 ◽  
Author(s):  
F Zenger ◽  
S Russmann ◽  
E Junker ◽  
C Wüthrich ◽  
M H Bui ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Risk Factor ◽  
Liver Injury ◽  
Toxic Liver Injury

scholarly journals Hepatoprotective Effect of Melatonin in Toxic Liver Injury in Rats

Medicina ◽  
2019 ◽  
Vol 55 (6) ◽  
pp. 304 ◽  
Author(s):  
Oleshchuk ◽  
Ivankiv ◽  
Falfushynska ◽  
Mudra ◽  
Lisnychuk
Keyword(s):  
Liver Injury ◽  
Hepatoprotective Effect ◽  
Male Rats ◽  
Saline Control ◽  
Control Group ◽  
Radical Scavenger ◽  
Thiobarbituric Acid Reactive Substance ◽  
Lipid Hydroperoxides ◽  
Significant Difference ◽  
Toxic Liver Injury

Background and objectives: toxic liver injury results in nitrooxidative stress. Melatonin is a potent free radical scavenger, an inducible nitric oxide synthase (iNOS) inhibitor and an activator of antioxidant enzymes. The aim of this study was to investigate the hepatoprotective effect of exogenous melatonin on animals with acute toxic hepatitis. Material and methods: 36 healthy Sprague-Dawley male rats were split into three equal groups and given carbon tetrachloride (CCl4), 2 g/kg (CCl4 group) or the same dose of CCl4 and melatonin, 10 mg/kg (CCl4/melatonin group) or saline (control group). The effect of melatonin on prooxidant and antioxidant system indexes, NO and NOS levels in serum and liver, data of mitochondrial chain functions and cytolysis in liver were evaluated in all three groups. Results: melatonin significantly decreased activities of AST, ALT, ceruloplasmine and thiobarbituric acid reactive substance (TBARS) in serum. Catalase activity was lowered in serum but not in the liver. Hepatic TBARS, lipid hydroperoxides and glutathione concentrations were decreased, while superoxide dismutase, mitochondrial cytochrome oxidase and succinate dehydrogenase activities increased. Melatonin inhibited synthesis of stable NO metabolites in serum: NO2-by 37.9%; NO3-by 29.2%. There was no significant difference in content NO2-in the liver, but concentration of NO3-increased by 32.6%. Melatonin significantly reduced iNOS concentrations both in serum (59.7%) and liver (57.8%) but did not affect endothelial isoform enzyme activities neither in serum, nor in liver. The histopathological liver lesions observed in the CCl4/melatonin group were less severe than those seen in the CCl4 group. Conclusions: we demonstrated an ameliorating effect of melatonin on prooxidants and antioxidants, NO-NOS systems balance, mitochondrial function and histopathological lesions in the liver in rats with CCl4-induced hepatitis.

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.

Role of plant metabolites in toxic liver injury

2002 ◽  
Vol 11 (1) ◽  
pp. 48-50 ◽  
Author(s):  
Mukul K Gole ◽  
S Dasgupta
Keyword(s):  
Liver Injury ◽  
Plant Metabolites ◽  
Toxic Liver Injury

Mitogen- and antigen-induced immunoregulatory cell activities in animals with toxic liver injury

1994 ◽  
Vol 1 ◽  
pp. 420 ◽  
Author(s):  
I.N. Alexeyeva ◽  
T.M. Bryzgina ◽  
T.V. Martinova
Keyword(s):  
Liver Injury ◽  
Toxic Liver Injury
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