title: Endogenous hydrogen sulfide formation mediates the liver damage in endotoxemic rats.
abstract: BACKGROUND
  Hydrogen sulfide (H2S) is a naturally occurring gaseous transmitter and may play important roles in normal physiology and liver disease.
  
  
  OBJECTIVE
  To investigate the relationships between the formation of liver H2S and liver damage in endotoxemic rats caused by lipopolysaccharide (LPS).
  
  
  METHODS
  Male SD rats were sacrificed to acute endotoxemia and pretreated with H2S donor sodium hydrogen sulfide (NaHS) or H2S inhibitor dl-propargylglycine (PAG). Liver H2S concentration, liver cystathionine-γ-lyase (CSE) mRNA, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) level, liver histopathological alteration in different time after treatment were determined.
  
  
  RESULTS
  Endotoxemia resulted in an increase in serum levels of ALT and AST. In the liver, endotoxemia induced a significant increase in the H2S concentration, and in the expression of the H2S-synthesizing enzymes CSE. Pretreatment with NaHS promoted the increase the liver H2S concentration and aggravated the LPS-induced liver damage, However, administration of PAG abolished the increase the liver H2S concentration and reduced the liver injury caused by endotoxemia.
  
  
  CONCLUSIONS
  These findings support the view that an enhanced formation of H2S contributes to the liver injury in endotoxemia. We propose that inhibition of H2S synthesis may be a useful therapeutic strategy against the liver injury associated with endotoxemia.
authors.affiliation: College of Animal Science and Technology, Yunnan Agricultural University, Kunming, PR China. yanyulin333@163.com
authors.forename: Yulin
authors.initials: Y
authors.lastname: Yan
authors.forename: Chao
authors.initials: C
authors.lastname: Chen
authors.forename: Hui
authors.initials: H
authors.lastname: Zhou
authors.forename: Hong
authors.initials: H
authors.lastname: Gao
authors.forename: Liping
authors.initials: L
authors.lastname: Chen
authors.forename: Ling
authors.initials: L
authors.lastname: Chen
authors.forename: Libo
authors.initials: L
authors.lastname: Gao
authors.forename: Ru
authors.initials: R
authors.lastname: Zhao
authors.forename: Yongke
authors.initials: Y
authors.lastname: Sun
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000480:Alkynes / Q000494:pharmacology; D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D003542:Cystathionine gamma-Lyase / Q000378:metabolism; D019446:Endotoxemia / Q000378:metabolism / Q000473:pathology*; D005998:Glycine / Q000031:analogs & derivatives / Q000494:pharmacology; D006862:Hydrogen Sulfide / Q000032:analysis / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008099:Liver / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000480:Alkynes; D008070:Lipopolysaccharides; C009055:propargylglycine; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D003542:Cystathionine gamma-Lyase; D005998:Glycine; D006862:Hydrogen Sulfide