Beneficial effects of histidine and carnosine on ethanol-induced chronic liver injury

Food Chem Toxicol. 2008 May;46(5):1503-9. doi: 10.1016/j.fct.2007.12.013. Epub 2008 Jan 25.

Abstract

Alleviative effects of histidine and carnosine in mice against ethanol-induced oxidative and inflammatory was examined. After chronic alcoholic liver injury was induced, histidine and carnosine at 0.5, 1, 2g/L were added to the drinking water for 3 weeks. Results showed that the post-intake of histidine or carnosine markedly decreased alanine aminotransferase and aspartate aminotransferase activities (P<0.05). Ethanol treatment increased malondialdehyde (MDA) level, decreased glutathione (GSH) content and catalase and glutathione peroxidase (GPX) activities, and increased cytochrome P450 2E1 (CYP2E1) activity in liver (P<0.05). The post-intake of histidine and carnosine significantly decreased MDA formations, increased GSH content, enhanced catalase and GPX activities, and suppressed CYP2E1 activity (P<0.05), in which the effects on catalase and CYP2E1 activities were dose-dependent (P<0.05). Ethanol treatment elevated hepatic levels of c-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) (P<0.05), the post-intake of histidine and carnosine significantly and dose-dependently diminished the release of CRP, IL-6, and TNF-alpha (P<0.05). Ethanol treatment caused down-regulation in both catalase and GPX mRNA expression, and up-regulated both IL-6 and TNF-alpha mRNA expression (P<0.05). Histidine and carnosine post-treatments significantly and dose-dependently upregulated catalase mRNA, and down-regulated mRNA expression of IL-6 and TNF-alpha (P<0.05). Based on the observed anti-oxidative and anti-inflammatory effects, the supplement of histidine or carnosine might be helpful for the treatment of chronic alcoholic liver injury.

MeSH terms

  • Alanine Transaminase / blood
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal
  • Antioxidants
  • Aspartate Aminotransferases / blood
  • C-Reactive Protein / biosynthesis
  • Carnosine / therapeutic use*
  • Catalase / metabolism
  • Central Nervous System Depressants / blood
  • Chemical and Drug Induced Liver Injury / pathology
  • Chemical and Drug Induced Liver Injury / prevention & control
  • Chronic Disease
  • Cytochrome P-450 CYP2E1 / metabolism
  • Dose-Response Relationship, Drug
  • Ethanol / blood
  • Glutathione / metabolism
  • Glutathione Peroxidase / metabolism
  • Histidine / therapeutic use*
  • Interleukin-6 / biosynthesis
  • Lipid Peroxidation / drug effects
  • Liver Diseases, Alcoholic / pathology
  • Liver Diseases, Alcoholic / prevention & control*
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Antioxidants
  • Central Nervous System Depressants
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Ethanol
  • Histidine
  • Carnosine
  • C-Reactive Protein
  • Catalase
  • Glutathione Peroxidase
  • Cytochrome P-450 CYP2E1
  • Aspartate Aminotransferases
  • Alanine Transaminase
  • Glutathione