title: Effect of protocatechuic acid on lipid profile and DNA damage in D-galactosamine-induced hepatotoxic rats.
abstract: BACKGROUND
  Our aim in this study is to investigate the effect of protocatechuic acid (PCA) on lipid profile and DNA damage in D-galactosamine (D-GalN)-induced hepatotoxic rats.
  
  
  METHODS
  Hepatotoxicity was induced by a single intraperitoneal dose of D-GalN in male Wistar rats. The activities of hepatic markers and levels of kidney function markers were determined. The plasma and tissue lipid levels were estimated. DNA damage was determined by COMET assay. Histopathological examination was also performed using portions of the liver and kidney tissues.
  
  
  RESULTS
  D-GalN-induced hepatotoxic rats showed increased in the activities of hepatic marker enzymes such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and γ-glutamyl transpeptidase (GGT) in serum. The levels of kidney function markers such as urea, uric acid, and creatinine increased in serum. Levels of lipid profile such as total cholesterol (TC), triglycerides (TG), free fatty acid (FFA), and phospholipids (PLs) in the plasma and tissues (liver and kidney) were significantly increased in D-GalN-induced rats. In plasma, levels of very low density lipoprotein cholesterol (VLDL-C) and low-density lipoprotein cholesterol (LDL-C) significantly increased, whereas high-density lipoprotein cholesterol (HDL-C) level decreased in D-GalN-induced rats. Furthermore, D-GalN-induced rats showed increased percentage of tail DNA and tail length and decreased percentage of head DNA. Oral administration of PCA (100 mg/ kg BW) for 20 days improved these levels when compared to D-GalN-induced rats. These biochemical changes were reflected on the attenuation and the structural alteration of the liver and kidney integrity.
  
  
  CONCLUSIONS
  The results of the study suggest that PCA has a potent hepatoprotective activity that may be linked to its antihyperlipidemic effect.
authors.forename: Thangaiyan
authors.initials: T
authors.lastname: Radhiga
authors.forename: Arjunan
authors.initials: A
authors.lastname: Sundaresan
authors.forename: Periyasamy
authors.initials: P
authors.lastname: Viswanathan
authors.forename: Kodukkur Viswanathan
authors.initials: KV
authors.lastname: Pugalendi
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001219:Aspartate Aminotransferases / Q000097:blood; D015415:Biomarkers / Q000097:blood; D004249:DNA Damage / Q000187:drug effects*; D005688:Galactosamine / Q000494:pharmacology*; D062385:Hydroxybenzoates / Q000494:pharmacology*; D000960:Hypolipidemic Agents / Q000494:pharmacology; D007668:Kidney / Q000187:drug effects; D008055:Lipids / Q000097:blood*; D008077:Lipoproteins, LDL / Q000097:blood; D008099:Liver / Q000187:drug effects*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D014280:Triglycerides / Q000097:blood; D005723:gamma-Glutamyltransferase / Q000097:blood
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D062385:Hydroxybenzoates; D000960:Hypolipidemic Agents; D008055:Lipids; D008077:Lipoproteins, LDL; D014280:Triglycerides; C009091:protocatechuic acid; D005688:Galactosamine; D005723:gamma-Glutamyltransferase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase