Pentraxin 3 as a potential biomarker of acetaminophen-induced liver injury

• Published in: Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie Vol. 65; no. 1-2; pp. 147 - 151
• Main Authors: Yaman, Halil, Cakir, Erdinc, Akgul, Emin O., Aydin, Ibrahim, Onguru, Onder, Cayci, Tuncer, Kurt, Yasemin Gulcan, Agilli, Mehmet, Aydin, Fevzi N., Gulec, Mustafa, Altinel, Ozcan, Isbilir, Salim, Ersoz, Nail, Yasar, Mehmet, Turker, Turker, Bilgi, Cumhur, Erbil, Kemal M.
• Format: Journal Article
• Language: English
• Published: Germany Elsevier GmbH 01.01.2013
• Subjects: Acetaminophen; Acetaminophen - toxicity; Administration, Oral; adults; Analgesics, Non-Narcotic - toxicity; Animals; biomarkers; Biomarkers - blood; Biomarkers - metabolism; blood; C-Reactive Protein - analysis; C-Reactive Protein - metabolism; Chemical and Drug Induced Liver Injury - diagnosis; Chemical and Drug Induced Liver Injury - etiology; Chemical and Drug Induced Liver Injury - metabolism; Chemical and Drug Induced Liver Injury - pathology; Dose-Response Relationship, Drug; histopathology; humans; Injury; laboratory animals; Liver; Liver - drug effects; Liver - metabolism; Liver - pathology; Male; Necrosis; overdose; Pentraxin 3; prediction; prospective studies; Rats; Rats, Wistar; Serum Amyloid P-Component - analysis; Serum Amyloid P-Component - metabolism; tissues; Pentraxin 3; Acetaminophen; Liver; Injury
• ISSN: 0940-2993; 1618-1433
• DOI: 10.1016/j.etp.2011.07.003

Overdose of acetaminophen (APAP) can lead to severe liver injury in humans and experimental animals. Pentraxin-3 (PTX-3) is produced and released by several cell types. In this study, we aimed to evaluate whether PTX-3 is a potential biomarker in the identification of APAP-induced liver injury. Thirty adult male Wistar rats were randomly divided into three groups: control, APAP-1 and APAP-2 groups. APAP-1 (1g/kg) and APAP-2 (2g/kg) group rats were given APAP by gastric tube. Liver tissues and blood samples were obtained for biochemical and histopathological analysis. Biochemical parameters, plasma and liver PTX-3 levels and degree of liver necrosis were measured in all groups. APAP treatments caused necrosis in liver and accompanied by elevated liver PTX-3 levels after 48h. In APAP-1 and APAP-2 groups when compared with control group (7.5±3.3ng/mg protein), mean liver PTX-3 concentrations were 14.1±3.0 (p=0.032) and 28.5±8.2 (p<0.001)ng/mg protein, respectively. All rats (100%) in the APAP-2 group had the degree 3 liver necrosis. However 10%, 40% and 50% of rats had the degree 1, the degree 2 and the degree 3 liver necrosis in the APAP-1 group, respectively. The degrees of liver necrosis of the APAP-1 and APAP-2 groups were higher than the group of control (p<0.001 and p<0.001, respectively). PTX-3 may have a role in the APAP-induced liver injury in the rats. The elevated liver PTX-3 in the APAP-induced hepatic necrosis might be a marker of acute histological liver damage. Further prospective studies are necessary to clarify the prognostic value of liver PTX-3 for prediction of histological hepatic necrosis in the APAP-induced liver injury.