Publication | Open Access
Observation of Esterase-Like-Albumin Activity during <i>N</i>'-Nitrosodimethyl amine Induced Hepatic Fibrosis in a Mammalian Model
16
Citations
39
References
2012
Year
PathologyHepatic FibrosisFatty Liver DiseaseOxidative StressHepatotoxicityStable Esterase-albumin ComplexHepatology FibrosisMetabolic SignalingHealth SciencesFibrosisBiochemistryNdma-induced HfLiver PhysiologyAlcohol-related Liver DiseasePharmacologyMammalian ModelDrug-induced Liver InjuryEsterase-like-albumin ActivityHepatologyPhysiologyLiver DiseaseMetabolismMedicineExtracellular Matrix
Aim: Hepatic fibrosis (HF) is characterized by irregular growth and amassing of fibrous scar tissues in the liver causing weakened hepatocytes metabolism and protein level alterations, including albumin. Albumin with Mr ~68-70 kDa is unglycosylated soluble plasma protein with various biological roles. In this study, we demonstrate ‘esterase-like activity’ of albumin during NDMA-induced HF in rats. Material and Methods: In rats, HF was induced by weekly i.p. injections of NDMA in doses of 10 mg/kg b.wt. Sera of controls (untreated) and treated rats were processed for biochemical tests, electrophoretic profiling and in-gel esterase activity localization using a, b-naphthyl acetates. H&E staining of liver sections (~ 5 m m) was done to confirm induction of HF. Results: NDMA satisfactorily induces hepatic fibrosis within 21 days which is also evident by significant increase in SALP, SGOT, SGPT and bilirubin levels in rats. ‘Esterase-like activity’ of albumin detected in animal sera remains stable throughout the course of treatment irrespective of other biochemical changes. Conclusion: During pathogenesis of HF, formation of stable esterase-albumin complex may have some important role and hence, prior recommending the use of albumin as diagnostic marker we propose further investigations to elucidate the mechanism of its formation.
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