Serum arylesterase and paraoxonase activity in patients with chronic hepatitis

AIM: To investigate the relationship between serum paraoxonase (PON1), AST, ALT, GGT, and arylesterase (AE) activity alterations and the degree of liver damage in patients with chronic hepatitis. METHODS: We studied 34 chronic hepatitis patients and 32 control subjects, aged between 35 and 65 years, in the Department of Infection and Clinical Microbiology at the Firat University School of Medicine. Blood samples were collected from subjects between 8: 00 and 10: 00 a. m. following a 12-h fast. Baseline and salt-stimulated PON1 activities were measured by the hydrolysis of paraoxon. Phenyl acetate was used as the substrate and formed phenol was measured spectrophotometrically at 270 nm after the addition of a 10-fold diluted serum sample in AE activity measurements. RESULTS: The results of this investigation revealed that the levels of AE activity decreased from 132 +/- 52 to 94 +/- 36 (29%), baseline PON1 activity from 452 +/- 112 to 164 +/- 67 (64%), salt-stimulated PON1 activity from 746 +/- 394 to 294 +/- 220 (61%), HDL from 58.4 +/- 5.1 to 47.2 +/- 5.6 (20%), triglyceride from 133 +/- 51.2 to 86 +/- 34.0 (35%), while a slight increase in the level of LDL (from 163 +/- 54.1 to 177.3 +/- 56.0; 9%) and significant increases in the levels of AST (from 29 +/- 9.3 to 98 +/- 44), ALP (from 57.2 +/- 13.1 to 91 +/- 38.1), ALT (from 27.9 +/- 3.32 to 89 +/- 19.1), GGT (from 24.3 +/- 2.10 to 94 +/- 48.2), total bilirubin (from 0.74 +/- 0.02 to 1.36 +/- 0.06; 84%) and direct bilirubin (from 0.18 +/- 0.01 to 0.42 +/- 0.04; 133%) were detected. However, the levels of albumin, total protein, cholesterol, and uric acid were almost the same in chronic hepatitis and the control subjects. CONCLUSION: Low PON1 and AE activity may contribute to the increased liver dysfunction in chronic hepatitis patients by reducing the ability of HDL to retard LDL oxidation and might be clinically useful for monitoring the disease of chronic hepatitis. (C) 2005 The WJG Press and Elsevier Inc. All rights reserved.