Open AccessImmunobiochemical analysis of paraoxonase1 (anti‐oxidant), xanthine oxidase (oxidant) enzymes and lipid profile of cardiac disease patients in Lahore Metropolitan, Pakistan
Author(s) -
Samra Zahoor Qadir,
Sana Adeela,
Bano Sadia,
Farooq Mariam,
Dar Nadia,
Athar Muhammad Amin
Publication year - 2010
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.20417
Subject(s) - xanthine oxidase , anti oxidant , enzyme , disease , lipid profile , chemistry , medicine , biochemistry , cholesterol , antioxidant
Cardiac diseases are the major cause of death. Paraoxonase1 (PON1) is known as free radicals scavenger/anti‐atherosclerosis, whereas xanthine oxidase (XO) is a free radicals generator. This study was undertaken to determine and compare the Paraoxonase and arylesterase activities of PON1 enzyme and activity of XO enzyme. The concentration of XO and PON1 enzymes along with lipid profile, lipid peroxides, and thiol level in plasma of cardiac patients ( n =200) and healthy persons ( n =200) of Lahore metropolitan, Pakistan was also determined. Anti‐PON1 and anti‐XO antibodies were developed, purified, and used to measure the concentration of PON1 and XO by competitive ELISA. It is observed that low paraoxonase ( P =0.0073)/arylesterase activity ( P =0.0038) of PON1 enzyme and its low concentration ( P =0.0049) were observed in cardiac patients, whereas elevated level of XO activity ( P =0.0129) and its concentration ( P =0.0097) was observed in cardiac patients as compared with healthy persons. Low levels of HDL ( P =0.0013), thiol ( P =0.0014) and high level of cholesterol ( P =0.0025), triglycerides ( P =0.0018), LPO ( P =0.0014), and LDL level ( P =0.05) were observed in cardiac patients admitted in intensive care unit as compared with hypertensive patients and control subjects. It is concluded that overall low PON1 and high XO activities do cause imbalance of free radical system which ultimately leads to or enhance the cardiac pathological conditions. J. Clin. Lab. Anal. 24:348–356, 2010. © 2010 Wiley‐Liss, Inc.