Study of oxidative stress and antioxidant status in ascitic patients with ovarian cancer in comparison to liver cirrhosis patients

Abstract

The pathological accumulation of abdominal fluid (ascites) is due to multiple causes often associated either with peritoneal and non-peritoneal diseases. In the process of ascites formation there is increased vascular permeability, decreased lymphatic resorption and gross change in the concentrations of functional proteins and metabolites. Liver cirrhosis is a chronic disorder in which ascites develop in advanced stages of the disease, where as in ovarian cancer, most of the cases develop ascites in the early stages after the onset of disease. Among malignant ascites, ovarian cancers are the most common primary tumors and sixth most common malignant neoplasm in women with highest mortality rate.1 Oxidative stress is caused by free radicals leading to oxidative destruction of poly unsaturated fatty acids constitutive of cellular membrane and give rise to lipid peroxides which are unstable and decompose to form reactive carbonyl compounds. Among them malondialdehyde (MDA) is the most abundant, and it readily combines with several functional groups on proteins and forms DNA-MDA adducts, which are highly mutagenic, cytotoxic, co-carcinogenic and acts as a tumor promoter.2–5 Oxidative stress induces cancer among the biological molecules and plays an important role in the pathogenesis of liver disease and other hepatic alterations.6 Intestinal permeability is increased in patients with cirrhosis and oxygen free radicals play an important role in gut epithelial damage. Hence measurement of MDA is widely used as an indicator of oxidative stress. The antioxidant enzyme superoxide dismutase (SOD) is widely distributed in the cells and present in higher levels in erythrocytes,7 and it plays an important role in scavenging and protects cells against superoxide radical by dismutation of the highly reactive superoxide anion to oxygen and less reactive oxygen species hydrogen peroxide.8 The low levels of SOD may be due to increased utilization of scavenger lipid peroxides. The imbalance between the free radicals and antioxidants results in oxidative stress. Ceruloplasmin is a copper binding protein which is increased in several carcinomas.