ABSTRACT
High rates of hepatocellular carcinoma [HCC] are primarily due to high prevalence of chronic hepatitis C or B virus infection which causes chronic necroinflammatory hepatic disease. Egypt has one of the world's highest prevalences of hepatitis C virus [HCV] infection. Glutathione S-transferases [GSTs] constitute a superfamily of enzymes that catalyse the metabolism of a wide range of carcinogens. Of the different isoforms of GSTs, GSTM1 and GSTT1 which have deletion polymorphisms. The aim of the present study was to investigate the possible association between GSTM1 and GSTT1 deletion polymorphisms and the risk of HCC in Egyptian patients with hepatitis C virus [HCV] infection. Subjects and The genotypes of GSTM1 and GSTT1 were analyzed in 24 HCV carriers with HCC, and 25 healthy controls using polymerase chain reaction [PCR] technique. The null genotypes of GSTM1 and GSTT1were significantly frequent in patients with HCC compared with controls. These results suggest that both The GSTM1 and GSTT1 null genotypes are associated with an increased risk of HCC in Egyptian population
Subject(s)
Humans , Male , Female , Glutathione Transferase/blood , Glutathione Transferase/genetics , Polymorphism, Genetic , Hepatitis C, Chronic , Risk FactorsABSTRACT
Paraoxonasel [PON1] is an esterase enzyme that has antioxidant acivity and is lightly associated with high density lipoprotein [HDL] in blood. Decreased activity of PONiwas reported in many diseases and could be partially attributed to PON1 glutamine 192 arginine polymorphism. In the present work we studied the effect of PON1 192 polymorphism on serum PON1 activity and lipid profiles in 30 non-insulin dependent diabetes mellitus [NIDDM] subjects and 30 healthy controls among the Egyptian populalion. Polymerase chain reaction-based restricion fragment was used to determine PON1 192 gene polymorphism. Fasing blood glucose, serum lipids, lipid peroxidalion [malondialdehyde-MDA] and PON1 acivity were measured by spectrophotometric method. Insulin serum levels were measured by ELISA technique and [HOMA] index was calculated as an index for presence insulin resistance. No significant difference was found in the distribution of PON1 192 genotypes [QQ, RR and QR] between patient and control groups. Also, the R allele was insignificantly predominant among diabetic palients. PON1 enzyme activity was significantly lower in diabetics than in control subjects. PON1 192 RR homozygote had significantly lower PON1 acivity and HDL-C level than QQ and QR genotypes among the NIDDM populations [p<0.001]. Total cholesterol, triglycerides, LDL-C serum level were significantly higher in patients than controls. Fasting serum insulin level and HOMA index were significantly increased in those patients compared to controls. This indicated the development of insulin resistance which could be attributed to the decrease of paroxonase antioxidant activity. the present results suggest that the paraoxonasel acivities are affected by PON1 genetic variability in NIDDM patients and may precipitate to insulin resistance among those patients