Catalase (CAT) is a major antioxidant enzyme and a number of polymorphisms in the CAT have been described as being associated with several diseases, such as hypertension, diabetes mellitus, Alzheimer's disease, and vitiligo.
(i) to determine the extent of oxidative stress and DNA damage and repair using a panel of selected markers in patients with type 1 and type 2 diabetes mellitus (T1DM, T2DM), (ii) to find their possible relationships with diabetes compensation and duration, and finally (iii) to test for the effect of functional polymorphisms in the 8-oxoguanin DNA glycosylase (rs1052133), catalase (rs1001179) and superoxide dismutase (rs4880) genes on respective intermediate phenotypes.
Whatever impaired glucose tolerance, insulin resistance on diabetes and whatever their occurrence or implications, the studies taken together converge toward the hypothesis that catalase polymorphisms play a role in glucose disorders.
The high (18.5%) prevalence of diabetes mellitus in inherited catalase deficient individuals and the earlier (10 years) manifestation of the disease may be attributed to the oxidative damage of oxidant sensitive, insulin producing pancreatic beta-cells.
The aim of this study is to examine association of decreased blood catalase activity and catalase exon mutations in patients (n=617) with diabetes (n=380), microcytic anemia (n=58), beta-thalassemia (n=43) and presbycusis (n=136) and in controls (n=295).
Catalase (CAT) is a major antioxidant enzyme and a number of polymorphisms in CAT have been shown to be associated with several diseases, including hypertension, diabetes mellitus, Alzheimer's disease, and vitiligo.
This paper describes the direct and indirect involvement of deficiency and/or modification of catalase in the pathogenesis of some important diseases such as diabetes mellitus, Alzheimer's disease, Parkinson's disease, vitiligo, and acatalasemia.
The early NAC treatment in DM rats reduced proteinuria, creatinine, urea, TBARS and iNOS and, increased creatinine clearance, NO and eNOS, increasing significantly the antioxidant defenses, promoting elevated catalase and glutathione compared to DM-E group, all p < 0.05.
The increase in total nitrite/nitrotyrosine in DM promoted significant compensatory increases in antioxidant activities of SOD, catalase and glutathione peroxidase/reductase probably to prevent cardiac oxidative damage.
Cardiac levels of GSH were increased in Smoking groups whereas activities of catalase and superoxide dismutase increased in DM, Smoking and DM + Smoking groups.
Levels of superoxide dismutase and catalase were both reduced and hydrogen peroxide was increased in vehicle-treated DM, but these changes were reversed by fenofibrate treatment.
Functionally, the antioxidants effect of NG is primarily attributed by reducing the free radical like reactive oxygen species (ROS) and enhancing the antioxidants activity such as superoxide dismutase (SOD), catalase, glutathione (GSH) in chronic diseases such as cardiovascular, neurodegenerative, diabetes, pulmonary, cancer and nephropathy.
The observed residue-specific modifications of catalase, peroxiredoxin, carbonic anhydrase, lactate dehydrogenase B and delta-aminolevulinic acid dehydratase were correlated with the literature report on their functional disorder in DM.
The effect of CE extract administration on the redox status of RBCs was evaluated by assessing lipid peroxidation, the ratio of reduced/oxidized glutathione (GSH/GSSG), the level of S-glutathionylated proteins (GSSP) and the enzymatic activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) in RBCs four weeks after diabetes onset.
Serum activity of antioxidant enzymes glutathione peroxidase, superoxide dismutase (SOD), and catalase was lower in DM than CTL; apocynin restored catalase and SOD levels in DM + APO.