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.
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.
Furthermore, the antioxidant enzyme activities of glutathione peroxidase and catalase in liver were increased and malondialdehyde level was decreased with AESA treatment compared with those in the DM group.
(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.
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.
L. rhamnosus NCDC 17 improved oral glucose tolerance test, biochemical parameters (fasting blood glucose, plasma insulin, glycosylated haemoglobin, free fatty acids, triglycerides, total cholesterol, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol), oxidative stress (thiobarbituric acid reactive substance and activities of catalase, superoxide dismutase and glutathione peroxidase in blood and liver), bifidobacteria and lactobacilli in cecum, expression of glucagon like peptide-1 producing genes in cecum, and adiponection in epididymal fat, while decreased propionate proportions (%) in caecum, and expression of tumour necrosis factor-α and interlukin-6 in epididymal fat of diabetic rats as compared to diabetes control group.
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.
In patients with impaired glucose regulation and diabetes, the number of coronary artery branches with stenosis and the Gensini scores were inversely correlated with the plasma levels of CAT, SOD, GSH, GH, and GSH-Px (P < 0.001).
Rats were studied 30 days after the STZ treatment, and the diabetes untreated model group presented significantly higher kidney index, blood glucose, triglyceride (TG), total cholesterol (TC), malondialdehyde (MDA), interferon-γ (IFN-γ), and IFN-γ/IL-4 levels, lower body weight, fasting blood insulin (FPI), IL-4, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and nitric oxide (NO) levels and worse renal function (higher blood urea nitrogen (BUN), serum creatinine (SCr), urine protein (UP) levels and glomerular extracellular matrix (relative area)) compared with the normal control group (p < 0.05).
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.