Search results for "DAS"
showing 10 items of 4164 documents
Modulation of selenium-dependent glutathione peroxidase by perfluorodecanoic acid in rats: effect of dietary selenium.
1990
Forty-eight male Sprague-Dawley rats fed a diet containing 0.4, 0.2 or 1.0 mg of selenium (Se)/kg of diet were injected with a single dose (35 mg/kg) of perfluorodecanoic acid (PFDA) in corn oil and killed 2 wk later. Control animals were pair-fed and treated with an equal volume of vehicle. PFDA treatment significantly increased Se-dependent glutathione peroxidase (Se-GSHPx) activity in liver cytosol of rats fed the 0.04 mg of Se/kg of diet but not in rats fed the other diets. The increase in liver cytosolic Se-GSHPx activity in rats fed 0.04 mg of Se/kg of diet paralleled increases in Se content and serum Se-GSHPx activity. Determination of Se-GSHPx by an enzyme-linked immunosorbent assay…
Formation and metabolism of catecholestrogens in depressed patients.
1990
Abstract The evidence that catecholestrogens are formed in the brain and exert behavioral effects in animal models suggests that these steroids might have psychotropic activities. In the present investigation, the formation and metabolism of catecholestrogens were studied in depressed patients. Twenty-four-hr urine samples were collected from 6 male patients (59 ± 8 years) with endogenous retarded depression (subtype primary, endogenous, and recurrent according to Research Diagnostic Criteria) and from 12 male control subjects (51 ± 4 years). The patients were treated with the monoamine oxidase inhibitor tranylcypromine (10–40 mg/day for 3–4 weeks). The concentrations of primary estrogens, …
The Clinical and Molecular Spectrum of GM1 Gangliosidosis
2019
Objective To evaluate the clinical presentation of patients with GM1 gangliosidosis and to determine whether specific clinical or biochemical signs could lead to a prompt diagnosis. Study design We retrospectively analyzed clinical, biochemical, and genetic data of 22 patients with GM1 gangliosidosis from 5 metabolic centers in Germany and Austria. Results Eight patients were classified as infantile, 11 as late-infantile, and 3 as juvenile form. Delay of diagnosis was 6 ± 2.6 months in the infantile, 2.6 ± 3.79 years in the late-infantile, and 14 ± 3.48 years in the juvenile form. Coarse facial features, cherry red spots, and visceromegaly occurred only in patients with the infantile form. …
Does increased serum creatine kinase activity reflect exercise-induced muscle damage in rats?
1995
To test a hypothesis that exercise-induced increase in serum creatine kinase activity and the concomitant necrotic muscle damage in unaccustomed rats may be interrelated phenomena, and that the first might largely be caused by changes in lymph flow, groups of rats were separately exposed to a swimming, combination of swimming and running, and running protocol. Their serum was then repeatedly analysed over a period of 72 h for creatine kinase activity, and their soleus and the red parts of quadriceps femoris muscles for beta-glucuronidase activity (damage marker) 72 h after the commencement of the experiment, i.e. at a moment when muscle damage is in the necrotic phase. The results clearly s…
The disruption of myofibre structures in rat skeletal muscle after forced lengthening contractions.
1998
Specific antibodies against structural proteins (actin, desmin, dystrophin, fibronectin) of muscle fibres were used to study the effect of forced lengthening contractions on muscle microarchitecture. Tibialis anterior (TA) muscle of male Wistar rats were subjected to 240 forced lengthening contractions. At consecutive time points (0, and 6 h, 2, 4, and 7 days) after stimulation, the TA muscle was excised for biochemical and histological assays. Beta-Glucuronidase activity, a quantitative indicator of muscle damage, showed increased values 2-7 days after the lengthening, peaking on day 4 (11.7-fold increase). A typical course of histopathological changes (myofibre swelling, necrosis and rege…
Prednisolone decreases exercise-induced acid hydrolase response in mouse skeletal muscle.
1984
Male NMRI-mice were subjected to exhaustive treadmill exercise. 3 and 6 days after the exertion, quadriceps femoris muscles were examined histologically and analyzed for acid hydrolases in order to follow the degree and progress of injuries. Prednisolone (PRED), an anti-inflammatory corticosteroid, was given to some of the animals in order to modify the exercise response. The PRED administration began 14 h before exercise and continued until the end of the experiment (6 days). The doses were 25 and 50 mg . kg-1 i.p. twice a day. The activities of both arylsulphatase and beta-glucuronidase increased significantly in the exercise control group after 3 and 6 days. The increase in activity corr…
Nephrosis in two siblings with infantile sialic acid storage disease
1990
The diagnosis of infantile sialic acid storage disease (ISSD) was established in two siblings on the basis of typical clinical signs and the biochemical findings of hyperexcretion and intracellular storage of free sialic acid. A severe, steroid resistant nephrosis occurred in both siblings. The activities of lysosomal enzymes, including sialidase, were normal. A combined detection method for sialic acids with Limax flavus agglutinin labelling and phosphotungstic acid staining showed severely alterated sialic acid components in epithelial kidney cells and indicate a causal relationship between the nephrosis and the underlying biochemical defect. Further observations of ISSD patients with ren…
Regulation of Oxygen Distribution in Tissues by Endothelial Nitric Oxide
2009
Nitric oxide (NO) decreases cellular oxygen (O 2 ) consumption by competitively inhibiting cytochrome c oxidase. Here, we show that endogenously released endothelial NO, either basal or stimulated, can modulate O 2 consumption both throughout the thickness of conductance vessels and in the microcirculation. Furthermore, we have shown that such modulation regulates O 2 distribution to the surrounding tissues. We have demonstrated these effects by measuring O 2 consumption in blood vessels in a hypoxic chamber and O 2 distribution in the microcirculation using the fluorescent oxygen-probe Ru(phen) 3 2+ . Removal of NO by physical or pharmacological means, or in eNOS −/− mice, abolishes this …
Mechanisms underlying recoupling of eNOS by HMG-CoA reductase inhibition in a rat model of streptozotocin-induced diabetes mellitus
2007
Abstract Objective HMG-CoA reductase inhibitors have been shown to upregulate GTP cyclohydrolase I (GTPCH-I), the key enzyme for tetrahydrobiopterin de novo synthesis and to normalize tetrahydrobiopterin levels in hyperglycemic endothelial cells. We sought to determine whether in vivo treatment with the HMG-CoA reductase inhibitor atorvastatin is able to upregulate the GTPCH-I, to recouple eNOS and to normalize endothelial dysfunction in an experimental model of diabetes mellitus. Methods and results In male Wistar rats, diabetes was induced by streptozotocin (STZ, 60mg/kg). In STZ rats, atorvastatin feeding (20mg/kg/d, 7 weeks), normalized vascular dysfunction as analyzed by isometric tens…
Chronic Therapy With Isosorbide-5-Mononitrate Causes Endothelial Dysfunction, Oxidative Stress and a Marked Increase in Vascular Endothelin-1 Express…
2011
Aims Isosorbide-5-mononitrate (ISMN) is one of the most frequently used compounds in the treatment of coronary artery disease predominantly in the USA. However, ISMN was reported to induce endothelial dysfunction, which was corrected by vitamin C pointing to a crucial role of reactive oxygen species (ROS) in causing this phenomenon. We sought to elucidate the mechanism how ISMN causes endothelial dysfunction and oxidative stress in vascular tissue. Methods and results Male Wistar rats ( n = 69 in total) were treated with ISMN (75 mg/kg/day) or placebo for 7 days. Endothelin (ET) expression was determined by immunohistochemistry in aortic sections. Isosorbide-5-mononitrate infusion caused si…