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Hypertension impairs cerebral vascular function. Vasodilator-stimulated phosphoprotein (VASP) mediates active reorganization of the cytoskeleton via membrane ruffling, aggregation and tethering of actin filaments. VASP regulation of endothelial barrier function has been demonstrated by studies using VASP−/− animals under conditions associated with tissue hypoxia. We hypothesize that hypertension regulates VASP expression and/or phosphorylation in endothelial cells, thereby contributing to dysfunction in the cerebral vasculature. Because exercise has direct and indirect salutary effects on vascular systems that have been damaged by hypertension, we also investigated the effect of exercise on maintenance of VASP expression and/or phosphorylation. We used immunohistochemistry, Western blotting and immunocytochemistry to examine the effect of hypertension on VASP expression and phosphorylation in brain endothelial cells in normotensive [Wistar-Kyoto (WKY)] and spontaneously hypertensive (SH) rats under normal and exercise conditions. In addition, we analyzed VASP regulation in normoxia- and hypoxia-induced endothelial cells. Brain endothelial cells exhibited significantly lower VASP immunoreactivity and phosphorylation at the Ser157 residue in SHR versus WKY rats. Exercise reversed hypertension-induced alterations in VASP phosphorylation. Western blotting and immunocytochemistry indicated reduction in VASP phosphorylation in hypoxic versus normoxic endothelial cells. These results suggest that diminished VASP expression and/or Ser157 phosphorylation mediates endothelial changes associated with hypertension and exercise may normalize these changes, at least in part, by restoring VASP phosphorylation. [ABSTRACT FROM AUTHOR]

Introduction. Vascular endothelial growth factor (VEGF) is known to influence testis function. Transforming growth factor alpha (TGF-α) is expressed in the postnatal testis, and has been demonstrated to stimulate testis development. Systemic diseases such as chronic renal failure (CRF) interfere with hypothalamic-pituitary-gonadal axis, which may cause defective steroidogenesis and gonadal functions. The aim of this study was to investigate the expression and localization of VEGF and TGF-α in testicular tissues of experimental CRF model. Material and methods. Experimental CRF was induced in rats by the resection of more than 85% of renal mass. The expression of VEGF and TGF-α in testicular tissues were assessed by immunohistochemistry on paraffin sections of control, CRF-nondialysed and CRF-dialysed rats. Results. The microscopic evaluation of the testicular structure showed that CRF did not affect testicular histology. Immunohistochemical evaluation showed that VEGF was expressed in the cytoplasm of primary and secondary spermatocyte series as well as the early spermatids. Staining intensity was lower in spermatocytes going through the first meiotic division. TGF-α was expressed in the nuclei of spermatogonia and primary spermatocytes with stronger staining intensity in spermatogonia. The intensity of VEGF staining was similar in control and experimental animals, however, TGF-α expression was lower in the CRF group. Conclusions. The continuous expression of VEGF in spermatocytes and spermatids suggests that the applied model of CRF does not directly disrupt morphology of seminiferous epithelium, thus also spermiogenesis. However, difference between control rats and CRF group in TGF-α immunopositivity, which was localised in spermatogonial mitosis step, may suggest the interference of CRF with early stages of spermatogenesis. [ABSTRACT FROM AUTHOR]

Study Design: A retrospective study. Purpose: The aim of this study was to evalute the effects of mitomycin-C, sodium hyaluronate and human amniotic fluid on preventingspinal epidural fibrosis.Overview of Literature: The role of scar tissue in pain formation is not exactly known, but it is reported that scar tissue causes adhesionsbetween anatomic structures. Intensive fibrotic tissue compresses on anatomic structures and increases the sensitivity of thenerve root for recurrent herniation and lateral spinal stenosis via limiting movements of the root. Also, neuronal atrophy and axonaldegeneration occur under scar tissue.Methods: The study design included 4 groups of rats: group 1 was the control group, groups 2, 3, and 4 receieved antifibrotic agents,mitomycin-C (group 2), sodium hyaluronate (group 3), and human amniotic fluid (group 4). Midline incision for all animals were doneon L5 for total laminectomy. Four weeks after the surgery, the rats were sacrificed and specimens were stained with hematoxylineosinand photos of the slides were taken for quantitive assesment of the scar tissue.Results: There was no significant scar tissue in the experimental animals of groups 2, 3, and 4. It was found that there was no significantdifference between drug groups, but there was a statistically significant difference between the drug groups and the controlgroup. Conclusions: This experimental study shows that implantation of mitomycin-C, sodium hyaluronate and human amniotic fluid reducesepidural fibrosis and adhesions after spinal laminectomy in rat models. Further studies in humans are needed to determine thecomplications of the agents researched. [ABSTRACT FROM AUTHOR]

It is known that aging is associated with marked effects on integrity and function of cell membrane. These effects may also be exacerbated by exogenous chemicals, e.g. sulfite. Thus, the aim of this paper is to examine the influence of sulfite on hemorheological and related hematological parameters in rats of various ages. In this study, male Wistar rats at the age of 3 and 18 months were used and the following parameters were evaluated: Mean Cell Volume (MCV), Mean Corpuscular Hemoglobin Concentration (MCHC), Red blood Cell (RBC) deformability and aggregation. The results show that aging is associated with a decrease in RBC deformability and MCHC, an increase in MCV. Sulfite administration significantly increased RBC deformability in both young and aged rats. Although MCHC was decreased in young rats, it was increased in aged rats in response to sulfite exposure. Additionally, sulfite induced a decrement in MCV of aged rats. Neither aging nor sulfite treatment caused significant alterations in RBC aggregation parameters in all experimental groups. In conclusion, these findings suggest that RBC deformability impairs with age and sulfite has ameliorating effects on RBC deformability in both young and aged rats. [ABSTRACT FROM AUTHOR]

Sulfites, which are commonly used as preservatives, are continuously formed in the body during metabolism of sulfur-containing amino acids. Sulfite oxidase (SOX) is an essential enzyme in the pathway of the oxidative degradation of sulfite to sulfate protecting cells from sulfite toxicity. This article investigated the effect of sulfite on Total Antioxidant Capacity (TAC), Total Oxidant Status (TOS), Lipid Hydroperoxide (LOOH) and total free sulphydryl groups (-SH) contents in normal and sulfite oxidase (SOX) deficient male albino rats' plasma. For this purpose rats were divided into four groups: control (C), sulfite treated (S), SOX-deficient (D), and sulfite treated SOX-deficient (DS) groups. Sulfite oxidase deficiency was established by feeding rats a low molybdenum diet and adding to their drinking water 200 ppm tungsten (W). Sulfite (70 mg/kg) was administered to the animals via their drinking water. SOX deficiency together with sulfite treatment caused a significant increase on the plasma LOOH and total oxidant status levels. -SH content of rats plasma significantly decreased by both sulfite treatment and SOX deficiency compared to the control. There was also significant decrease in plasma TAC level by sulfite treatment. In conclusion, sulfite treatment affects the antioxidant/oxidant balance of the plasma cells of the rats toward oxidants in SOX deficient groups. [ABSTRACT FROM AUTHOR]