Superoxide radicals (SR) in the pathophysiology of ischemic acute renal failure (ARF).
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Acute Kidney Injury↗
Biomedical subjects
F Turrini
Publications and source records attributed to F Turrini.
Measurement of phagocytosis utilizing [14C]cyanate-labelled human red cells and monocytes.
Human red cells were labelled with [14C]cyanate, non-oxidant, permeant reagent that binds irreversibly to amino groups in proteins. Cyanate did not modify GSH levels, nor glucose-6-phosphate dehydrogenase (G6PD) activity when added at the labelling concentration i.e. c. 0.5 mM. Phagocytes were human monocytes, isolated and plated on 16 mm diameter plastic wells. Each well was plated with 40-70 X 10(3) cells. Monocytes were quantified by DNA assay with the DNA intercalating fluorescent compound Hoechst 33,258. The basal phagocytic rate of normal red cells by monocytes was 0.34 +/- 0.21 red cell per monocyte. Treatment of normal red cells with 20 microM diamide, or 50-100 microM chromate enhanced this rate 10-15-fold. 10 microM diamide or chromate were sufficient to stimulate phagocytosis of G6PD-deficient (Mediterranean variant) red cells.
Carbon Radioisotopes↗
In vitro effects of epinephrine on Na influx into brush border vesicles from the rat kidney.
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Animals↗
Increased red cell calcium, decreased calcium adenosine triphosphatase, and altered membrane proteins during fava bean hemolysis in glucose-6-phosphate dehydrogenase-deficient (Mediterranean variant) individuals.
RBCs from four glucose-6-phosphate dehydrogenase (G6PD)-deficient (Mediterranean variant) subjects were studied during fava bean hemolysis. In the density-fractionated RBC calcium level, Ca2+-ATPase activity, reduced glutathione level, and ghost protein pattern were studied. In the bottom fraction, containing most heavily damaged RBCs, calcium level ranged from 143 to 244 mumol/L RBCs (healthy G6PD-deficient controls: 17 +/- 5 mumol/L RBCs). The Ca2+-ATPase activity ranged from 0.87 to 1.84 mumol ATP consumed/g Hb/min (healthy G6PD-deficient controls: 2.27 +/- 0.4). Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) of ghosts showed: (1) the presence of high mol wt aggregates (in three cases they were reduced by dithioerythritol; in one case, only partial reduction was possible); (2) the presence of multiple, scattered new bands; and (3) the reduction of band 3. Oxidant-mediated damage to active calcium extrusion, hypothetically associated with increased calcium permeability, may explain the large increase in calcium levels. They, in turn, could activate calcium-dependent protease activity, giving rise to the profound changes in the ghost protein pattern.
Adolescent↗
Prevention of acute renal failure by diuretics.
Experiments were performed on 26 rats to evaluate the effect of furosemide and muzolimine in an experimental model of acute renal failure (ARF). After control clearance measurements from both the left and the right kidney, an acute hydronephrosis was produced on the left side only, to completely interrupt urine flow rate. At the 17th minute of stop-flow, placebo (4 animals), furosemide (4 mg i.v. in 5 animals) or muzolimine (1.2 mg i.v. in 5 rats) were injected and three minutes later the renal arteries were clamped bilaterally for 20 minutes. The arterial clamps and the left hydronephrosis were removed at the 20th minute of ischemia and then 5 consecutive clearance periods were performed from either side to assess recovery from post-ischemic ARF. There was no difference in the entity of GFR depression and speed of recovery of either kidney between placebo, muzolimine and furosemide. The left, post-hydronephrotic kidney consistently exhibited a post-ischemic renal function more depressed than that measured in the contralateral side, although the speed of recovery was the same. The ATP content of the renal tissue was significantly larger in the right kidney compared to the contralateral side in the group receiving furosemide. In the animals treated with muzolimine ATP was significantly depressed in both kidneys. In the post-ischemic period the urinary Na excretion and the fractional water excretion rose significantly with either diuretic compared to placebo. However, this did not influence the recovery in GFR.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Kidney Injury↗
Mechanism of action of divicine in a cell-free system and in glucose-6-phosphate dehydrogenase-deficient red cells.
Favism is an acute hemolysis occurring in glucose-6-phosphate dehydrogenase (G6PD)-deficient (Mediterranean variant) individuals after intake of fava beans. Divicine (D), 2,6-diamino-4,5-dihydroxypyrimidine, is present in high amounts in the beans, and is suspected to play a role in hemolysis. Its mechanism of action was studied in a cell-free system and in G6PD (Mediterranean variant)-deficient red cells (RBC). Upon hydrolysis of the inactive beta-glucoside vicine, reduced divicine is formed. Oxygen acts as a one- or two-electron acceptor; superoxide anion and hydrogen peroxide are formed, respectively, together with the semiquinoid free-radical form of D. This free radical gives an electron spin resonance (ESR) signal, which is similar to that of the alloxan free radical. Added reduced glutathione (GSH) is rapidly oxidized with a stoichiometry of one to one, and the ESR signal is abolished. Additional GSH is oxidized by hydrogen peroxide and by a slow redox cycle which continuously regenerates oxidized D. The fast-direct and the slow-indirect oxidation result in nonstoichiometric oxidation of GSH. D added to G6PD-deficient RBC rapidly oxidizes GSH with an end point kinetics and a stoichiometry of one to one. Hydrogen peroxide and superoxide anion are scavenged in the RBC and no redox cycling is taking place. No GSH is regenerated even after long incubation periods. After the primary event, i.e., oxidation of GSH and--SH groups, a number of metabolic, rheologic, and membrane modifications, together with increased erythrophagocytosis take place in G6PD-deficient, D-treated RBC only.(ABSTRACT TRUNCATED AT 250 WORDS)
Ascorbic Acid↗
Mechanisms of red cell clearance in favism.
Divicine (2,6-diamino-4,5-dihydroxypyrimidine) is a quinoid compound contained in high amounts in all fava bean strains. It elicits a number of metabolic and rheological modifications in G6PD-deficient RBC. Besides this, it stimulates erythrophagocytosis by mouse peritoneal macrophages and formation of crossbonded red cells. The latter are intracellularly membrane-bonded red cells, which form during hypertonic incubation and subsequent swelling. All effects observed in vitro were also observed in vivo in the early phases of fabic hemolysis. In particular, phagocytosis and crossbonding offer a basis for understanding extravasal hemolysis.
Animals↗
Red cell G6PD decay in circulating cells: a possible marker for variants identification.
The age dependent decay of G6PD activity was studied in G6PD deficient red cells free of leukocytes and platelets and separated on a density gradient. The pattern of decay can be a useful additional parameter to characterize enzyme variants.
Erythrocyte Aging↗
Acute haemolysis in childhood falciparum malaria.
Acute haemolysis associated with clinical episodes of high-level Plasmodium falciparum parasitaemia was studied in 20 children from an holoendemic area (coastal Tanzania). The change in blood haemoglobin (Hb) concentration ranged from -46 to g/L during the 72-h observation period and was linearly related to maximum parasitaemia. Balance studies between loss of blood Hb, increase in plasma Hb and appearance of Hb in the urine indicated that extravascular clearance of red cells was the predominant mode of erythrocyte clearance. Most subjects, however, showed minor signs of intravascular haemolysis. The plasma Hb was << 1% of blood Hb and haemoglobinuria was detected in 14/20 children but the excretion of Hb in urine was < 0.5% of total Hb loss. Haemoglobinuria was, however, a marker of severe haemolysis, since the maximum blood Hb loss in children without haemoglobinuria was 10 g/L. Erythrocyte-bound opsonins known to induce erythrophagocytosis, i.e., complement C3c fragments and autologous IgG, were increased in all patients. In the patients with major haemolysis, the changes correlated to the haemolysis over time. Hence, a similar mechanism for predominantly extravascular erythrocyte clearance may be operative in acute malarial anaemia, normal erythrocyte senescence and other forms of acute haemolysis.
Acute Disease↗
Antimalarial drugs inhibit the phagocytosis of erythrocytes infected with Plasmodium falciparum.
Phagocytic cells constitute the first line of defence against malarial parasites. They perform their role by delivering oxidative radicals and by phagocytosing infected red blood cells (IRBC). Phagocytosis is mediated by antibody binding to clustered band 3 antigen in the IRBC membrane and activation of the alternative complement pathway. In this study we showed that treatment of IRBC containing Plasmodium falciparum with therapeutically-relevant concentrations of antimalarial drugs considerably reduced the binding of immunoglobulin G (IgG) to, and the phagocytosis of, IRBC. Opsonization of IRBC by fresh serum before drug treatment prevented this inhibitory action of drugs. Removal of the drug restored IgG binding and the phagocytic susceptibility of IRBC in a time-dependent fashion. Direct measurement of the effect of chloroquine on the clustering of band 3 in IRBC, however, failed to reveal any disruption of the aggregation. We conclude that antimalarial drugs are able to alter, by an as yet unresolved mechanism, the affinity of IgG to clustered band 3. This affinity of IRBC seems to be determined by a dynamic process that depends on the metabolic activity of the parasite.
Antibody Affinity↗
Indices of membrane alterations in beta-thalassemic erythrocytes.
Analytical protocols for the study of thalassemic erythrocyte membrane alterations are described. Denatured hemoglobin derivatives and aggregated band 3 are separated from detergent membrane extracts by gel-filtration as high-molecular-weight aggregates and quantitated spectrophotometrically. Membrane-bound, low-molecular-weight iron is measured on SDS-solubilized ghosts by a ferrozine-based colorimetric test. We adapted these methods for microscale preparation and analysis of erythrocyte ghosts in order to have suitable tools to estimate oxidative membrane damage in human samples. Data from 11 beta-thalassemia intermedia patients and from 10 normal controls are reported as an example of the application of these methods.
Adult↗
Castleman's disease.
Castleman's disease (CD) is a rare atypical lymphoproliferative disorder whose morphology, soon after the original presentation of Castleman et al., has been definitely subdivided in a hyaline vascular (HV) and plasma cell (PC) histopathological pattern, with intermediate variants. The former occurs much more frequently than the latter and is usually localized to the mediastinum or pulmonary hilum. The latter involves lymph nodes separately or in aggregations and often displays multicentricity with systemic symptoms including autoimmune phenomena and aggressive course. Infections are the most frequent causes of patient demise in these cases, followed by malignancies such as Kaposi's sarcoma, malignant lymphoma or epithelial neoplasia. Increase of follicular dendritic reticulum cells (FDRC), often dysplastic, in the germinal center (GC) and marginal zone (MZ), broad MZ expansion with prominence of immunophenotypically aberrant B cells (Ki B3-negative, CD5-positive), possible predominance of paracortical plasma cells often with clusters of clonal l-light chain restricted plasma cells, increase of paracortical plasmacytoid monocytes, represent common hallmarks of CD. However, small hyalinized and hypervascular GCs with hypervascular interfollicular stroma and sinus effacement are common features of the HV variant, whereas hyperplastic GCs with plasma cell aggregates in lymph node paracortex and partially spared sinuses are characteristic features of the PC variant. The frequent concomitance of the HV and PC types at separate sites, together with transient morphological patterns from one type to the other and from the localized to multicentric form during the course of the disease, along with B and T cell impaired functions, with frequent development of autoantibodies, have suggested that CD is a single disorder related to immune dysregulation. A key event in the pathogenesis of CD has been recently suggested to be an abnormal production of a B cell growth factor, such as IL-6, leading to lymphoproliferation and plasma cell differentiation and being involved in the oncogenesis of plasmacytoma. In this event, Kaposi's sarcoma associated virus (HHV-8), which has been found in many cases of CD, especially in the multicentric form, could play a crucial role both in producing IL-6 and releasing angiogenic factors. A possible differentiation block may lead to the development of a malignant lymphoma. Kaposi's sarcoma or other malignant neoplasias can be supposed to be consequences of the immunodeficiency typical of CD.
Blood Vessels↗
[Fracture of the orbit-malar-zygomatic complex: a review of surgical treatment].
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Fracture Fixation↗
Mesenteric vein thrombosis: a rare cause of abdominal pain in cirrhotic patients--two case reports.
Mesenteric vein thrombosis is a rare disorder which can develop rapidly with intestinal infarction or subacutely with abdominal pain due to intestinal ischemia. Despite the availability of modern diagnostic tools, which allow an early diagnosis in most cases, the mortality from this disease has not significantly diminished over the years. The problem is that the syndrome is rare and unusual and the clinical presentation is usually vague or confusing. Particularly in cirrhotic patients, this diagnosis requires the exclusion of several other complications of liver disease, like spontaneous bacterial peritonitis, tense ascites or portal thrombosis. Here, we report the occurrence of acute mesenteric vein thrombosis in two patients with liver cirrhosis. Severe subcontinuous abdominal pain out of proportion to the physical findings and abdominal distension were the major symptoms in both patients. Magnetic resonance imaging in one case and ultrasound scan with color Doppler followed by computed tomography in the other patient confirmed the diagnosis and enabled an appropriate early therapy to be undertaken.
Abdominal Pain↗