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T Zima

Publications and source records attributed to T Zima.

At least 91 records · Page 5Linked to original sources
PubMed1996

Activity of the antioxidant enzymes superoxide dismutase and glutathione peroxidase in fetal erythrocytes.

It is generally accepted that the balance between the formation and inactivation of reactive oxygen species may be abolished within the perinatal period, as a consequence of rapid changes in tissue oxygen concentration and the development of antioxidant defence enzyme activities. We studied the ontogeny of the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx) in fetal blood samples. The activity of SOD in fetal erythrocytes taken in the 17th gestational week was the same as that in erythrocytes of healthy blood donors. On the other hand, GPx activity was significantly lower between the 17th and 25th gestational week and at the time of delivery, compared with the healthy adult control. Our results suggest that the supposed underdevelopment of the antioxidant system in the lungs or in the other organs of premature infants cannot be monitored by SOD and GPx activities in erythrocytes, because these reach adult levels before the 17th week for SOD and from the 26th to the 35th gestational week for GPx, with lower levels from the 17th to the 25th week and at term.

Antioxidants↗
PubMed1996

Antioxidant enzymes--superoxide dismutase and glutathione peroxidase--in haemodialyzed patients.

The biological effect of oxygen-reactive species controlled by antioxidant mechanisms are exerted on the basis of antioxidant enzymes and substrates. In this study, the activities of antioxidant enzymes-superoxide dismutase (SOD) and glutathione peroxidase (GPx)-were determined in the erythrocytes of patients on regular haemodialysis treatment. The SOD activity was significantly lower (1,810.38 +/- 609.85 vs. 2,347.13 +/- 502.51 U/g haemoglobin, p < 0.05, or 70.71 +/- 11.50 vs. 100.13 +/- 24.28 mU/10(6) erythrocytes, p < 0.0001), as was the GPx activity (18.80 +/- 4.22 vs. 23.26 +/- 3.61 U/g haemoglobin, p < 0.01), when compared with the control group. A positive correlation between GPx activity and number of haemodialysis sessions was found (p = 0.0038), but no correlation between SOD activity and number of HD sessions. An inpaired antioxidant enzyme defence system, here represented by SOD and GPx levels, can potentiate injury caused by free radicals in haemodialysis patients.

Antioxidants↗
PubMed1996

Lipid peroxidation and antioxidant enzymes in CAPD patients.

The mechanisms of free-radical injury include reactions with proteins, nucleic acids, and polysaccharides; and covalent binding to membrane components and initiation of lipid peroxidation. Cells have developed antioxidant defense to prevent free-radical injury including superoxide dismutase (SOD) and glutathione peroxidase (GPx). Significantly higher concentrations of total malondialdehyde (MDA) in plasma (1.22 +/- 0.42 vs. 0.64 +/- 0.22 micromol/L, p < 0.0001) as well as erythrocytes (2.56 +/- 1.28 vs. 1.03 +/- 0.44 micromol/L, p < 0.0001) of the CAPD patients were found when compared to the control group. The free MDA in plasma and the erythrocytes do not differ significantly in continuous ambulatory peritoneal dialysis (CAPD) patients and the control group. A significantly lower activity of GPx in erythrocytes of CAPD patients (17.85 +/- 2.63 U/g Hb vs. 23.26 +/- 3.61 U/g Hb, p < 0.0001) was found when compared to the control group, but the SOD activity in erythrocytes is not different (2272.36 +/- 579.92 U/g Hb vs. 2347.13 +/- 502.51 U/g Hg, NS). Our results show an increase of total MDA in erythrocytes and plasma. MDA is the product of lipid peroxidation with decreasing activity of GPx, which is capable of detoxifying peroxides. The activity of SOD did not change in CAPD patients. These results propose a possible role of free radicals with reduced antioxidant activity of GPx in CAPD patients and indicate that they could play some role in other pathological conditions such as atherogenesis and hemolysis.

Adult↗
PubMed1996

The influence of pefloxacine on experimental adriamycin-induced nephrotic syndrome in rats.

Initial reports on antiproteinuric effect of pefloxacine in small groups of patients with minimal-change nephropathy (MCN) and focal and segmental glomerulosclerosis (FSGS) have not been confirmed in other papers. To assess its antiproteinuric effect in experimental animals we administered pefloxacine to rats with adriamycin nephropathy showing morphological changes resembling human minimal-change disease or focal segmental glomerulosclerosis, and clinically with full-blown nephrotic syndrome. Pefloxacine treatment was at least partially effective in preventing further increase of proteinuria in rats with adriamycin nephropathy. The mechanism of this effect remains unclear and deserves further studies concentrating on the glomerular cytokine network and glomerular production of reactive oxygen species.

Animals↗
PubMed1996

[Lipid metabolism in the nephrotic syndrome].

BACKGROUNDS: Hyperlipidemia is a common and serious complication in patients with chronic nephrotic syndrome which unremitted may result in accelerated atherosclerosis. Accumulation of lipids in glomeruli may moreover contribute to the progression of renal insufficiency in these patients. METHODS: Total cholesterol, HDL-cholesterol and its HDL2 a HDL3 subfractions, LDL-cholesterol, triglycerides, free fatty acids, apoprotein B, apoprotein A1 and lipoprotein (a) were determined before any immunosuppressive and/or hypolipidemic therapy in 15 patients (pts) with nephrotic syndrome (8 pts with proteinuria higher than 10 g/24 hrs-NS-A, 7 with proteinuria between 5 and 10 g/24 hrs-NS-B), 7 pts with glomerulonephritis with low proteinuria (GN) and 6 pts with autosomal dominant polycystic kidney disease (PKD). All pts had normal glomerular filtration rate. RESULTS: Plasma cholesterol (10.26 +/- 2.22 vs. 4.75 +/- 0.66 mmol/1, p < 0.001), plasma triglycerides (4.03 +/- 1.64 vs. 2.17 +/- 0.12 mmol/1, p < 0.05), LDL-cholesterol (7.16 +/- 1.55 vs. 2.62 +/- 0.67 mmol/1, p < 0.001) and apoprotein B (1.92 +/- 0.47 vs. 1.11 +/- 0.31 g/1, p < 0.01) were significantly higher in NS-A than in PKD. There was no difference in total HDL-cholesterol and the ratio HDL2/HDL3 between investigated groups of pts. Lipoprotein (a) was higher in NS-A than in other investigated groups of pts. The differences between NS-B and PKD were less significant. CONCLUSIONS: Disorder of lipid metabolism is more serious in patients with more severe nephrotic syndrome than in nephrotic patients with milder proteinuria. Hypercholesterolemia is complicated in these subjects by hypertriglyceridemia and by the increase of apoprotein B and A1 and lipoprotein (a). Metabolic and renal consequences of these disorders depend undoubtedly on their duration and probably also on other factors (e.g. age, hypertension, long-term therapy with corticosteroids., etc.).

Female↗
PubMed1996

Antioxidant enzymes and lipid peroxidation in patients with multiple myeloma.

Reactive oxygen species and other free radicals are known to be the mediators of phenotypic and genotypic changes that lead from mutation to neoplasia. The imbalance in tumor cell antioxidant defense mechanism can influence also the sensitivity to cytoreductive therapy. In erythrocytes it can result to hemolysis which is one of the pathogenetic mechanisms of anemia in cancer patients. Parameters of lipid peroxidation (malondialdehyde-MDA) and antioxidant enzymes here represented by superoxide dismutase (SOD) and glutathione peroxidase (GPx) in multiple myeloma (MM) have been investigated. Nine patients of various clinical stages and activities of the disease were studied. Significantly higher concentrations of total MDA in plasma (1.20 +/- 0.24 mumol/l vs. 0.64 +/- 0.22 mumol/l, p < 0.0001) as well as in erythrocytes (2.72 +/- 0.81 mumol/l vs. 1.03 +/- 0.44 mumol/l, p < 0.0001) were found comparing to the control group. The levels of free MDA in plasma (0.31 +/- 0.09 mumol/l vs. 0.49 +/- 0.17 mumol/l, p < 0.05) and in erythrocytes (0.29 +/- 0.20 mumol/l vs. 0.59 +/- 0.22 mumol/l, p < 0.001) were decreased in myeloma patients. Significantly lower activities of GPx (19.17 +/- 4.07 U/g Hb vs. 23.26 +/- 3.61 U/g Hb, p < 0.05) and SOD (1882.46 +/- 181.73 U/g Hb vs. 2347.13 +/- 502.51 U/g Hb, p < 0.05) in erythrocytes were found. We did not observe evident relationship between the concentration of MDA or the activities of SOD and GPx and either the stage of the disease, or the level and the type of paraprotein. These results propose possible role of free radicals with reduced antioxidant activities of SOD and GPx in multiple myeloma.

Aged↗
PubMed1996

[Clinical problems in kidney disorders associated with myeloma and other paraproteinemias].

An overview of constantly enlarging spectrum of renal lesions in monoclonal gammapathies and new insights in possible pathogenesis of renal disturbances is given. Between the different types of renal affections a predominant role is played by the "myeloma kidney", induced by the presence of casts, primary amyloidosis with light chains deposition and tubular dysfunctions. Case stories of 3 patients, affected by myeloma kidney (with acute and chronic renal failure) and primary amyloidosis (with pronounced nephrotic syndrome) in context of monoclonal gammapathy are presented. Clinical problems of patients necessitating intensive hematologic and nephrologic care are highlighted, as well as need of early diagnosis and complex care.

Adult↗
PubMed1995

[The role of oxygen radicals in the pathogenesis of glomerulonephritis].

In the pathogenesis of glomerulonephritis, acute renal failure, pyelonephritis and other diseases of the kidneys oxygen radicals are involved. Some types of glomerulonephritis are characterized by infiltration of the glomeruli by neutrophils and monocytes which can form oxygen radicals (superoxide, hydrogen peroxide). The increased amount of cAMP in glomeruli can be due to oxygen radicals. Cyclic nucleotides modulate the inflammatory or immune response in glomerular disease and play a part in the action of local mediators of the inflammation. Oxygen radicals act as second messenger for the activation of cytokines via NF-kappaB transcription factor, they stimulate the formation of TNF-alpha, IL-1, IL-6 and influence the expression of monocyte-specific cytokines (CSF-1 and MCP-1). Radicals formed by the system myeloperoxidase--hydrogen peroxide--halogen derivatives activate proteolytic enzymes (proteinases) which break down collagen and other components of the extracellular matrix present in the basal membrane of glomeruli and in the mesangium. Oxygen radicals and proteinases can cause and amplify glomerular damage. Glucocorticoid administration leads to an increased activity of endogenous antioxidant enzymes in the glomerulus and reduced the of lipid peroxidation.

Free Radicals↗
PubMed1995

[The effect of pefloxacin on nephrotic syndrome in experimental adriamycin nephropathy].

BACKGROUND: Antiproteinuric effect of pefloxacine was demonstrated in a small group of patients with minimal change nephropathy (MCN) and focal and segmental glomerulosclerosis (FSGS). This finding was not, however, confirmed by other papers. Adriamycine nephropathy is an experimental model of nephrotic syndrome with morphological changes resembling MCN and/or FSGS in patients. METHODS AND RESULTS: Nephrotic syndrome was induced in rats by the i.v. administration of adriamycine. One part of nephrotic animals was treated from the beginning of the 4th week by daily intraperitoneal application of pefloxacine. Administration of adriamycine led in experimental animals after 3 weeks to the development of full-blown nephrotic syndrome with further progression of proteinuria in the next 3 weeks (from 1.4 +/- 1.25 to 2.23 +/- 1.89 g of protein/mmol of urinary creatinine, p < 0.05). Proteinuria did not change in nephrotic rats treated by pefloxacine (from 1.04 +/- 0.97 to 1.26 +/- 1.11 g of protein/mmol of urinary creatinine, p = n.s.). The difference in proteinuria between both groups was also significant (0.83 +/- 0.73 vs. 0.23 +/- 0.67 g of protein/mmol of urinary creatinine, p < 0.05). CONCLUSIONS: Pefloxacine was antiproteinuric in experimental adriamycine nephropathy. The mechanism of this effect remains unclear and deserves further studies concentrating on glomerular cytokine network and glomerular production of reactive oxygen species.

Animals↗
PubMed1995

[Free radicals in the pathogenesis of selected diseases].

Free radicals are chemical substances which contain one or more unpaired electrons, which is the cause of their high reactivity with a series of biologically important substances such as fatty acids, DNA, RNA, amino acids. The source of radicals are immunological reactions and reactions in the endoplasmatic reticulum during detoxication of xenobiotics. Free radicals can act on the organism by a number of reactions, the most frequent on being lipid peroxidation when important toxic products are formed such as 4-hydroxy 2,3 trans-nonenal (4-HNE) and malondialdehyde. Direct assessment of free radicals due to their short life span is difficult in clinical practice. The majority of measurements is based on the assessment of substances which are formed by the reaction of free radicals in the organism. The most frequent method is assessment by means of thiobarbituric acid. Oxidative stress (the reaction produced by the action of free radicals) of tissues and cells is caused by the increased formation of free radicals and/or reduced capacity of antioxidant systems. Free radicals are involved in the process of ageing, cancerogenesis, inflammatory and degenerative diseases, atherogenesis, and play a part in the ischaemic and toxic damage of the organism. During evolution antioxidant defence mechanisms developed which under physiological conditions are sufficient to inactivate free radicals. Antioxidant systems can be divided into two groups--antioxidant enzymes (superoxide dismutase, glutathione peroxidase, catalase etc) and antioxidant substrates (tocopherols, carotenoids, ascorbic acid, glutathione, transferrin, ceruloplasmin etc).

Animals↗
PubMed1995

Activity of the antioxidant enzyme, glutathione peroxidase, on autosomal dominant polycystic kidney disease patients.

Reactive oxygen species are generated physiologically in cells with a significant increase in certain pathological conditions, such as inflammation, cancer, aging, degenerative disease. If endogenous antioxidant systems, in our study represented by glutathione peroxidase, are exceeded by this oxidant flux, tissue injury may occur. Activity of glutathione peroxidase (GPx) was determined using Beutler's modified spectrophotometric assay in erythrocytes from autosomal dominant polycystic kidney disease patients. Activity of glutathione peroxidase was significantly (at p < 0.0001) lower there (17.75 +/- 3.69 U/g haemoglobin) compared to the control group (23.26 +/- .61 U/g Hb). Lower antioxidant enzyme defence system of ADPKD patients, here represented by GPx, can potentiate injury caused by free radicals and possibly play a role in the progression of autosomal dominant polycystic kidney disease.

Adult↗
PubMed1995

Lipid peroxidation and superoxide dismutase activity in umbilical and maternal blood.

Oxygenation of both mother and child tissues oscillate frequently during labour. We tested the lipid peroxidation caused by reactive oxygen species which are produced in consequence of tissue reoxygenation and the inactivation of these species by the maternal and newborn superoxide dismutase. Total malondialdehyde in concentrations (mean +/- SE) of 1.04 +/- 0.17, 1.57 +/- 0.22, 1.33 +/- 0.14 and 1.36 +/- 0.21 mumol/L was found in maternal plasma and red blood cells and newborn plasma and red blood cells, respectively, after uncomplicated deliveries and 4.93 +/- 1.34, 7.12 +/- 1.37, 4.77 +/- 1.29 and 7.37 +/- 1.51 mumol/L, respectively, after deliveries with clinical signs of foetal hypoxia. In newborns, erythrocyte superoxide dismutase activity reached only 82% of the maternal level (p < 0.05). The results indicate that the maternal and foetal antioxidant defence systems can be overloaded during deliveries with abnormal oxygenation, where increased lipid peroxidation occurred.

Acidosis↗
PubMed1995

The influence of chronic ethanol administration on adriamycin-induced nephrotic syndrome in rats.

Alcoholic liver disease may be frequently complicated by mesangial proliferation with the deposition of IgA in glomeruli and glomerulosclerosis, but these glomerular lesions are usually mild and without greater impact on renal function. To evaluate the putative role of ethanol in glomerular pathology we studied the influence of chronic ethanol administration on the development of experimental adriamycin nephropathy in rats. Nephrotic syndrome was induced by a single i.v. dose of adriamycin (5 mg/kg body wt) both in rats given ethanol at a dose of 4 g/day for 3 months and control rats given standard chow. Further controls on both diets without adriamycin administration were also studied. Blood and urine were examined before and 3 and 6 weeks after adriamycin administration. All rats were killed and examined histologically 6 weeks after adriamycin administration. Ethanol fed nephrotic rats were more catabolic than control nephrotic rats (with higher free fatty acids, lower glycaemia, higher urea with similar creatinine) and had lower proteinuria (0.55 +/- 0.34 versus 5.79 +/- 3.15 g of protein/nmol of creatinine, P < 0.05), higher albuminaemia (5.41 +/- 2.62 versus 1.92 +/- 1.94 g/l, P < 0.01), lower plasma cholesterol (6.54 +/- 2.6 versus 10.57 +/- 2.92 mmol/l, P < 0.01) and triglycerides. The development of nephrotic syndrome and renal morphological changes after adriamycin administration in rats seemed to be ameliorated, or at least delayed by chronic ethanol feeding with much milder and focal glomerulosclerosis as compared with more severe and diffuse glomerulosclerosis in control nephrotic animals. The mechanism of this effect of chronic ethanol feeding remains to be elucidated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

The effect of calcium channel blockers on cyclosporine A (Cs A) induced nephrotoxicity in rats.

The limiting factor in the therapeutical use of cyclosporine A (Cs A) is its nephrotoxicity, which may lead to renal failure. Cs A nephrotoxicity may present itself as an acute decrease in GFR, or as a chronic renal injury. Nephrotoxicity is caused by the indirect vasoconstriction effect mainly on proximal tubule and afferent arteriols. In our study we have concentrated on the effect of Ca-channel blockers on Cs A nephrotoxicity. As parameters of toxic kidney damage we have used the urine levels of the following enzymes: N-acetyl-beta-D-glucosaminidase (NAG), gama-glutamyltransferase (GMT) and alkaline phosphatase (ALP). Daily intragastric application of verapamil (V) (dose 1.0 mg/kg BW) or nifedipine (N) (dose 0.1 mg/kg BW) was started in a group of male Wistar rats. Cs A (Sandimun Sandoz, Switzerland) was applied daily intraperitoneally 30 minutes after the application of V or N. The dose of Cs A ranged from 5 mg/kg BW to 25 mg/kg BW in individual groups. The animals were observed for 10 days after the drugs application. Urine samples were collected and examined at the end of the whole experiment. The individual parameters were evaluated in the groups receiving the 3 different doses of Cs A (5-25 mg/kg BW). The serum creatinine rose moderately during the experiment. When the Ca-channel blockers were administered, the rise was not as steep, but when the highest dose of Cs A was administered, the Ca-channel blockers did not influence the elevation of the serum creatinine. Using the standard dose of Cs A (5 mg/kg BW) the protective effect of Ca-channel blockers can be found. In higher doses of Cs A this protective effect was not expressed.

Animals↗
PubMed1995

[The effect of lovastatin on the development of adriamycin nephropathy in rats].

BACKGROUNDS: Hyperlipidemia is not only a prominent complication of nephrotic syndrome, but it may also contribute to the further non-immunologic damage of glomeruli. Analogy between atherosclerosis and glomerular sclerosis was suggested. Treatment of hyperlipidemia may decrease proteinuria in nephrotic animals and subjects and possibly prevent the progression of glomerulosclerosis and renal failure. We decided to study the influence of therapy with the inhibitor of cholesterol synthesis, lovastatin, on the development of the experimental nephrotic syndrome induced by the administration of adriamycine in rats. METHODS AND RESULTS: Nephrotic syndrome was induced in rats by the intravenous administration of adriamycine. One group of animals was treated from the time of adriamycine adminstration with lovastatin. Lovastatin was also given to one group of control animals. Proteinuria increased significantly during 4 weeks in untreated adriamycine rats (from 0.93 + 0.57 to 12.76 + 11.95 g/mmol of urinary creatinine, p < 0.01), but it did not change significantly in adriamycine rats treated with lovastatin (from 0.98 + 0.69 to 1.90 + 4.25 g/mmol of creatinine, p = n.s.) and it was significantly lower than in untreated animals (p < 0.01). Plasma albumin decreased 12 weeks after adriamycine administration in untreated rats (from 21.16 + 1.45 to 10.58 + 3.83 g/l, p < 0.001) significantly more (p < 0.05) than in rats treated with lovastatin (from 20.01 + 2.18 to 15.34 + 2.66 g/l, p < 0.01). Lovastatin also ameliorated the increase of plasma cholesterol and eliminated the increase of plasma triglycerides in adriamycine rats. Metabolic changes were in all groups characterized by the increase of free fatty acids, possibly due to exaggerated lipolysis, but without significant change of glycaemia and plasma urea. Proteinuria was decreasing at the end of the observed period. Histologically there were only minimal changes in glomeruli, without significant glomerulosclerosis. CONCLUSIONS: Administration of lovastatin prevented the development of nephrotic syndrome in experimental adriamycine nephropathy in rats. This finding suggests the possible role of hyperlipidemia in the pathogenesis of glomerular damage and suggests the posibility to prevent glomerulosclerosis and renalisufficiency in some form on nephrotic syndrome by the effective hypolipidemic therapy.

Animals↗
PubMed1994

[Rapidly progressive glomerulonephritis in a solitary kidney positive for anti-glomerular basement membrane antibodies and antineutrophil cytoplasmic antibodies].

The authors describe the case-report of a 72-year-old female patient with acute failure of a solitary kidney with complete functional breakdown which developed within several days and was due to rapidly progressive glomerulonephritis (RPGN) with concurrent positivity of antineutrophil cytoplasmatic autoantibodies (ANCA) and anti-glomerular basement antibodies (AGBMA). Intensive combined immunosuppressive therapy with methyl prednisolone, cyclophosphamide and azathioprine and concurrent plasmaphereses led to negativity of both types of antibodies but were not able to restore sufficient renal function and regular dialysis treatment to be started. Subsequently AGBMA remained negative, while ANCA became again positive. Despite this partial restoration of renal function was manifested by an increased diuresis and the frequency of dialyses could be reduced. The case-report has several remarkable features. An uncommon RPGN of the antirenal type is involved, moreover in a solitary kidney with concurrent C-ANCA positivity. The concurrent presence of ANCA and AGBMA autoantibodies in RPGN has been described in the literature only in several tens of cases. So far it was not described in our country. Based on their experience the authors conclude: 1. a solitary kidney cannot be considered in case of suspected RPGN as a strict contraindicatio of renal biopsy, 2. RPGN with concurrent positivity of ANCA and AGBMA is indicated for long-term immunosuppressive therapy on account of a more favourable prognosis than simple antirenal RPGN, and also with regard to a possible suspected systematic vasculitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗