Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The glutathione redox system, haemoglobin (Hb) oxidation, the activity of antioxidant enzymes and the lipid peroxidation product malonyl dialdehyde (MDA) were studied in red blood cells (RBCs) during administration of recombinant human erythropoietin (rhEPO) over 12 weeks in ten children maintained on haemodialysis. A rapid increase in the reticulocyte count was accompanied by a slower rise in total Hb concentration. The mean level of oxidized glutathione (GSSG) increased from 13.2 +/- 5.3 nmol/g Hb to 56.7 +/- 15.8 nmol/g Hb 4 weeks after the start of rhEPO (P < 0.001), followed by a fall to the basal value. Reduced glutathione (GSH) levels showed a smaller though constant elevation during rhEPO therapy (P < 0.001). Before rhEPO treatment, incubation of RBCs for 1 h with acetylphenylhydrazine induced a decrease in GSH concentration compared with controls (P < 0.001), which became more pronounced in the first few weeks of rhEPO therapy (P < 0.001). In addition, the percentage of Hb derivatives (metHb and haemichrome) increased in the first 4 weeks of rhEPO therapy (P < 0.001). Although there was no significant difference between the values obtained preEPO and during EPO treatment, MDA levels were continuously higher and superoxide dismutase, catalase and glutathione peroxidase concentrations were lower than in the controls (P < 0.001). These results are compatible with oxidative damage to the RBCs in the early period of rhEPO therapy in children with end-stage renal failure. The GSH-GSSG system, as an important cellular defence mechanism of the RBCs, appears to be severely affected.
 ...
PMID:The effect of erythropoietin on the cellular defence mechanism of red blood cells in children with chronic renal failure. 148 41

Based on recent reports that reactive oxygen metabolites may play a role in endotoxin-induced injury in other tissues, we postulated that reactive oxygen metabolites may be important mediators of endotoxin-induced acute renal failure. Superoxide dismutase, a scavenger of superoxide, or catalase, which destroys hydrogen peroxide, did not protect against endotoxin-induced renal failure. Similarly, neither the hydroxyl radical scavenger dimethylthiourea nor the iron chelator deferoxamine (which presumably would act by preventing the generation of hydroxyl radical via the iron-catalyzed Haber-Weiss reaction) prevented the endotoxin-induced fall in renal function. In separate experiments, we found no increase in renal cortical lipid peroxidation (a marker of reactive oxygen metabolite-mediated tissue injury) in endotoxin-treated rats, providing further evidence against a role for reactive oxygen metabolites in endotoxin-induced renal injury. Finally, using the aminotriazole-induced inhibition of catalase (a measure of in vivo changes in the hydrogen peroxide generation) we found no evidence of enhanced hydrogen peroxide generation in the renal cortex in endotoxin-treated rats. Taken together, the data from these three separate experimental approaches suggest that reactive oxygen metabolites are not important mediators of endotoxin-induced acute renal failure.
 ...
PMID:Reactive oxygen metabolites in endotoxin-induced acute renal failure in rats. 212 35

A novel bacterium, Protomonas extorquens was isolated from sputum, pleural effusion and ascitis in four cases of pulmonary infection by buffered charcoal yeast extract agar (B-CYE) which was generally used for Legionella spp. Three cases were so-called immunocompromised hosts (2 malignant diseases, 1 renal failure), and they died from underlying diseases. Protomonas extorquens was newly named by Komagata in 1984, which was characterized by production of pink pigment, growth in methanol medium and positive production of oxidase and catalase. This organism is ordinarily isolated from soil and dead leaves. This is the first report for isolation of P. extorquens from clinical specimens in Japan and it seems to have a significant role in immunocompromised hosts.
 ...
PMID:[Clinical and bacteriological studies in four cases of pulmonary infection caused by Protomonas extorquens]. 221 63

The effects of antioxidant therapy with probucol were evaluated in rats subjected to 1 h renal ischemia and to 24 h reperfusion. Probucol exerted significant antioxidant effects in renal cortical tubules in vitro when exposed to a catalase-resistant oxidant. At 24 h probucol treatment (IP) improved single nephron glomerular filtration rate (SNGFR) (28.1 +/- 3.3 nl/min) in comparison to untreated ischemic (I) rats (15.2 +/- 3.0), primarily as a result of improving SNGFR in a population of low SNGFR, low flow and/or obstructed nephrons. However, absolute proximal reabsorption remained abnormally low in IP rats at 24 h (5.9 +/- 0.8 nl/min), and cell necrosis was greater than in I rats. Kidney GFR remained low in IP rats due to extensive tubular backleak of inulin measured by microinjection studies. Evaluations after 2 h of reperfusion revealed a higher SNGFR in IP (36 +/- 3.1 nl/min) than I rats (20.8 +/- 2.7 nl/min). Absolute proximal reabsorption was essentially normal (11.6 +/- 1.3 nl/min) in IP rats, which was higher than IP rats at 24 h and the concurrent I rats. Administration of the lipophilic antioxidant, probucol, increased SNGFR and proximal tubular reabsorption within 2 h after ischemic renal failure. Although SNGFR remained higher than I rats at 24 h, absolute reabsorption fell below normal levels and tubular necrosis was more extensive in IP rats. Early improvement in nephron filtration with antioxidants may increase load dependent metabolic demand upon tubules and increase the extent of damage and transport dysfunction.
 ...
PMID:Ischemic acute renal failure and antioxidant therapy in the rat. The relation between glomerular and tubular dysfunction. 283 99

During renal failure, polyamines and oxalate levels are elevated in the serum and the glomerular filtrate and are dumped by the kidney. Both of these compounds can be catabolized by oxidative reactions. We have, therefore, investigated the intracellular distribution of oxalate oxidase and of a polyamine oxidase in normal female rat kidney and liver. Polyamine oxidase was demonstrable, using spermidine as substrate in the cerous peroxyhydrate procedure of Briggs et al., in peroxisomes of kidney tubule cells and of hepatocytes. Oxalate oxidase could not be studied with this technique due to precipitation of cerium oxalate in the incubation medium. To demonstrate oxalate oxidase, and to confirm the polyamine oxidase localization, we incubated aldehyde-fixed tissue in a diaminobenzidine medium at pH 8, following the approach of Veenhuis et al., in which oxidases are demonstrated by virtue of their production of H2O2, which then serves as a substrate for endogenous catalase. Using oxalate or spermidine as substrate with this approach, we found reaction product in typical renal peroxisomes; we also found reaction product, with the polyamine substrate, in hepatocyte peroxisomes. To strengthen the conclusion that the oxidases themselves are present in peroxisomes, we used a light microscopic method, based on the tetrazolium procedures of Allen and Beard to demonstrate polyamine and oxalate oxidase activities in bodies with the distribution of renal peroxisomes.
 ...
PMID:Oxidation of oxalate and polyamines by rat peroxisomes. 392 4

During experimental renal ischemia and reperfusion in rabbits, morphine as well as naloxone significantly inhibited the increased superoxide anion (O2-) generation by resting and opsonized zymosan-stimulated phagocytes in renal venous blood. Morphine with naloxone in combination inhibited O2- generation to a lesser extent than that observed when these drugs were used separately. Morphine and/or naloxone did not significantly affect erythrocyte superoxide dismutase (SOD-1), glutathione peroxidase (GPx) and catalase activities or malonyldialdehyde (MDA) concentrations in venous blood during renal ischemia. During reperfusion there was a tendency to a slight reduction of erythrocyte catalase activity in morphine-treated animals, and to slight diminutions of erythrocyte SOD-1 and GPx activities and erythrocyte MDA concentrations in rabbits treated with naloxone and morphine in combination. These results indicate that opioid receptor agonists and antagonists modify the response of the kidney to acute injury. These effects may have relevance to the pattern of oxidative stress seen in patients with acute ischemic renal failure.
 ...
PMID:Effect of morphine and naloxone on oxidative metabolism during experimental renal ischemia and reperfusion. 785 38

Tyrosinase-positive albinism, previously diagnosed as Hermansky-Pudlak Syndrome (HPS), has been examined in four generations from a village of the canton Valais, Switzerland. Homozygotes, obligate heterozygotes and putative heterozygotes in this geneology yielded lower than normal membrane-associated thioredoxin reductase (TR) activities compared with normal family members and controls. All of the homozygotes and 50% of each the obligate and putative heterozygotes showed an increase in bleeding time associated with storage-pool-deficient platelets lacking dense bodies. The TR activity profile and the platelet-dense body deficiency in the Swiss albinos was the same as that in the HPS population from Puerto Rico. However, in albinos from Puerto Rico, there is an accumulation of ceroid/lipofuscin-like pigment in lysosomal structures causing tissue damage, and, upon kidney involvement, this leads to increased urinary dolichol excretion. Approximately half of the Puerto Rican HPS cases had clinical evidence of storage disease with restrictive lung disease, granulomatous colitis, kidney failure and cardiomyopathy. By comparison, the Swiss HPS geneology had a normal life expectancy with no significant evidence for ceroid accumulation or urinary dolichol excretion. An examination of antioxidant enzymes, catalase, TR and glutathione reductase in epidermal suction blisters from Swiss HPS homozygotes showed a similar result for catalase and TR levels to the depigmented epidermis of patients with vitiligo, except that intracellular TR was found to be calcium free in HPS compared with vitiligo. Intracellular glutathione reductase levels were highest in HPS. Both the Swiss and Puerto Rican HPS homozygotes and heterozygotes have giant melanosomes in skin melanocytes.
 ...
PMID:Hermansky-Pudlak syndrome in a Swiss population. 827 81

Subtotally nephrectomized rats were found to have decreased activities of superoxide dismutase (SOD) and catalase, and spin trapping with 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) showed that the amount of hydroxyl radical in the residual kidney tissue was greater than that in normal rat kidney. This indicated both direct and indirect involvement of free radicals in renal failure. In contrast, rats given magnesium lithospermate B (10 mg/kg body weight) orally for 30 days after subtotal nephrectomy showed restoration of SOD and catalase activities to almost normal levels. Hydroxyl radical, which is highly reactive and for which there is no scavenger system in the body, was decreased markedly in kidney homogenates obtained from rats given magnesium lithospermate B and in an experimental system for hydroxyl radical production to which magnesium lithospermate B was directly added. The increased levels of uremic toxins in the blood were also low in rats given magnesium lithospermate B. This indicates that magnesium lithospermate B helps to inhibit the progression of renal failure by scavenging radicals.
 ...
PMID:Magnesium lithospermate B suppresses the increase of active oxygen in rats after subtotal nephrectomy. 903 Dec 76

To determine whether magnesium lithospermate B ameliorates renal injury induced by cephaloridine, the effect of cephaloridine was investigated in rats given magnesium lithospermate B for 20 days preceding cephaloridine administration and in control rats given no magnesium lithospermate B. In the control rats, blood and urinary parameters and the activity of radical-eliminating enzymes in the renal tissue deviated from the normal range, indicating damage to the kidneys. In contrast, rats given magnesium lithospermate B showed decreased urine volume, increased urinary osmotic pressure, and decreased urinary levels of glucose, protein, sodium and potassium, denoting less damage to the kidney. In this group, the urinary nitrite/nitrate ratio, and the activities of superoxide dismutase and catalase in the renal tissue were increased, while the malondialdehyde levels were decreased, suggesting the involvement of radicals in the normalizing of kidney function. The increased levels of urea nitrogen in the blood of rats with induced renal failure were also lowered by administering magnesium lithospermate B.
 ...
PMID:Magnesium lithospermate B ameliorates cephaloridine-induced renal injury. 945 78

Oxidant injury is considered to be an important mechanism in the pathophysiology of acute renal failure. It has been thought that decrease in extracellular and intracellular fluid and endotoxemia seen in obstructive jaundice may cause an increase in production of oxygen free radicals and impairment in antioxidant defense mechanism. This study is designed to investigate the possible role of oxidant injury in renal failure seen in jaundiced patients. In this study, 28 rats were divided into four groups: Control (C)(N = 7); Renal ischemia (RI)(N = 7); Obstructive jaundice+renal ischemia (OJ+RI)(N = 7); Obstructive jaundice (OJ)(N = 7). All groups were compared with each other according to renal failure findings and enzyme activities, such as Xanthine oxidase (XOD), Superoxide Dismutase (SOD) and Catalase in renal cortex and Glutathione Peroxidase (GSH-Px), in blood at 3rd day after ischemia and reperfusion. Renal failure findings monitored by blood urea and creatinine levels, seemed more evident in OJ+RI than RI group (p < 0.05). When compared with RI, in OJ+RI group, increase in XOD activity at 3rd day was statistically significant [0.259 +/- 0.01 U/g (tissue) and 0.362 +/- 0.03 U/g (tissue) respectively] (p < 0.05). SOD and GSH-Px activities of each ischemic group at 3rd day were decreased compared to non-ischemic groups. This fall was significant (p < 0.05). But there was no statistical difference between jaundiced and non-jaundiced groups. Alterations in catalase activities also had no statistical significance. These findings may suggest that the injury induced by oxygen free radicals at re-oxygenation of tissue after ischemia may also play a role in the pathogenesis of acute renal failure developed in obstructive jaundice.
 ...
PMID:The role of oxygen free radicals in acute renal failure complicating obstructive jaundice: an experimental study. 951 37


1 2 3 4 5 6 7 8 9 Next >>