Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of cyclosporin (CS) on intrinsic glomerular level of antioxidants in puromycin aminonucleoside (PAN) nephrosis was examined. A single intravenous dose of PAN (50 mg/kg body weight) given to Sprague-Dawley rats resulted in marked proteinuria. Ten days after PAN injection, the rats were treated with daily intraperitoneal injection of CS (10 mg/kg body weight/day) for 10 days. PAN-treated rats without CS treatment (PAN rats) had significantly lower activities of glomerular superoxide dismutase (SOD) and catalase (CAT) than normal rats (p < 0.05, respectively). When compared with PAN rats, CS-treated PAN rats had significantly less proteinuria and higher activities of glomerular SOD and CAT (p < 0.01 and p < 0.05, respectively). Significant elevation of glomerular malondialdehyde (MDA) level characteristic of PAN rats was absent in CS-treated PAN rats. Moreover, segmental sclerosis with capsular adhesion, hyalinosis, epithelial cell foot process fusion and microvillous transformation seen in PAN rats were apparently attenuated in CS-treated PAN rats. When compared with normal rats, rats receiving CS only had a significantly higher CAT activity and MDA level (p < 0.01 and p < 0.05, respectively). Assessment of glomerular reduced glutathione revealed no significant differences among PAN rats, CS-treated PAN rats, normal rats, and rats receiving only CS. These data indicate that glomerular antioxidant enzyme activities are modulated by CS.
Nephron 1993
PMID:Amelioration of antioxidant enzyme suppression and proteinuria in cyclosporin-treated puromycin nephrosis. 828 93

The purpose of the study was to investigate the effects of parathyroid hormone (PTH) infusion on antioxidant enzyme activity and lipid peroxidation of erythrocytes in five-sixths nephrectomized (Nx) rats. Five-sixths Nx rats had a higher osmotic fragility in red blood cells (RBC). Thyroparathyroidectomy (TPTX) effectively decreased the abnormality of osmotic fragility in RBC in Nx rats. PTH infusion in Nx-TPTX rats markedly increased the osmotic fragility in RBC. Total glutathione was measured by using the enzyme-recycling method. We found elevated glutathione levels in RBC of five-sixths Nx rats, but this elevation could be inhibited by TPTX and recovered by PTH infusion in Nx-TPTX rats. Five-sixths Nx rats had a lower glutathione peroxidase activity in RBC, but TPTX or PTH infusion was not found to alter the decrease of the glutathione peroxidase activity in RBC of five-sixths Nx rats. These rats had a higher activity in RBC superoxide dismutase as compared with sham-operated controls (p < 0.05), but the higher activity in RBC superoxide dismutase in Nx rats had been inhibited by TPTX. PTH infusion recovered the higher activity in RBC superoxide dismutase in five-sixths Nx-TPTX rats. Nx rats were not found to alter the activity of catalase in RBC. Neither could TPTX or PTH infusion in Nx rats influence the activity of catalase in RBC. A high lipid peroxidation in RBC was found in five-sixths Nx rats, namely, increased formation of malondialdehyde (MDA) in RBC had been induced to produce lipid peroxidation by H2O2, but neither TPTX nor PTH infusion could inhibit or enhance the increase of lipid peroxidation in RBC of Nx rats. These results indicate that PTH infusion did not increase the susceptibility to lipid peroxidation in RBC of five-sixths Nx rats. Thus, the increased osmotic fragility in RBC induced by PTH infusion may not result from the reduction in the RBC defense mechanism against free radical toxicity.
Nephron 1996
PMID:Effect of parathyroid hormone on antioxidant enzyme activity and lipid peroxidation of erythrocytes in five-sixths nephrectomized rats. 877 50

Cyclosporin A (CsA) was shown to reduce proteinuria in nephrotic syndrome, but its potential to increase lipid peroxidation may play a role in cyclosporin nephrotoxicity. The influence of cyclosporin treatment on the lipid peroxidation (assessed as malondialdehyde (MDA) in plasma and kidney homogenates using HPLC and reaction with thiobarbituric acid) and the activity of superoxide dismutase (SOD) in erythrocytes was studied in rats with nephrotic syndrome induced by single intravenous injection of adriamycin. Rats with nephrotic syndrome treated from the beginning with cyclosporin had lower proteinuria than untreated nephrotic rats. Free MDA in blood and kidney homogenates was significantly elevated in untreated nephrotic rats in comparison with controls. Activity of SOD in erythrocytes was significantly elevated in nephrotic rats treated with cyclosporin (113.40 +/- 34.31 mU/10(6) erythrocytes) in comparison with the control group (55.63 +/- 9.90 mU/10(6) erythrocytes, p < 0.001), rats treated with cyclosporin (65.7 +/- 17.49 mU/10(6) erythrocytes, p < 0.01) and untreated nephrotic rats (65.07 +/- 17.49 mU/10(6) erythrocytes, p < 0.001). In conclusion, cyclosporin reduced proteinuria in rats with mild adriamycin nephropathy (similar to human minimal change disease). Cyclosporin also partially counteracted adriamycin-induced lipid peroxidation probably due to the stimulation of antioxidant enzyme SOD. The possible contribution of decreased lipid peroxidation to the antiproteinuric effect of cyclosporin deserves further study.
Nephron 1997
PMID:The influence of cyclosporin on lipid peroxidation and superoxide dismutase in adriamycin nephropathy in rats. 912 35

In rats with five-sixth nephrectomy (remnant kidney), glomerulosclerosis was significantly reduced by dietary administration of vitamin E (alpha-tocopherol) during 11 and 16 weeks after reduction of nephron number. The activity of catalase and the production of H2O2 in remnant kidney cortex homogenate were not influenced by the vitamin E diet; however, the activities of glutathione peroxidase and superoxide dismutase were significantly increased (up to 140 and 180%, respectively, after 16 weeks). Lipid peroxidation, evaluated by malonaldehyde and 4-hydroxynonenal concentrations, was decreased in cortex homogenates and in urine. Though the extent of the effect of vitamin E on antioxidant enzyme levels and lipid peroxidation is small, the important reduction of glomerulosclerosis is in favor of dietary supplementation with vitamin E.
Nephron 1997
PMID:Effect of vitamin E on antioxidant enzymes, lipid peroxidation products and glomerulosclerosis in the rat remnant kidney. 917 4

Nephron loss leads to increased production of reactive oxygen intermediates. We measured the effect of carvedilol, a beta-blocking drug with radical scavenging properties, on renal function, glomerulosclerosis, antioxidant enzyme status and in vivo hydrogen peroxide (H2O2) production in rats with chronic renal failure caused by 5/6 nephrectomy (remnant kidney) and compared results to data obtained with propranolol, a beta-blocking drug without scavenging characteristics. Carvedilol and propranolol were administered during 11 weeks following reduction of nephron number. Kidneys were examined using enzymatic and histological techniques. Both carvedilol and propranolol decreased systolic blood pressure. Compared to propranolol, carvedilol offered some additional beneficial effects on renal function, particularly with regard to glomerulosclerosis. Lipid peroxidation, evaluated by malonaldehyde and 4-hydroxynonenal concentration in cortex homogenates, was decreased in carvedilol-treated rats only. Superior beneficial effect of carvedilol treatment is not linked to a significant up-regulation of the activities of the remnant kidney antioxidant enzymes (catalase, glutathione peroxidase and superoxide dismutase) or to a decreased in vivo H2O2 production.
Nephron 1997
PMID:Carvedilol protects against glomerulosclerosis in rat remnant kidney without general changes in antioxidant enzyme status. A comparative study of two beta-blocking drugs, carvedilol and propanolol. 937 27

In rats with five-sixths nephrectomy (remnant kidney), blood pressure, glomerulosclerosis, and proteinuria are significantly reduced by administration of the angiotensin-converting enzyme inhibitor enalapril, during 16 weeks after reduction of the nephron number. The activity of catalase in remnant-kidney cortex homogenate is not influenced by enalapril treatment; the activities of superoxide dismutase and glutathione peroxidase are significantly increased. Elevated lipid peroxidation in cortex homogenates, evaluated by malondialdehyde and 4-hydroxynonenal concentrations, is not changed by treatment. Supplementation of dietary vitamin E to enalapril treatment does not alter antioxidant enzyme activities when compared to enalapril monotherapy. These results show that enalapril improves the balance between reactive oxygen intermediates and antioxidant enzymes in the remnant-kidney cortex of the rat. This finding may in part explain the protective effect of angiotensin-converting enzyme inhibitors on the progression of glomerulosclerosis.
Nephron 1998 Oct
PMID:Enalapril increases antioxidant enzyme activity in renal cortical tissue of five-sixths-nephrectomized rats. 1052 41

The present study investigated the effects of melatonin, an antioxidant, on gentamicin-induced nephrotoxicity in rats. Melatonin (5 mg/kg p.o.) was used 3 days before and 8 days simultaneously with gentamicin (80 mg/kg i.p.) Saline-treated animals served as controls. Determinations of urinary creatinine, N-acetyl-beta-D-glucosaminidase, glucose, protein, blood urea, serum creatinine, plasma and kidney tissue malondialdehyde (MDA), and antioxidant enzyme levels in kidney tissue were done after 8 days of gentamicin treatment. The kidneys were also examined for morphological changes using histological techniques. Gentamicin caused nephrotoxicity as evidenced by marked elevation in blood urea and serum creatinine. Mean blood urea and serum creatinine levels were 289+/-50, and 2.5+/-0.5 mg/dl, respectively, in rats treated with gentamicin. Melatonin significantly protected the rats from gentamicin-induced nephrotoxicity; blood urea and serum creatinine levels were 23+/-2.7 and 0.88+/-0.19 mg/dl, respectively. The creatinine clearance was decreased with gentamicin treatment (0.048+/- 0.007 ml/min) as compared with controls (0.41+/-0.08 ml/h/kg). In rats treated with melatonin plus gentamicin, the creatinine clearance was similar to controls (0.41+/-0.08 ml/h/kg). The product of lipid peroxidation (MDA) was markedly increased in plasma (2.10+/-0.15 nmol) and kidney tissue (8.87+/-3.2 nmol/mg protein) with gentamicin treatment. Melatonin prevented the gentamicin-induced rise in plasma MDA (1.03+/-0.27 nmol) and kidney tissue MDA (2.57+/-0.87 nmol/mg protein). An increased excretion of urinary N-acetyl-beta-D-glucosaminidase, glucose, and protein by gentamicin was also prevented by melatonin. Kidneys from gentamicin-treated rats showed tubular epithelial loss with intense granular degeneration involving more than 50% of renal cortex, while there were findings comparable to controls in melatonin plus gentamicin treated rats. The present study indicates that melatonin significantly protects against gentamicin-induced renal toxicity in Wistar rats.
Nephron 2000 Jun
PMID:Melatonin, a pineal hormone with antioxidant property, protects against gentamicin-induced nephrotoxicity in rats. 1086 23

Excessive generation of reactive oxygen intermediates can induce changes in the cellular antioxidant defence system. In this study we examine the antioxidant enzyme status and the expression of fibrosis-related marker proteins in the Adriamycin model of chronic renal failure in the rat. Twenty weeks after Adriamycin treatment, rats have overt nephrotic syndrome and renal failure with development of tubulo-interstitial fibrosis and glomerulosclerosis. Lipids accumulate in blood and in both glomeruli and tubulo-interstitial tissue. Desmin and alpha-smooth muscle actin expression increases in glomeruli and in the tubulo-interstitial area. Renal cortex antioxidant enzyme activities are decreased 20 weeks after Adriamycin injection (to 41% for catalase, to 56% for total superoxide dismutase and to 69% for glutathione peroxidase). The mRNA levels of catalase, Cu/Zn-superoxide dismutase and glutathione peroxidase-1 evaluated by Northern blot are decreased by more than 50% for catalase, Cu/Zn-superoxide dismutase and glutathione peroxidase-1. We conclude that in the rat Adriamycin-induced model of chronic renal failure with fibrosis, the combination of decreased antioxidant enzyme status in renal cortex with high concentrations of lipids in blood and renal tissue facilitates oxidative damage. Development of fibrosis is paralleled by increased expression of desmin and alpha-smooth muscle actin.
Nephron 2000 Oct
PMID:Renal antioxidant enzymes and fibrosis-related markers in the rat adriamycin model. 1101 87

Heme oxygenase-1 (HO-1) is an antioxidant enzyme and is believed to protect against oxidative stress-induced tissue injury. Renal ischemia-reperfusion (IR) injury seems at least in part to be caused by the oxidative stress. The aim of this study was to improve the renal IR injury by clinically available means. When littermate hemolysate was intravenously administered into rats, HO-1 was markedly induced in the kidneys. To investigate whether prior induction of HO-1 by the hemolysate injection ameliorates the subsequent renal IR injury, we assessed the levels of blood urea nitrogen (BUN) and serum creatinine (SCr), markers for renal injury, in rats with 45 min of ischemia followed by 18 h of reperfusion. To avoid the nephrotoxicity induced by hemolysate, small but effective amounts of hemolysate was injected into rats at 48 h prior to the ischemia. The levels of BUN and SCr values were significantly improved as compared to the rats with renal IR injury alone. Administration of HO inhibitor abolished the efficacy of hemolysate pretreatment. Our findings indicated that the prior induction of HO-1 by treatment of littermate hemolysate ameliorated the subsequent renal IR injury. Prior injection of self-hemolysate would be clinically useful for the protection against the renal IR injury induced by kidney transplantation and kidney surgery without immunological and infectious problems.
Nephron 2002 Oct
PMID:Hemolysate pretreatment ameliorates ischemic acute renal injury in rats. 1221 21