Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxygen free radicals have been implicated in the pathogenesis of tissue injury consequent to ischemia/reperfusion in several different organs, including heart, bowel, and kidney. In this study, the protective effect of FOY, SOD, and PEG-SOD against kidney damage resulting from warm ischemia and reperfusion was investigated in the rat. FOY (Gabexate mesilate), one of protease inhibitor, has been suggested to inhibit the activity of superoxide in polymorphonuclear leucocyte in recent reports. PEG-SOD (polyethyleneglycol-modified SOD), recently synthesized on the basis of SOD, has an additional value in comparison with SOD. WKA rats underwent right nephrectomy, and occlusion of the left renal artery, vein, and ureter for 60 minutes. FOY (50mg/kg, DIV.) was administrated from 5 minutes before reperfusion to 5 minutes after reperfusion to the rat. SOD (2mg/kg, 5mg/kg, 10mg/kg, IV.) and PEG-SOD (2mg/kg, 5mg/kg, IV.) were administrated at 10 minutes before reperfusion. 48 hours after operation, the measurement of urine output (60 minutes) was made, and BUN, Cr, K, UUN, UCr were measured at this point. Creatinine clearance was calculated from these results. The left kidney was removed and histological examination was performed. Serum BUN, Cr level were greatly elevated, and creatinine was diminished in the group of ischemic untreated rats (n = 8). In the groups of rats treated with FOY (n = 9), SOD (5mg/kg, 10mg/kg; n = 5, respectively), and PEG-SOD (2mg/kg, 5mg/kg; n = 5, respectively), serum Cr was significantly lower and creatinine clearance was significantly higher than control untreated group. Furthermore, tubular injury was less in histological examination in these groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Experimental study on renal protection against damage in kidneys subjected warm ischemia--protective effect of FOY, SOD, and PEG-SOD on ischemic acute renal failure]. 251 Nov 30

Bovine copper/zinc superoxide dismutase (SOD) was labelled with 125I using the chloramine-T method. The tissue distribution of 125I-SOD (dose of SOD 5 mg/kg) was studied with whole-body and microautoradiography at various times after an intravenous injection. The distribution of 125I-SOD showed a remarkable organ specificity in that the localization of the enzyme to the kidneys and the urinary tract completely dominated the autoradiograms. The time pattern of localization of 125I-SOD also gives a clear picture of the renal handling of the enzyme in that, as a consequence of the renal elimination, the enzyme rapidly disappears from the circulation with an elimination half time of about 6 min. Up to 20 min. after the injection, there were high concentrations of 125I-SOD in the renal pelvis, ureter and urinary bladder showing that in addition to renal uptake there was an initial substantial urinary excretion of the enzyme. From the microautoradiography it is clear that the grains were exclusively localized over proximal tubular cells and tended to be concentrated at the luminal rather than the peritubular side of tubule. This would be compatible with renal uptake secondary to glomerular filtration of 125I-SOD, which is what one would expect from the renal handling of a protein with a molecular weight around 31,000 and an isoelectric point around pH 5.4. Pretreatment with a large dose of SOD (88 mg/kg) tended to competitively decrease the renal uptake of labelled SOD after 5 min. and apparently further increase its renal excretion. However, a noticeable renal uptake of 125I-SOD was still apparent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tissue distribution of 125I-labelled bovine superoxide dismutase (SOD) in the rat. 335 58

Hydrogen has been demonstrated to have effective protection against tissue injuries caused by oxidative stress, inflammation, and apoptosis. This study investigated the efficacy of hydrogen-rich saline (HS) on the prevention of renal injury induced by unilateral ureteric obstruction (UUO) in rats. Male Sprague-Dawley rats were divided randomly into 4 groups: sham group, UUO group, UUO+saline group, and UUO+HS group. UUO was induced by ligation of the left ureter. 5ml/kg HRSS or saline was administered beginning 1day after UUO and for 10days thereafter. Rats were killed at 10days after UUO. Left kidneys were excised immediately for the tissue histologic examinations and biochemical assays. Renal injury scores in the UUO group and the UUO+saline group were significantly higher compared with those in the sham group. However, administration of HS significantly reduced the injury score. Apoptosis index was significantly increased in UUO group and the UUO+saline group. HS treatment also reduced the apoptosis index. Interstitial fibrosis and macrophage infiltration were obvious in UUO kidneys. However, HS treatment significantly reduced the fibrosis and infiltration of macrophage in UUO kidneys. Significant increase in the MDA level and decrease in the SOD activity were observed in UUO group and the UUO+saline group. MDA level of UUO+HS group was significantly reduced. In addition, SOD activity of was significantly improved after treatment of HS. The data provide a biochemical and histologic basis for HS acting as a novel therapeutic strategy for preventing the renal injury induced by UUO.
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PMID:Hydrogen-rich saline ameliorates renal injury induced by unilateral ureteral obstruction in rats. 2387 Dec 46