Role of endotoxin and nitric oxide in the pathogenesis of renal failure in obstructive jaundice

Inan, Murat; Sayek, İskender; Tel, Banu Cahide; Şahin-Erdemli, İnci

doi:10.1002/bjs.1800840710

Cited by 46 publications

(18 citation statements)

References 30 publications

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“…Endotoxin shows direct toxic activity on the kidney and also decreases renal blood flow through cytokine activation and increase in catecholamine release [17,18]. In addition, endotoxin affects the arachidonic acid metabolism and increases leukotriene B 4 and thromboxane A 2 production. In studies on sepsis and endotoxemia, leukocyte accumulations in the tubuli were demonstrated.…”

Section: Discussionmentioning

confidence: 99%

“…In studies on sepsis and endotoxemia, leukocyte accumulations in the tubuli were demonstrated. Leukocytes produce proteases and FORs and cause glomerular basal membrane [4,11,16].…”

Section: Discussionmentioning

confidence: 99%

“…Decrease in the glomerular filtration rate and acute renal failure (ARF) are observed in 60-75 and 4-18% of the patients respectively. The mortality of patients with renal failure varies between 32 and 100% [1][2][3][4].…”

Section: Introductionmentioning

confidence: 99%

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Role of Oxygen Free Radical Scavengers in Acute Renal Failure Complicating Obstructive Jaundice

Küçük¹,

Sözüer²,

Ikizceli³

et al. 2003

Eur Surg Res

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Obstructive jaundice is associated with high morbidity and mortality. Major complications such as pulmonary dysfunction, renal failure and sepsis are frequently encountered. Recent studies and observations suggest that the free oxygen radicals (FORs) produced in obstructive jaundice may play a significant role in the etiopathogenesis of acute renal failure (ARF). Thirty rats were divided into three groups, as sham, control and treatment groups containing 10 rats each. Laparatomy was performed on each animal in the control and treatment groups and common bile ducts were ligated. Common bile duct was observed but was not ligated for the rats in the sham group. Saline solution injection was begun on the first day of surgical procedure and repeated once a day during the following 5 days. The same procedure was performed with oxygen radical scavenger dimethyl sulfoxide (1.5 mg/kg/day i.p.) instead of saline in the treatment group. The rats were sacrificed on the 7th postoperative day. On the 7th postoperative day, the bilirubin, urea and creatinine levels of the control and treatment groups were significantly higher in comparison with the sham group (p < 0.01). Although there was no statistically significant difference between the bilirubin levels of the control and treatment groups (p > 0.05), the urea and creatinine levels in the treatment group were significantly lower (p < 0.01). On the 7th postoperative day, the erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels of the control and treatment groups were significantly lower than those of the sham group (p < 0.01), whereas renal and erythrocyte malondialdehyde (MDA) levels were significantly higher (p < 0.01). Although SOD and GSH-Px levels did not differ significantly between the treatment and control groups (p > 0.05), renal and erythrocyte MDA levels of the treatment group were significantly lower than those of the control group (p < 0.01). The histopathological scores were significantly higher in the control and treatment groups (p < 0.01); there was no significant difference between the control and treatment groups (p > 0.05). FORs seem to play a significant role in the etiopathogenesis of renal failure in obstructive jaundice. Antioxidant treatment may decrease oxidative damage due to FORs and may prevent renal failure.

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Section: Discussionmentioning

confidence: 99%

“…In studies on sepsis and endotoxemia, leukocyte accumulations in the tubuli were demonstrated. Leukocytes produce proteases and FORs and cause glomerular basal membrane [4,11,16].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Role of Oxygen Free Radical Scavengers in Acute Renal Failure Complicating Obstructive Jaundice

Küçük¹,

Sözüer²,

Ikizceli³

et al. 2003

Eur Surg Res

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“…The rat and human renal proximal tubules (PTs) are capable of generating nitric oxide (NO) [6,7], and thus generated NO participates in the cytotoxicity associated with hypoxia/reoxygenation injury [8] and endotoxemia [9]. NO is generated by two types of enzymes: constitutive Ca 2+ -dependent NO synthase (cNOS) and Ca 2+ -independent, cytokine-dependent inducible NOS (iNOS) [7,10,11].…”

Section: Introductionmentioning

confidence: 99%

Grass Carp (Ctenopharyngodon idellus) Bile may Inhibit the Release of Renal Dipeptidase from the Proximal Tubules by Nitric Oxide Generation

Choi

Park²,

Lee³

et al. 2000

Kidney Blood Press Res

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There are many reports on acute renal failure (ARF) after ingestion of grass carp bile (CB; Ctenopharyngodon idellus). Renal dipeptidase (RDPase; EC 3.4.13.19) is a glycosylphosphatidylinositol–anchored ectoenzyme within the renal proximal tubules (PTs) and is proposed as a diagnostic enzyme of renal disease. We examined the release of RDPase following treatment with CB and various nitric oxide (NO) related compounds in porcine PTs. The RDPase release from PTs was inhibited by CB in a concentration–dependent manner and was also inhibited by sodium nitroprusside (direct NO donor) and L–arginine (NO synthase substrate) in the tested range (0–12 mM). CB–treated (0.1 mg/ml) PTs showed a decreased RDPase activity in comparison with the control group. This inhibition was blocked by 2 mM L–NAME (NO synthase inhibitor) and U73122 (inhibitor of phosphatidylinositol–specific phospholipase C) in a concentration–dependent manner. Eel bile (0–0.1 mg/ml), used as the control, did not significantly affect the RDPase release from PTs. The NO concentration was observed as nitrite, the degradation product of the NO metabolism, increased in proportion to CB and L–arginine. The increase of nitrite to 151.5% by CB treatment (0.1 mg/ml) was blocked by 2 mM L–NAME (95.5%). When the phospholipase C pathway was blocked by 10 and 20 μM U73122, the nitrite generation decreased to 122.7 and 89.4%, respectively. These results strongly suggest that NO generation and the phospholipase C pathway affect the RDPase release from the PTs and that they may be involved in the development of ARF in vivo following CB ingestion. The release of RDPase from PTs could be a useful tool not only for this CB–caused ARF, but also for the elucidation of other biochemical mechanisms.

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“…The gastric wall blood response to exogenous NO/cyclic guanosine-3 ,5 -monophosphate (cGMP)-dependent vasodilators is impaired in bile duct-ligated rats (32). Cause of NO overproduction in the BDL-only group may be due to an elevated incidence of endotoxemia after BDL (33). On the other hand, the low levels of NO in resveratrol-treated rats may be due to inhibition of NO and peroxynitrite (ONOO¯) by resveratrol (34,35).…”

Section: Discussionmentioning

confidence: 94%

Resveratrol, a Red Wine Constituent Polyphenol, Protects Gastric Tissue Against the Oxidative Stress in Cholestatic Rats

et al. 2006

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This experimental study was designed to determine the effects of resveratrol on the level of malondialdehyde (MDA), reduced glutathione (GSH), and nitric oxide (NO) in gastric tissue after bile duct ligation (BDL). Swiss albino rats were divided into three groups: Group 1, sham (n = 7); Group 2, BDL (BDL only group; n = 7); and Group 3, BDL plus resveratrol (n = 7). Animals in the resveratrol group were treated with 10 mg/kg resveratrol (i.p.) once a day throughout 28 days. In the resveratrol group, levels of MDA and NO in gastric tissue were significantly lower than in the BDL-only group (P < 0.001). The level of GSH in the resveratrol group was significantly higher than in the BDL-only group (P < 0.001). The present study demonstrates that intraperitoneal administration of resveratrol maintains antioxidant defenses and reduces oxidative gastric damage. This effect of resveratrol may be useful to preserve gastric tissue under oxidative stress due to cholestasis.

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Role of endotoxin and nitric oxide in the pathogenesis of renal failure in obstructive jaundice

Abstract: Endotoxaemia in obstructive jaundice may induce overproduction of nitric oxide that may lead to impairment of cGMP-associated vasodilatation and disrupt autoregulation of the renal vascular bed. This may contribute to renal failure in obstructive jaundice.

Cited by 46 publications

References 30 publications

Role of Oxygen Free Radical Scavengers in Acute Renal Failure Complicating Obstructive Jaundice

Role of Oxygen Free Radical Scavengers in Acute Renal Failure Complicating Obstructive Jaundice

Grass Carp (Ctenopharyngodon idellus) Bile may Inhibit the Release of Renal Dipeptidase from the Proximal Tubules by Nitric Oxide Generation

Resveratrol, a Red Wine Constituent Polyphenol, Protects Gastric Tissue Against the Oxidative Stress in Cholestatic Rats

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