Increase by NO synthase inhibitor of lead-induced release of N-acetyl-β-d-glucosaminidase from perfused rat kidney

Dehpour, Ahmad Reza; Essalat, Mostafa; Ala, Shahram; Ghazi‐Khansari, Mahmoud; Ghafourifar, Pedram

doi:10.1016/s0300-483x(98)00143-7

Cited by 13 publications

(5 citation statements)

References 30 publications

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“…Dehpour et al in 1999 have shown significant increase in NAG level with LA administration. 26 similar results are seen in the present study, that LA administrated groups showed a significant increase in NAG level indicating nephrotoxicity occurrence. Lead produce its deleterious effect by attributed its ability to induce oxidative injury by generate ROS in the kidney by two separate, although related, pathways.…”

Section: Discussionsupporting

confidence: 93%

Nephroprotective Effect of Low Viscosity Sodium Alginate on Lead Acetate-Induced Nephrotoxicity in Rats

Kaur¹,

Sharma²

2017

IJPER

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Objective: Renal failure in majority of population is considered to be idiopathic. Heavy metals like lead in drinking water are usually the hidden cause of these renal consequences. Thus, this study has been designed to investigate the effect of low viscosity sodium alginate (LvSA) in Lead-induced nephrotoxicity. Methods: Lead (0.2% lead acetate in drinking water for 5 weeks) was administered in rats to produce nephrotoxicity assessed in terms of histopathological changes, increase in serum creatinine, blood urea nitrogen, urinary N-acetyl-β D glucosaminidase (NAG), proteinuria, Thiobarbituric acid reactive substances (TBARS) and decrease in reduced glutathione level. Results : Lead acetate (LA) intoxication shown elevations in serum creatinine, Proteinuria, glomerular filtration rate (GFR), blood urea nitrogen (BUN), Thiobarbituric acid reactive substances (TBARS), altered urinary N-acetyl-β D glucosaminidase (NAG), kidney weight/ body weight ratio (KW/BW %), and creatinine clearance that indicate renal damage. Treatment with Low viscosity sodium alginate (LvSA) show significant decrease in serum creatinine, BUN, urinary NAG, protein in urine, KW/BW %, TBARS level and increase in GSH, creatinine clearance and GFR. Conclusion: Thus, on the basis of results it may be concluded that LvSA significantly attenuated Lead-induced nephrotoxicity.

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Section: Discussionsupporting

confidence: 93%

Nephroprotective Effect of Low Viscosity Sodium Alginate on Lead Acetate-Induced Nephrotoxicity in Rats

Kaur¹,

Sharma²

2017

IJPER

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“…NAG is a sensitive hydrolytic lysosomal enzyme that is released after renal tubular damage [26]. In the rat, urinary NAG is a useful early marker of renal injury induced by acetaminophen, aspirin, lead, and gentamicin [30][31][32]. In our previous clinical protocol, we successfully implemented ion supplementation, as well as vigorous hydration of patients, as nephroprotective measures to prevent AmB-induced acute decrease in renal function [25].…”

Section: Discussionmentioning

confidence: 99%

Reduced Nephrotoxicity of Conventional Amphotericin B Therapy after Minimal Nephroprotective Measures: Animal Experiments and Clinical Study

Mayer

Doubek

et al. 2002

J INFECT DIS

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Amphotericin B (AmB)-treated rats develop severe polyuria, polydypsia, impairment of renal concentrating ability, and morphologic signs of tubular damage. However, renal insufficiency develops quickly only in animals in which water intake is restricted to the median volume drunk by rats of the control group. Therefore, vigorous hydration seems crucial for prevention of AmB-induced nephrotoxicity. In a clinical study, 61 patients with hematologic malignancies receiving AmB therapy were massively hydrated to ensure urine output of > or =4000 mL/day. Urine sodium, potassium, and magnesium were also measured, and all losses were supplemented (potassium as a 7.45% solution via central venous catheter). AmB-treated patients developed signs of renal tubular damage (increased fractional excretion of sodium and potassium) and required large amounts of ion supplementation. The serum ion concentration and creatinine clearance remained stable. No clinically significant renal damage developed to force premature cessation of AmB treatment.

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“…α, β and γ Ig [20,21], serum alanin aminotransferase (ALT), aspartate aminotransferase (AST) activities [22], serum alkaline phosphatase, (ALP) activity (kits of bioMerieux/ France) [23], serum urea level (kits bioMerieux) [24], serum creatinine (kits bioMerieux) [25], serum cholesterol [26] and Lipid peroxidation (LPO) (kits (Biodiaguostic) ® ) [27] were determined. Serum Lead level was estimated using an atomic absorption spectrophotometer/flame [28]. The concentrations of T3 and T4 were assayed according to the method described by Nussey and Whitehead [29] using enzymelinked immunosorbent assay (ELISA) kits (Microwell T3, T4 kits; Synthron Bioresearch, Inc, USA).…”

Section: Serum Biochemical Analysismentioning

confidence: 99%

Effect of Aqueous Extract of Punica granatum Peel on the Oxidative Damage Induced by Lead Intoxication in Rats

Zaglool

Hassan

El-shamy

2017

Zagazig Veterinary Journal

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The present investigation aimed to evaluate the effect of aqueous extract of local pomegranate peel on the oxidative damage induced by lead intoxication in rats. Forty-eight female Albino rats were divided into four equal groups. Group (1) kept as a control group, while Group (2) was fed on 1000 ppm lead acetate in drinking water. Group (3) received 1000 ppm lead acetate in drinking water plus 1 mL of distilled water containing 43 mg/rat of pomegranate peel aqueous extract via gastric intubation and Group (4) received 1 mL of distilled water containing 43 mg/rat of Pomegranate peel aqueous extract via gastric intubation. All rats were treated with the respective regime daily for five weeks. Administrations of lead acetate for 5 weeks caused significant decrease of total proteins, globulins (α, β & γ), triiodothyronine (T3) and thyroxine hormone (T4) with significant increase of the urea, creatinine, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lead residue in liver and lipid peroxidase. Mild degenerative and necrobiotic changes in liver and kidney were detected histopathologically. Administration of pomegranate peel extract revealed minor ameliorative effect on serum proteins, aminotransferases and urea levels. Treating rats with both of lead acetate and Punica granatum peel aqueous extract for 5 weeks revealed focal hepatic necrosis, hypercellularity of renal glomeruli and degeneration in the epithelial cells lining of renal tubules. Administration of aqueous extract of Punica granatum peel for 5 weeks to healthy rats induced congestion of central vein of liver and degeneration in the epithelial cells lining of renal tubules. This study figure out that administration of Punica granatum peel aqueous extract had a mild deleterious effect on healthy rats with a slight improvement on the oxidative damage induced by lead intoxication in rats.

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Increase by NO synthase inhibitor of lead-induced release of N-acetyl-β-d-glucosaminidase from perfused rat kidney

Cited by 13 publications

References 30 publications

Nephroprotective Effect of Low Viscosity Sodium Alginate on Lead Acetate-Induced Nephrotoxicity in Rats

Nephroprotective Effect of Low Viscosity Sodium Alginate on Lead Acetate-Induced Nephrotoxicity in Rats

Reduced Nephrotoxicity of Conventional Amphotericin B Therapy after Minimal Nephroprotective Measures: Animal Experiments and Clinical Study

Effect of Aqueous Extract of Punica granatum Peel on the Oxidative Damage Induced by Lead Intoxication in Rats

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