Detection of the Early Steps of Cadmium Nephropathy – Comparison of Light- and Electron-Microscopical Patterns with the Urinary Enzymes Excretion

Gatta, Angelo; Bazzerla, G.; Amodio, Piero; Menon, F.; Angeli, P.; Schiaffino, E; Schmid, Christopher H.

doi:10.1159/000185235

Cited by 19 publications

(10 citation statements)

References 10 publications

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“…In agreement with other reports, we have noted a vesiculation of cells and mitochondrial and lysosomal alterations [41][42][43]. Long-term morpho logical reports in experimental cisplatin intoxication were rarely found in the literature.…”

Section: Discussionsupporting

confidence: 92%

Cisplatin Nephrotoxicity in Cadmium-Pretreated Rats

Bompart¹,

Orfila²,

Manuel³

1991

Nephron

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Treatment of rats with cisplatin or with cisplatin after chronic pre-exposure to cadmium induced a decrease in kidney cytochrome P-450 and glutathione levels, and in glutathione peroxidase and reductase activities. Furthermore, cadmium and cisplatin enhanced lipid peroxidation, oxidized glutathione and N-glucuronyl transferase activity. Glutathione S-transferase (substrate: 1-chloro-2,4-dinitrobenzene) was increased and decreased by cadmium and cisplatin respectively. On morphological observation, cadmium nephrotoxicity was characterized by tubular proximal damage with mitochondrial and lysosomal changes and a widespread vesiculation of tubular cells. A marked focal tubular necrosis associated with cyst formation was observed in cisplatin nephrotoxicity. On the basis of the measured biochemical, functional and histological parameters, it is concluded that cadmium pretreatment did not potentiate the nephrotoxic effect of cisplatin.

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Section: Discussionsupporting

confidence: 92%

Cisplatin Nephrotoxicity in Cadmium-Pretreated Rats

Bompart¹,

Orfila²,

Manuel³

1991

Nephron

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“…Chronic Cd exposition caused a nephropathy with peculiar damage of the renal proximal tubule. Atrophy and degeneration of proximal tubules with vacuolization of tubular cells were the most striking lesions seen (21). Cd exposure has been shown to cause large cytoplasmic vacuoles containing membranous material in proximal tubular lining cells.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Quercetin Against Renal Toxicity Induced by Cadmium in Rats

Aktoz¹

2012

Balkan Med J

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Objective: The aim of the present study was to examine the protective effect of quercetine (QE) against cadmium (Cd)-induced renal toxicity. Material and Methods:A total of 24 male Wistar albino rats were divided into three groups: control, Cd-treated and Cd-treated with QE; each group containing 8 animals. The Cd-treated group was injected subcutaneously with CdCl2 dissolved in saline in the dose of 2 ml/kg/day for 30 days, resulting in a dosage of 1 mg/kg Cd. The rats in the QE treated groups were given QE (15 mg/kg body weight) once a day intraperitoneally starting 2 days prior to Cd injection during the study period.Results: The renal histology in Cd-treated rats showed mesangial expansion, thickening of capsular basement membranes, glomerular basement membranes and tubular basement membranes, characterized by an increase in periodic acid Schiff (PAS)-positive areas as compared with control animals. With the QE treatment, despite the presence of only a few swollen glomeruli, we noticed a marked protection of renal structure when compared with the Cd-treated rats. Furthermore, QE pretreatment resulted in increased proliferating cell nuclear antigen (PCNA) immunoreactivity and decreased the activity of Terminal Transferase dUTP Nick End Labeling (TUNEL). Conclusion:These findings suggest that QE may attenuate Cd-induced renal toxicity.

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“…The urinary excretion of y-glutamy ltransferase, an enzyme of the brush border of proxi mal tubular cells [20], and that of a-glucosidase, a tubular lysosomal enzyme [21], showed a trend for an increase in CS-treated rats, in keeping with a slight tubular damage detectable with this diagnostic tool [15,22].…”

Section: Discussionmentioning

confidence: 94%

Effects of Defibrotide on Renal Function and Urinary Prostanoid Excretion in Ciclosporin-Treated Rats

Rigotti

Amodio²,

Sacerdoti³

et al. 1991

Nephron

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Defibrotide (DF) has been proposed as a new antithrombotic agent in renal transplantation. Because it was also found to increase prostacyclin synthesis, a reduction in ciclosporin (CS) nephrotoxicity could be supposed. To ascertain this hypothesis, renal function and urinary prostanoids were evaluated in four groups of rats after 10 days of oral treatment (doses in mg/kg/day): CS 50 (group A), CS 50 + DF 400 (group B), DF 400 (group C) and controls (group D). Compared to controls, creatinine clearance (C_Cr) was significantly lower in groups A and B (In C_Cr: A = 6.62 ± 0.28, B = 6.83 ± 0.24 vs. 8.17 ± 0.13 μl/min, p < 0.01), whereas it did not change in group C (8.03 ± 0.24 μl/min). The urinary excretion of prostaglandin E₂ (PGE₂) was significantly (p < 0.05) higher in group A (In PGE₂: 3.98 ± 0.98 nmol/mol Cr) and more evidently in groups B and C (6.89 ± 0.38 and 6.01 ± 0.32 nmol/mol Cr, respectively) compared to controls (1.43 ± 0.45 nmol/mol Cr). The urinary excretion of 6-keto-PGF₁α and of thromboxane B₂ (TxB₂) were higher only in groups A and B (In 6-keto-PGF_1α and In TxB₂: A = 6.45 ± 0.22 and 4.97 ± 0.20, B = 7.06 ± 0.31 and 5.43 ± 0.41 vs. group D = 5.53 ± 0.22 and 3.79 ± 0.42 nmol/mol Cr; p < 0.05). The 6-keto-PGF_1α/Tx molar ratio was not significantly affected, although a trend for a reduction in the ratio was found in the treated rats. In conclusion, DF enhanced urinary prostanoid excretion in CS-treated rats but did not significantly affect renal function.

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Detection of the Early Steps of Cadmium Nephropathy – Comparison of Light- and Electron-Microscopical Patterns with the Urinary Enzymes Excretion

Cited by 19 publications

References 10 publications

Cisplatin Nephrotoxicity in Cadmium-Pretreated Rats

Cisplatin Nephrotoxicity in Cadmium-Pretreated Rats

Protective Effect of Quercetin Against Renal Toxicity Induced by Cadmium in Rats

Effects of Defibrotide on Renal Function and Urinary Prostanoid Excretion in Ciclosporin-Treated Rats

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