Transport of Inorganic Phosphate in Renal Cortical Brush-Border Membrane Vesicles of Cadmium-Intoxicated Rats

Ahn, Do Whan; Park, Yang Saeng

doi:10.1006/taap.1995.1147

Cited by 25 publications

(20 citation statements)

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“…Nephropathy due to chronic Cd exposure in humans and experimental animals is characterized by defects of reabsorptive and secretory functions in the proximal tubule that clinically resemble acquired Fanconi's syndrome. Glucosuria [1,[17][18][19], proteinuria [1, 4, 17 19], aminoaciduria [1,17,20], phosphaturia [1,2,4,17,18], hypercalciuria [18,26], hyperosmolar polyuria [17][18][19], impared p-aminohippurate (PAH) secretion [18], and increased fractional excretion of Na +, K +, and C1-are common signs of the Cd-damaged kidney in humans and experimental animals.…”

Section: Introductionmentioning

confidence: 99%

Renal type II Na/Pi-cotransporter is strongly impaired whereas the Na/sulphate-cotransporter and aquaporin 1 are unchanged in cadmium-treated rats

Herak-Kramberger

Spindler

Biber

et al. 1996

Pflugers Arch - Eur J Physiol

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The cellular mechanisms of cadmium (Cd) nephrotoxicity are poorly understood. In this study we investigated the cellular causes of the Cd-induced phosphaturia in the rat. Compared to controls, Cd-treated rats (2 mg Cd/kg body weight, s.c. for 14 days) showed a marked polyuria, proteinuria and phosphaturia. As studied by the rapid filtration technique in isolated cortical brush-border membrane vesicles (BBMV), Na+-gradient-driven uptake of phosphate ([32Pi]) and of [3H] glucose were markedly decreased in Cd-treated rats, whereas uptake of sulphate ([35S]) remained unchanged. By Western blotting of BBMV proteins and by indirect immunocytochemistry in 4-micron thick frozen fixed kidney sections, using an antibody against the type II Na/Pi-cotransporter (NaPi-2), we found a diminished expression of this protein in the brush-border membrane from Cd-treated rats. How ever, the expression of the water channel aquaporin 1, estimated from the specific antibody staining in brush-border membranes, remained unchanged by Cd. Northern blot analysis showed a strong reduction of 2.7 kb NaPi-2-related mRNA in Cd-affected kidneys. Our data indicate that: (1) Cd may reduce reabsorption of Pi in proximal tubules by affecting the expression of the functional Na/Pi-cotransporters in the luminal membrane, and (2) Cd effects on brush-border transporters are selective.

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Section: Introductionmentioning

confidence: 99%

Renal type II Na/Pi-cotransporter is strongly impaired whereas the Na/sulphate-cotransporter and aquaporin 1 are unchanged in cadmium-treated rats

Herak-Kramberger

Spindler

Biber

et al. 1996

Pflugers Arch - Eur J Physiol

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“…This nephrotoxicity causes reabsorptive and secretory dysfunction of the renal tubule. The main signs include proteinuria, ion losses, glucosuria, aminoaciduria, and polyuria (1,2,21,24,29,31). Experimental chronic intoxication with Cd 2ϩ has been performed at various doses over several weeks (9,30,48) and causes a Fanconi-like syndrome with predominant tubular dysfunction that develops into renal failure (47,48).…”

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confidence: 99%

Zinc protects renal function during cadmium intoxication in the rat

Jacquillet¹,

Barbier²,

Cougnon³

et al. 2006

American Journal of Physiology-Renal Physiology

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This study investigates the effect in the rat of chronic CdCl2 intoxication (500 μg Cd2+/kg, daily ip injection for 5 days) on renal function and the changes in tight junction proteins claudin-2, claudin-3, and claudin-5 present in rat kidney. We also studied the effect of coadministration of ZnCl2 (500 μg Zn2+/kg) during chronic CdCl2 intoxication. Our results indicate that 1) most of the filtered Cd2+ is reabsorbed within the kidney; 2) chronic Cd2+ intoxication can induce a change in renal handling of ions without altering glomerular filtration rate; 3) a delayed nephropathy, showing Fanconi-like features, appears more than 5 days after the end of CdCl2 exposure; 4) epithelial integrity is altered by chronic Cd2+ intoxication affecting the expression and localization of claudin tight junction proteins; and 5) cotreatment with Zn2+ protects against the renal toxic effects of Cd2+, preventing altered claudin expression and inhibiting apoptosis. In conclusion, these results show that Cd2+ toxicity and cellular toxic mechanisms are complex, probably affecting both membrane transporters and tight junction proteins. Finally, Zn2+ supplementation may provide a basis for future treatments.

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“…Moderate exposure to Cd is known to cause the leakage of IAP (Kido et al, 1995). The significantly high AP activity detected in the serum in this study could have come from any of the tissues/organs enumerated above, particularly the kidney and bone, which are established target organs of cadmium toxicity (Kido et al, 1995;Ahn and Park, 1995). However, there was no corresponding decrease in bone and kidney AP relative to the Cd-free controls, which would have been the case if they were merely damaged by this toxicant.…”

Section: Resultsmentioning

confidence: 38%

Effects of Cadmium Exposure on Bone and Kidney Alkaline Phosphatase Activity and Acid Phosphatase Activity in Testis and Prostate Gland in the Male Rat

O¹,

Olabode²

2002

Journal of Applied Sciences and Environmental Management

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This paper examines the effects of varying doses of cadmium on bone and kidney alkaline phosphatase and on testis and prostate acid phosphatase after 4 weeks of administration to separate groups of rats. Relative to the cadmium-free control rats femur bone alkaline phosphatase activity was significantly (P<0.05) elevated in rats exposed to 2 mg cadmium /kg body weight and in those exposed to 3 mg/kg. Compared to control rats kidney alkaline phosphatase activity was also statistically significantly (P<0.05) elevated in separate groups of rats exposed to 1, 2 and 3 mg cadmium/kg body weight. Prostatic acid phosphatase activities in the testis and prostate were significantly (P<0.05) decreased in the groups of rats separately exposed to 1, 2 and 3 mg cadmium/ kg. At the highest dose nonprostatic acid phosphatase activity increased significantly (P<0.5) in testis and prostrate. In serum at the highest dose nonprostatic acid phosphatase decreased while the prostatic isoform and

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Transport of Inorganic Phosphate in Renal Cortical Brush-Border Membrane Vesicles of Cadmium-Intoxicated Rats

Cited by 25 publications

References 0 publications

Renal type II Na/Pi-cotransporter is strongly impaired whereas the Na/sulphate-cotransporter and aquaporin 1 are unchanged in cadmium-treated rats

Renal type II Na/Pi-cotransporter is strongly impaired whereas the Na/sulphate-cotransporter and aquaporin 1 are unchanged in cadmium-treated rats

Zinc protects renal function during cadmium intoxication in the rat

Effects of Cadmium Exposure on Bone and Kidney Alkaline Phosphatase Activity and Acid Phosphatase Activity in Testis and Prostate Gland in the Male Rat

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