Changes in Renal Function in Cadmium‐Intoxicated Rats

Kim, Y. K.; Choi, Jong-Soon; Kim, J. S.; Park, Y. S.

doi:10.1111/j.1600-0773.1988.tb00966.x

Cited by 38 publications

(19 citation statements)

References 31 publications

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“…It seems that the duration of treatment and the doses used were not enough to produce significant renal damage. However, these results are in homogeny with other similar studies [37,38]. Dudley et al [39] showed that hepatic injury occurs prior to renal damage following Cd administration, which confirms that over long period of Cd exposure, the hepatic release of Cd-metallothionein with its subsequent translocation to kidney produces renal damage.…”

Section: Discussionsupporting

confidence: 81%

Effect of Cadmium and Aluminum Intake on the Antioxidant Status and Lipid Peroxidation in Rat Tissues

El-Maraghy

Gad

Fahim

et al. 2001

J Biochem & Molecular Tox

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This work aimed to study the relationship between the accumulation of cadmium (Cd) or aluminum (Al) in certain tissues and the levels of lipid peroxides as well as tissue antioxidants. To carry out such investigations, CdCl2 was given to rats in two dose levels; 0.5 or 2.0 mg/kg i.p for 1 day or daily repeated doses for 2 weeks. Al was given as AlCl3 either in a single dose of 100 mg/kg or daily repeated doses of 20 mg/kg for 2 and 4 weeks. The measured parameters were tissue malondialdehyde (MDA, index of lipid peroxidation) and reduced glutathione (GSH) levels as well as the activities of glutathione peroxidase (GSH-PX), glutathione reductase (GSSG-R), and glucose-6-phosphate dehydrogenase (G-6-PDH) enzymes. Liver and kidney functions were assessed by measuring serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities as well as serum urea and creatinine concentrations. Cd and Al concentrations in the studied tissues were also measured. Results indicated that tissue Cd was significantly increased after administration of either Cd doses. After a single dose of 0.5 or 2.0 mg/kg CdCl2, the increase in tissue Cd levels were accompanied by an increase in MDA and a decrease in GSH levels. On the other hand, after repeated administration of Cd, tissue Cd accumulation was accompanied by increased hepatic and renal GSH levels with decrease in MDA content and a decrease in GSH-PX activity in liver. Liver function was affected at all dose regimens, whereas kidney function was affected only after 2 weeks administration of the higher dose. In Al treated rats, Al concentration was shown to be increased in liver much more than in brain. This was accompanied by a slight decrease in hepatic GSH level after 2 weeks and a decrease in GSH-PX activity after 4 weeks. Liver function was affected only after repeated injection of Al for 2 or 4 weeks. In general, Al administration exhibited safer pattern than Cd.

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Section: Discussionsupporting

confidence: 81%

Effect of Cadmium and Aluminum Intake on the Antioxidant Status and Lipid Peroxidation in Rat Tissues

El-Maraghy

Gad

Fahim

et al. 2001

J Biochem & Molecular Tox

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“…Pathological changes in the kidneys due to cadmium have been noted frequently in many experiments (Bernard et al, 1992;Chin and Templeton, 1992;Groten et al, 1991;Hewitt et al, 1991;Itokawa et al, 1974Itokawa et al, , 1978Kim et al, 1988;Ś wiergosz et al, 1998;Waalkes et al, 1992b). It is known that there is a clear difference in the toxicity in rats fed inorganic cadmium (CdCl 2 ) from those fed cadmium bound to MT.…”

Section: Kidneymentioning

confidence: 95%

Cadmium distribution and toxicity in tissues of small rodents

Świergosz-Kowalewska

2001

Microscopy Res & Technique

110

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The aim of the present paper is to discuss the accumulation and distribution of cadmium (Cd) in the various tissues of animals, the interactions of cadmium with other elements, and the damage to tissues caused by this metal. Cadmium is not physiologically or biochemically essential to an organism. It is absorbed via the gastrointestinal tract and lungs and accumulated in various tissues, mainly the kidneys and liver. The distribution of cadmium between various tissues depends on many endogenous and exogenous factors. Cadmium is bound to a low-molecular-weight protein, metallothionein (MT), and to high-molecular-weight proteins. This metal has a great affinity to thiol groups. Cadmium binds also to O- and N-containing ligands. The distribution of cadmium between organs differs markedly depending on the chemical form of administered Cd and the duration of exposure. Acute exposure results in a different distribution pattern throughout the body than does chronic exposure. Long-term exposure to high doses of cadmium may cause biochemical and functional changes in some critical organs. Cadmium can influence the absorption and distribution of essential elements and can replace them in enzymes. Metallothionein and glutathione play important roles in the transport of metals and in detoxification processes. Reported findings are mainly the results of experiments on laboratory animals. The lack of data concerning the localization of cadmium in various tissues of wild species is noticeable and there is a great need for such data.

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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).…”

mentioning

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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Changes in Renal Function in Cadmium‐Intoxicated Rats

Cited by 38 publications

References 31 publications

Effect of Cadmium and Aluminum Intake on the Antioxidant Status and Lipid Peroxidation in Rat Tissues

Effect of Cadmium and Aluminum Intake on the Antioxidant Status and Lipid Peroxidation in Rat Tissues

Cadmium distribution and toxicity in tissues of small rodents

Zinc protects renal function during cadmium intoxication in the rat

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