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This Article Full Text Full Text (PDF) All Versions of this Article: 293/5/F1450    most recent 00223.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Jacquillet, G. Articles by Cougnon, M. Search for Related Content PubMed PubMed Citation Articles by Jacquillet, G. Articles by Cougnon, M.

Cadmium causes delayed effects on renal function in the offspring of cadmium-contaminated pregnant female rats

¹Unité Mixte de Recherche-Centre National de la Recherche Scientifique 6548, Université de Nice-Sophia Antipolis, Nice, France; ²Departamento de Fisiologia y Biofisica and ³Seccion Externa de Toxicologia, Centro de Investigacion y de Estudios Avanzados, Avenida Instituto Politécnico Nacional 2508, Colonia San Pedro Zacatenco, Mexico City, Mexico

Submitted 14 May 2007 ; accepted in final form 6 August 2007

In the adult rat, chronic cadmium intoxication induces nephropathy with Fanconi-like features. This result raises the question of whether intoxication of pregnant rats has any deleterious effects on renal function in their offspring. To test this hypothesis, we measured the renal function of 2- to 60-day-old postnatal offspring from female rats administered cadmium chloride by the oral route (0.5 mg·kg^–1·day^–1) throughout their entire gestation. Investigations of rat offspring from contaminated pregnant rats showed the presence of cadmium in the kidney at gestational day 20. After birth, the cadmium kidney concentration increased from postnatal day 2 to day 60 (PND2 to PND60), presumably because of 1) milk contamination and 2) neonatal liver cadmium content release. Although the renal parameters (glomerular filtration, U/P inulin, and urinary excretion rate) were not significantly affected until PND45, renal failure appeared at PND60, as demonstrated by a dramatic decrease of the glomerular filtration rate associated with increased excretion of the main ions. In parallel, an immunofluorescence study of tight-junction protein expression of PND60 offspring from contaminated rats showed a disorganization of the tight-junction proteins claudin-2 and claudin-5, specifically expressed in the proximal tubule and glomerulus, respectively. In contrast, expression of a distal claudin protein, claudin-3, was not affected. In conclusion, in utero exposure of cadmium leads to toxic renal effects in adult offspring. These results suggest that contamination of pregnant rats is a serious and critical hazard for renal function of their offspring.

heavy metals; renal failure; newborn; claudins