Developmental effects of lead acetate on the chick embryo metanephros

• Published in: Journal of submicroscopic cytology and pathology Vol. 33; no. 3; p. 261
• Main Authors: Errede, M, Elia, G, Bertossi, M, Mulas, M L, Riva, A, Virgintino, D, Benagiano, V, Girolamo, F, Roncali, L, Ambrosi, L
• Format: Journal Article
• Language: English
• Published: Italy 01-07-2001
• Subjects: Abnormalities, Drug-Induced; Allantois - chemistry; Allantois - drug effects; Animals; Chick Embryo - abnormalities; Chick Embryo - drug effects; Chorion - chemistry; Chorion - drug effects; Connexin 43 - analysis; Embryonic and Fetal Development; Gap Junctions - drug effects; Gap Junctions - ultrastructure; Kidney - abnormalities; Kidney - drug effects; Lead - analysis; Lead - pharmacokinetics; Lead - toxicity; Organometallic Compounds - pharmacokinetics; Organometallic Compounds - toxicity
• ISSN: 1122-9497

The developmental effects of lead acetate were studied in the chick embryo metanephros, the third renal rudiment that acquires morphological characteristics of functioning kidney already during the prenatal life. Lead exposure was obtained by applying a lead acetate solution on the chick embryo chorioallantoic membrane at the days 9, 10 and 11 of incubation. Quantitative evaluation of the lead concentration assessed by furnace atomic absorption spectrophotometry at the days 14 and 21 of incubation demonstrated metal presence both in the chorioallantoic membrane (CAM) and in metanephros (MN). The lead concentration was higher in CAM than in MN; the metal amount was similar in the CAM of 14 and 21 day embryos, but significantly higher in the 14day embryo MN than in the 21 day embryo MN. Morphological observations on metanephros tissue of control and lead-treated embryos were performed under light, electron transmission and electron scanning microscopes. Peculiar attention was devoted to the expression of the junctional protein connexin 43, the major component of the gap junctions in the renal cells. The results indicated that lead treatment does not intervene in the general differentiation of the metanephric nephrons. The lead is reabsorbed by the proximal tubule cells that are engulfed by endocytotic vacuoles and metal deposits and show long term degenerative changes. Expression of Cx43 protein and ultrastructure of gap junctions between proximal tubule cells appeared to be unchanged. The morphological aspects of the MN corpuscles and tubules agree with the suggestion of a lead cytotoxic effect but do not corroborate, at least in this experimental model, the view of primary damage exerted by lead on the gap junctions of the renal epithelial cells.