Renal morphological alterations induced by perinatal exposure to Di(2-ethylhexyl) phthalate: analysis of an experimental model

The high human exposure to Di(2-ethylhexyl) phthalate (DEHP), a synthetic chemical used to provide flexibility, transparency, and durability to plastic materials, could induce chronic kidney disease. Until now, studies have focused on evaluating the effects of DEHP on oxidative stress in renal tubul...

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Autores principales: Moyano, F, Faure, E, Pérez, P, Gutierrez, S, Mukdsi , J
Formato: Artículo revista
Lenguaje:Español
Publicado: Universidad Nacional Córdoba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología 2023
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Acceso en línea:https://revistas.unc.edu.ar/index.php/med/article/view/42700
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Sumario:The high human exposure to Di(2-ethylhexyl) phthalate (DEHP), a synthetic chemical used to provide flexibility, transparency, and durability to plastic materials, could induce chronic kidney disease. Until now, studies have focused on evaluating the effects of DEHP on oxidative stress in renal tubular epithelial cells in adult animal models. The objective of our research was to analyze and characterize the renal morphological alterations induced by perinatal exposure to DEHP. To achieve this, a perinatal exposure model to DEHP (200 μg/kg/day) was used in both male and female Wistar rats (n: 9/sex), with rats of the same strain exposed to corn oil used as controls (n: 9/sex). The employed methodologies included photonic microscopy (10% formaldehyde fixative in 0.1M PBS, paraffin embedding, and 3 μm sections stained with H&E, PAS, and Masson's Trichrome), as well as transmission electron microscopy (4% Karnovsky fixative, epoxy resin embedding, heavy metal salt contrast, observation using a Zeiss Leo 906-E electron microscope). Through photonic microscopy, and only in the animals exposed to DEHP, multisegmented adherence of the glomerular capillary tuft to Bowman's capsule was observed. At the tubular level, signs of acute tubular damage were prominent, with small areas of interstitial fibrosis being relevant, irregularly distributed within the organ parenchyma. Ultrastructural study identified changes in podocytes and glomerular basement membrane (GBM). Mild and multisegmented pedicel fusion was observed, along with discrete folding and changes in the texture of GBMs. Fenestrations and the honeycomb appearance of the glomerular endothelium were preserved in all groups. This study allows us to conclude that early (perinatal) exposure to DEHP induces renal morphological changes which, although mild and with focal and segmental distribution, affect the glomerular and tubulointerstitial compartments. These changes could serve as a triggering factor for progressive kidney damage.