ArticlePediatric nephrology (Berlin, Germany)2011
Alpha-tocopherol prevents intrauterine undernutrition-induced oligonephronia in rats.
Article in Pediatric nephrology (Berlin, Germany), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 17 citations in OpenAlex.
- Preterm Birth and Kidney Health: From the Womb to the Rest of Life.Children (Basel, Switzerland) · 2024Review
- Implication of Oxidative Stress in Fetal Programming of Cardiovascular Disease.Frontiers in physiology · 2018Review
- Developmental Origins of Chronic Kidney Disease: Should We Focus on Early Life?International journal of molecular sciences · 2017Review
- How the kidney is impacted by the perinatal maternal environment to develop hypertension.Biology of reproduction · 2013Review
- Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of α-tocopherol during nephrogenesis was investigated in rats subjected to maternal undernutrition, which reduces the number of nephrons. α-tocopherol (350 mg/kg, p.o.) was administered daily to well-nourished or malnourished Wistar dams during pregnancy, or to prenatal undernourished rats during lactation. The kidneys of 1- and 25-day-old offspring were removed to evaluate expression of angiotensin II (Ang II) and to correlate this with expression of proliferating cell nuclear antigen, α-smooth muscle actin, fibronectin and vimentin in the glomeruli and tubulointerstitial space. One-day-old prenatally undernourished rats had reduced expression of Ang II and of kidney development markers, and presented with an enlarged nephrogenic zone. Maternal administration of α-tocopherol restored the features of normal kidney development in undernourished rats. Twenty-five-day-old prenatally undernourished progeny had fewer glomeruli than the control group. Conversely, animals from mothers that received α-tocopherol during lactation presented with the same number of glomeruli and the same glomerular morphometrical profile as the control group. Analyzing the levels of thiobarbituric acid reactive substances in the liver in conjunction with kidney development markers, it is plausible that α-tocopherol had antioxidant and non-antioxidant actions. This study provides evidence that α-tocopherol treatment restored Ang II expression, and subsequently restored renal structural development.
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