Bisphenol A (BPA) is a chemical found in plastics that resembles oestrogen in organisms. Developmental exposure to endocrine-disrupting chemicals, such as BPA, increases the susceptibility to type 2 diabetes (T2DM) and cardiovascular diseases. Animal studies have reported a nephron deficit in offspring exposed to maternal diabetes. The aim of this study was to investigate the prenatal BPA exposure effects on nephrogenesis in a mouse model that was predisposed to T2DM. This study quantitatively evaluated the renal structural changes using stereology and histomorphometry methods. The OF1 pregnant mice were treated with a vehicle or BPA (10 or 100 μg/kg/day) during days 9-16 of gestation (early nephrogenesis). The 30-day-old offspring were sacrificed, and tissue samples were collected and prepared for histopathological and stereology studies. Glomerular abnormalities and reduced glomerular formation were observed in the BPA offspring. The kidneys of the BPA10 and BPA100 female offspring had a significantly lower glomerular number and density than those of the CONTROL female offspring. The glomerular histomorphometry revealed a significant difference between the female and male CONTROL offspring for the analysed glomerular parameters that disappeared in the BPA10 and BPA100 offspring. In addition, the kidney histopathological examination showed typical male cuboidal epithelial cells of the Bowman capsule in the female BPA offspring. Exposure to environmentally relevant doses of BPA during embryonic development altered nephrogenesis. These structural changes could be associated with an increased risk of developing cardiometabolic diseases later in life.

Hyperglycemia characteristic of diabetes mellitus triggers pathological processes in fetal development of various structures such as the retina, peripheral nerves, renal glomerulus, and arterial and venous beds. Women with diabetes prior to conception have children with birth defects three to five times more frequently than women without diabetes. There is no specific pattern of birth defects, but the central nervous and cardiovascular systems are the most affected. Hyperglycemia leads to mitochrondrial superoxide radical production, which activates five metabolic pathways that mediate damage leading to diabetic embryopathy. Once oxidative stress is established, there is modification of gene expression controlling embryonic development in critical periods. Vitamin E application in animal models has greatly lowered occurrence of birth defects in embryonic and fetal stages, consistent with an etiologic role for oxidative stress in dysmorphogenesis. Effective metabolic control before and during pregnancy, achieved in Cuba by implementing programs for control of birth defects in children of diabetic pregnant women, has been found effective.

Background: Previous studies have shown alpha-tocopherol favorable effects on biochemical markers of kidney function and tissue damage in experimental models of diabetes. However, few reports highlight its effect in organ morphology and even less its impact during pregnancy. The main goal of this study was to evaluate the effect of alpha-tocopherol supplementation on the renal tissue morphology of diabetic pregnant rats. Methods: Diabetes was induced in female Wistar rats after intraperitoneal administration of streptozotocin. Healthy rats without any preparation were used as control subjects. Diabetic and control rats were grouped by receiving oral alpha-tocopherol 150 mg/kg/day or the vehicle during pregnancy. Euthanasia was practiced by bleeding under anesthesia at 20 days of gestation. Metabolic markers in plasma were analyzed and the kidney cortex morphology was studied by optical and electron microscopy. Statistic studies were performed using Kruskal Wallis, U Mann-Withney, Dunn and Fisher tests; significant differences were considered with p<0.05. Results: Diabetic rats presented a lower weight gain than the control group, hyperglycemia, hypercholesterolemia and morphological alterations on renal cortex, with increase in glomerular volume and 70% of tubular damage. A lower incidence of kidney lesions was observed in diabetic rats that received alpha-tocopherol, with similar glomerular volumes to the control and improved of tubular cells with only 36% of damage. Conclusions: The administration of alpha-tocopherol to diabetic rats during gestation showed a protective effect on the morphology kidney. This result would be related to the antioxidant action of alpha-tocopherol, but further studies are needed to confirm this.