There is increasing evidence that environmental exposures early in fetal development influence phenotype and give rise to disease risk in the next generations. We previously found that lifelong exposure to uranium, an environmental contaminant, induced subtle testicular and hormonal defects; however, its impact on the reproductive system of multiple subsequent generations was unexplored. Herein, rats were exposed to a supra-environmental and non-nephrotoxic concentration of natural uranium (U, 40 mg·L of drinking water) from postnatal life to adulthood (F0), during fetal life (F1), and only as the germ cells from the F1 generation (F2).
View Article and Find Full Text PDFPurpose: A protocol of chronic exposure to low dose of uranium was established in order to distinguish the sexual differences and the developmental process that are critical windows for epigenetic effects over generations.
Methods: Both male and female rats were contaminated through their drinking water with a non-toxic solution of uranyl nitrate for 9 months. The exposed generation (F0) and the following two generations (F1 and F2) were examined.
We recently reported augmentation of lipid peroxidation products in the liver of intrauterine growth-restricted (IUGR) piglets fed a high load of Maillard reaction products (MRPs) during suckling period. The underlying mechanisms of MRPs effects remain unknown. Here, we studied the long-term impact of MRPs exposure on liver oxidative status of IUGR juvenile pigs.
View Article and Find Full Text PDFIntroduction: An increased health problem in industrialised countries is the contemporary concern of public and scientific community as well. This has been attributed in part to accumulated environmental pollutants especially radioactive substances and the use of nuclear power plants worldwide. However, the outcome of chronic exposure to low doses of a radionuclide such as uranium remains unknown.
View Article and Find Full Text PDFIncreasing evidence indicates that chlorpyrifos (CPF), an organophosphorus insecticide, is involved in metabolic disorders. We assess the hypothesis whether supplementation with prebiotics from gestation to adulthood, through a modulation of microbiota composition and fermentative activity, alleviates CPF induced metabolic disorders of 60 days old offspring. 5 groups of Wistar rats, from gestation until weaning, received two doses of CPF pesticide: 1 mg/kg/day (CPF1) or 3.
View Article and Find Full Text PDFObjective: the present study has been conducted to evaluate the impact of the consumption of high MRP formula on changes in the microbiota and the oxidative status, during development, in the colons of intrauterine growth restricted (IUGR) juvenile pigs.
Methods: over a 3-week period, fifteen-day old piglets received formula with two different heat treatments. A formula heated at high temperature (HHF, n = 8) and another one heated at a low temperature (LHF, n = 8).
Scope: Formula-derived dietary advanced glycation end products (AGEs) may promote programming of inflammation and oxidative stress in the kidney of intrauterine growth retardation (IUGR) piglets.
Methods And Results: IUGR piglets received either a low temperature heated formula (n = 8) or a high temperature heated formula (HHF: n = 8) or suckled naturally for 3 wk postnatally. Then they were fed with normal ad libitum regular diet.
Aim. Chronic diseases are the leading cause of death worldwide. Advanced glycation end products, known as AGEs, are a major risk factor for diabetes onset and maintenance.
View Article and Find Full Text PDFNutritional insults during developmental plasticity have been linked with metabolic diseases such as diabetes in adulthood. We aimed to investigate whether a low-protein (LP) diet at the beginning of adulthood is able to program metabolic disruptions in rats. While control rats ate a normal-protein (23%; NP group) diet, treated rats were fed a LP (4%; LP group) diet from 60 to 90 days of age, after which an NP diet was supplied until they were 150 days old.
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