Article

Oxidative stress in development: nature or nurture?

Department of Pediatrics, University of Pennsylvania School of Medicine, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.
Free Radical Biology and Medicine (Impact Factor: 5.71). 10/2010; 49(7):1147-51. DOI: 10.1016/j.freeradbiomed.2010.07.011
Source: PubMed

ABSTRACT An unavoidable consequence of aerobic respiration is the generation of reactive oxygen species (ROS). These may negatively impact development. Nevertheless, a certain amount of oxidative stress is required to allow for the normal progression of embryonic and fetal growth. Alterations in placental oxidative stress results in altered placental function and ultimately altered fetal growth and/or developmental programming leading to long-term consequences into adulthood. This article reviews the role of redox in fetal development and will focus on how developmental programming is influenced by the fetal and placental redox state as well as discuss potential therapeutic interventions.

0 Followers
 · 
139 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: This paper aimed to clarify whether maternal inhalation of engineered nanoparticles (NP) may constitute a hazard to pregnancy and fetal development, primarily based on experimental animal studies of NP and air pollution particles. Overall, it is plausible that NP may translocate from the respiratory tract to the placenta and fetus, but also that adverse effects may occur secondarily to maternal inflammatory responses. The limited database describes several organ systems in the offspring to be potentially sensitive to maternal inhalation of particles, but large uncertainties exist about the implications for embryo-fetal development and health later in life. Clearly, the potential for hazard remains to be characterized. Considering the increased production and application of nanomaterials and related consumer products a testing strategy for NP should be established. Due to large gaps in data, significant amounts of groundwork are warranted for a testing strategy to be established on a sound scientific basis. Copyright © 2015. Published by Elsevier Inc.
    Reproductive Toxicology 06/2015; 11. DOI:10.1016/j.reprotox.2015.05.015 · 2.77 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: PurposeIncreasing evidence exists that maternal obesity and overnutrition (MO) during pregnancy and lactation have long-lasting consequences for progeny metabolism, cardiovascular and endocrine function. Data on effects of MO on offspring reproduction are limited. We hypothesized that MO during pregnancy and lactation in founder F0 rat mothers would increase testicular and sperm oxidative stress (OS) and adversely impact male fertility in their F1 offspring.Methods We induced pre-pregnancy MO by feeding F0 females a high fat diet from weaning through pregnancy and lactation. After weaning all F1 rats ate control (C) diet. We determined serum testosterone, malonaldialdehyde (MDA), reactive oxygen species (ROS), and superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity in F1 testes and sperm at postnatal days (PND) 110, 450 and 650.ResultsAt PND 450 and 650 MO offspring had lower LH while testosterone levels were lower at all ages. Testicular MDA and ROS concentrations and SOD and GPx activity were higher in MO F1 at all ages. Nitrotyrosine immunostaining was higher at all ages in MO F1 testes than C F1. At PND 450 and 650, MO F1 spermatozoa showed higher MDA concentrations and lower SOD and GPx activity with reduced sperm concentration, viability and motility and more sperm abnormalities. Fertility rate was not affected at PND 110 but was lower in MO F1 at PND 450 and 650.Conclusions We conclude that MO during pregnancy and lactation increases F1 testicular and sperm OS leading to premature aging of reproductive capacity.International Journal of Obesity accepted article preview online, 15 December 2014. doi:10.1038/ijo.2014.209.
    International journal of obesity (2005) 12/2014; 39(4). DOI:10.1038/ijo.2014.209 · 5.39 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective: In offspring with intrauterine growth restriction (IUGR), where oxidative stress may play an important role in inducing metabolic syndrome, nutrition restriction has been shown to improve oxidative status. In this study, we aimed to investigate the effect of postnatal nutrition restriction on the oxidative status of IUGR neonates. Methods: A total of twelve pairs of piglets, of normal birth-weight (NBW) and with IUGR (7 days old), respectively, were randomly allocated to have adequate nutritional intake (ANI) and restricted nutritional intake (RNI) for a period of 21 days, respectively. This design produced 4 experimental groups: NBW-ANI, IUGR-ANI, NBW-RNI and IUGR-RNI (n = 6 per group). Serum, ileum and liver samples were analyzed for antioxidant parameters and the mRNA expression of genes with regard to oxidative status. The data were subjected to general linear model analysis and Duncan's test with a 5% significance level. Results: Irrespective of nutritional intake, the IUGR pigs had markedly lower activity of glutathione peroxidase (GPX), gene expressions of liver mitochondrial manganese superoxide dismutase (Mn-SOD) and ileum cytoplasmic copper/zinc (CuZn)-SOD and, accordingly, there was a markedly higher malondialdehyde concentration in the liver of these pigs compared to in the NBW pigs. Irrespective of body weight, pigs receiving ANI treatment had significantly lower activities of antioxidant enzymes in the serum (total antioxidative capability, CuZn-SOD and GPX) and liver (total SOD and glutathione reductase) and decreased gene expression of liver CuZn-SOD and Mn-SOD compared to the pigs receiving RNI. In addition, the IUGR pigs had a markedly lower concentration of liver reduced glutathione (GSH), ratio of GSH to oxidized glutathione, gene expression of ileum CuZn-SOD and extracellular SOD than the NBW pigs when receiving ANI, but not all of these differences were observed in those receiving RNI. Conclusion: IUGR neonates may have poor antioxidant defense systems, and postnatal nutrition restriction has the potential to prevent oxidative stress. © 2014 S. Karger AG, Basel.
    Neonatology 11/2014; 107(2):93-99. DOI:10.1159/000368179 · 2.37 Impact Factor