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: 5.74). 10/2010; 49(7):1147-51. DOI: 10.1016/j.freeradbiomed.2010.07.011
Source: PubMed


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.

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    • "Embryonic development entails the complex interaction of fundamental cellular processes such as proliferation , differentiation, migration, and cell death. Over the past years, the involvement of cellular redox state as well as redox regulation pathways in the fine modulation of these processes has been clearly established (Covarrubias et al., 2008; Dennery, 2010; Hernandez- Garcia et al., 2010). In the context of CNS development, Prdx1 has been directly linked to spinal motor neuron differentiation through its interaction with GDE2 (Yan et al., 2009). "
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    ABSTRACT: Reactive oxygen and nitrogen species (ROS/RNS) are natural byproducts of cellular metabolism. Though these molecules are deleterious at high concentrations, moderate levels of ROS/RNS are essential to normal cell function and take part in numerous cellular processes. The regulation of ROS/RNS is largely attended by peroxiredoxins (Prdxs) and their main reductants, thioredoxins (Trxs). Through their oxidoreductase activities, the members of the Trx/Prdx system can also affect certain cellular processes, notably implicated in central nervous system (CNS) development. Although several studies have investigated the expression of Prdxs and Trxs in mouse, rat and human adult CNS, few data are available concerning embryonic stages. In this work, we used immunofluorescence analyses to study the distribution of these enzymes during prenatal mouse spinal cord development. Our results highlight several patterns that contrast with available data in the adult. Indeed, Prdx1, Prdx4 and Prdx6 which are expressed in glial cells in the adult CNS, present clear neuronal localization in mouse spinal cord during embryonic development. Additionally, Prdx1, Prdx2 and to a lesser extent Prdx4, Prdx6 and Trx1 are mainly localized in the nucleus of neural cells. Finally, we identified a consistent intense expression of all Prdxs and Trxs in groups of cells located in ventral regions of the spinal cord that express motor neuronal markers. These striking expression patterns suggest novel functions of these enzymes at these stages and offer clues as to the role of Trx/Prdx system during the embryonic development of the spinal cord. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    The Journal of Comparative Neurology 05/2015; DOI:10.1002/cne.23807 · 3.23 Impact Factor
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    • "The throughput of reactive oxygen increases along PE developing during the pregnancy. This may lead to OS (Dennery 2010). The most important enzymatic oxidants are catalase, superoxide dismutase, glutathione-S-transferase, glutathione reductase and glutathione peroxidase (Kaur et al. 2008). "
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    ABSTRACT: Pre-eclampsia is a serious pathological state affecting 5-10% of pregnant women. Currently, it is diagnosed in the second half of pregnancy, particularly after the 20th week. Symptoms mostly correspond to the changes of blood vessels and kidneys. The severity of pre-eclampsia is proportional to symptomatic manifestations, thus the more symptoms present, the higher is of pre-eclampsia development. Although there are several studies dealing with pre-eclampsia pathology, the complete etiology is still unknown. In this review paper, several theories are presented and discussed.
    Brazilian Archives of Biology and Technology 10/2014; 57(5):701-705. DOI:10.1590/S1516-8913201402449 · 0.55 Impact Factor
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    • "In the kidneys of both humans and experimental models, developmental programming reduces nephron numbers, alters the renin-angiotensin system (RAS), and impairs natriuresis, leading to adult kidney disease and hypertension [2] [3] [4] [5]. A number of hypotheses have been proposed to explain the developmental programming phenomenon [6]. Oxidative stress is proposed as the underlying link between developmental programing and elevated risks of hypertension and kidney disease in adulthood [7] [8]. "
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    ABSTRACT: Nitric oxide (NO) deficiency is involved in the development of hypertension, a condition that can originate early in life. We examined whether NO deficiency contributed to programmed hypertension in offspring from mothers with calorie-restricted diets and whether melatonin therapy prevented this process. We examined 3-month-old male rat offspring from four maternal groups: untreated controls, 50% calorie-restricted (CR) rats, controls treated with melatonin (0.01% in drinking water), and CR rats treated with melatonin (CR + M). The effect of melatonin on nephrogenesis was analyzed using next-generation sequencing. The CR group developed hypertension associated with elevated plasma asymmetric dimethylarginine (ADMA, a nitric oxide synthase inhibitor), decreased L-arginine, decreased L-arginine-to-ADMA ratio (AAR), and decreased renal NO production. Maternal melatonin treatment prevented these effects. Melatonin prevented CR-induced renin and prorenin receptor expression. Renal angiotensin-converting enzyme 2 protein levels in the M and CR + M groups were also significantly increased by melatonin therapy. Maternal melatonin therapy had long-term epigenetic effects on global gene expression in the kidneys of offspring. Conclusively, we attributed these protective effects of melatonin on CR-induced programmed hypertension to the reduction of plasma ADMA, restoration of plasma AAR, increase of renal NO level, alteration of renin-angiotensin system, and epigenetic changes in numerous genes.
    Oxidative medicine and cellular longevity 04/2014; 2014:283180. DOI:10.1155/2014/283180 · 3.36 Impact Factor
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