Effects Of Chronic Prenatal Exposure Research Articles

Effect of chronic prenatal exposure to the food additive titanium dioxide E171 on respiratory activity in newborn mice.

Nanoparticles (NPs) possess unique properties that make their use valuable in all industries. Titanium dioxide (TiO2) NPs are extensively used as a white pigment in food (labeled under the European number E171) and personal care products, which creates a significant potential for chronic consumer exposure. Concerns about the potential toxic effects of TiO2 NPs have arisen, particularly in vulnerable populations, including pregnant women and infants. Recently, human materno-fetal transfer of E171 was demonstrated, and simultaneously, we reported that chronic prenatal exposure to reference P25 TiO2 NPs was found to alter the developing respiratory neural networks. In this study, using whole body plethysmography from postnatal day (P) 0 to P7, we assessed the respiratory function of newborn mice born to mothers fed with E171 during pregnancy. We also evaluated the potential alterations to respiratory centers by using brainstem-spinal cord electrophysiological recordings from P0 to P6. Our study reveals that E171-prenatally exposed animals displayed an abnormally elevated breathing rate from P3 onwards. From P5 to P6, the respiratory-related burst frequency generated by the isolated brainstem-spinal cord preparations was significantly higher in E171-exposed animals than in non-exposed animals. These findings demonstrate prenatal toxicity of E171 to the developing respiratory function and may contribute to policy-making regarding the use of TiO2 NPs.

In vitro cellular and proteome assays identify Wnt pathway and CDKN2A-regulated senescence affected in mesenchymal stem cells from mice after a chronic LD gamma irradiation in utero

Reliable data on the effects of chronic prenatal exposure to low dose (LD) of ionizing radiation in humans are missing. There are concerns about adverse long-term effects that may persist throughout postnatal life of the offspring. Due to their slow cell cycle kinetics and life-long residence time in the organism, mesenchymal stem cells (MSCs) are more susceptible to low level genotoxic stress caused by extrinsic multiple LD events. The aim of this study was to investigate the effect of chronic, prenatal LD gamma irradiation to the biology of MSCs later in life. C3H mice were exposed in utero to chronic prenatal irradiation of 10 mGy/day over a period of 3 weeks. Two years later, MSCs were isolated from the bone marrow and analyzed in vitro for their radiosensitivity, for cellular senescence and for DNA double-strand break recognition after a second acute gamma-irradiation. In addition to these cellular assays, changes in protein expression were measured using HPLC–MS/MS and dysregulated molecular signaling pathways identified using bioinformatics. We observed radiation-induced proteomic changes in MSCs from the offspring of in utero irradiated mice (leading to ~ 9.4% of all detected proteins being either up- or downregulated) as compared to non-irradiated controls. The proteomic changes map to regulation pathways involved in the extracellular matrix, the response to oxidative stress, and the Wnt signaling pathway. In addition, chronic prenatal LD irradiation lead to an increased rate of in vitro radiation-induced senescence later in life and to an increased number of residual DNA double-strand breaks after 4 Gy irradiation, indicating a remarkable interaction of in vivo radiation in combination with a second acute dose of in vitro radiation. This study provides the first insight into a molecular mechanism of persistent MSC damage response by ionizing radiation exposure during prenatal time and will help to predict therapeutic safety and efficacy with respect to a clinical application of stem cells.

Modulation of Some Insulin Signaling Genes Due to Prenatal Rice Consumption

Objective: A clinically observable metabolic disorder often takes its root from modulation of transcriptional factors which in turn are responsible for perturbed protein expressions and their sequelae. Perinatal perturbations due to chronic prenatal exposure to a certain type of rice could predispose parents exposed to such ‘insult’ and their subsequent offsprings to metabolic diseases.
 Materials and Methods: We investigated the effect of chronic prenatal exposure to different types of rice (in context of a balanced normal diet and a high-fat diet) on some insulin signaling genes using nulliparous Sprague Dawley rats. The rats were exposed to various predetermined rice diets for 90 days. After returning them to standard chow, they were mated with male rats raised on standard chow. The resulting pups (F1) and dams were sacrificed and their tissues were examined for modulation of genes related to insulin signaling.
 Results: Our results show that dams fed with white rice in context of standard diet modulated MAPK 1 , M A F A 1 and S L C 2 A 2 . Also, germinated brown rice prevented dysregulation of MAPK1, and SLC2A2 in both dams and pups exposed to this diet in the context of a high-fat diet. In general, germinated brown rice retarded dysregulations due to high-fat diet exposure while white rice enhanced the dysregulatory effects of high-fat diet.
 Conclusion: We conclude that chronic prenatal exposure to a certain type of rice, could be a factor to modulation of some genes related to insulin signaling pathways and that these modulation could be inherited by at least one generation of offsprings.

Effects of psychological or physical prenatal stress on attention and locomotion in juvenile rats

Background: Prenatal stress has been shown to affect the cognition of offspring, including memory and learning abilities.Methods: In the current study, the long-term effects of chronic prenatal exposure to the physical or psychological stress on locomotion and attention were evaluated by using open field test (OFT) and prepulse inhibition (PPI) of the acoustic startle reflex (ASR). In addition, the level of corticosterone was measured after the ASR trial.Results: Male and female rodents that underwent prenatal physical and psychological stress had an augmented velocity in OFT, and only male animals showed an increased ASR. Neither male nor female offsprings had an alteration in the level of corticosterone and PPI values regardless of the stress type.Conclusion: Our results revealed that exposure to stress during the development of fetus increases ASR in a sex-dependent manner. This finding might implicate the effect of prenatal stress on attention in male offspring regardless of the stress type.

Long term effects of chronic prenatal exposure to hypercarbia on organ growth and cardiovascular responses to adrenaline and hypoxia in common snapping turtles

Reptilian embryos often face challenging environmental gas compositions during incubation, which may inflict long-lasting effects in the individuals' physiological responses. These conditions can have a lasting effect on the animal into juvenile life as chronic prenatal exposure to hypercarbia results in enlarged hatchling organ size, higher growth rate and resting metabolic rate, although relatively smaller increment in metabolic scope during digestion. Therefore, we wanted to verify whether prenatal hypercarbia exposure would cause persistent effects on morphology and physiological responses in C. serpentina. We measured organ masses and cardiovascular parameters in five years old turtles incubated either under 3.5% hypercarbia (H3.5) or normoxia (N21). We expected that: i) organ masses of H3.5 would be bigger than N21; ii) acute exposure to hypoxia should decrease blood flows in H3.5, since metabolic scope is presumably reduced in this group. As hypoxia exposure elicits catecholamine release, we also tested cardiovascular responses to adrenaline injection. Lungs and stomach exhibited higher growth rates in H3.5. Divergent cardiovascular responses between groups to adrenaline injection were observed for heart rate, pulmonary blood flow, pulmonary mean arterial pressure, blood shunt, systemic stroke volume, and stomach perfusion. Hypoxia caused decreased systemic blood flow and cardiac output, systemic and total stroke volume, and systemic vascular conductance in H3.5. These variables were unaffected in N21, but pulmonary flow and stroke volume, and stomach blood perfusion were reduced. These data support the hypothesis that exposure to hypercarbia during embryonic development has long term effects on organ morphology and cardiovascular responses of C. serpentina.

Brain growth spurt-prenatal ethanol exposure and the guinea pig hippocampal glutamate signaling system

This study tested the hypothesis that prenatal ethanol exposure (PEE) during the brain growth spurt (BGS) in the guinea pig suppresses the glutamate–NMDA receptor–nitric oxide synthase (NOS) signaling system in the developing hippocampus. Pregnant guinea pigs [term, about gestational day (GD) 68] received daily oral administration of 2 g ethanol/kg maternal body weight/day on GD 43 and/or GD 44 and then 4 g ethanol/kg maternal body weight/day from GD 45 to GD 62, isocaloric-sucrose/pair-feeding or water. Offspring were studied at GD 63 (near-term fetus) and postnatal day (PD) 10 (young postnatal life). Maternal blood ethanol concentration during ethanol treatment, pregnancy outcome variables, no change in spontaneous locomotor activity, and decreased brain and cerebral cortical weight data were reported previously [Neurotoxicol. Teratol. 23 (2001) 355]. This BGS-PEE regimen did not affect hippocampal stimulated glutamate release in young postnatal offspring, NMDA receptors as assessed by [ 3H]MK-801 binding, or NOS activity in near-term fetal offspring. Furthermore, BGS-PEE did not affect the number of hippocampal CA1 and CA3 pyramidal cells and dentate gyrus granule cells in defined locations of these three regions in the hippocampal formation. These findings are in contrast to the effects of chronic prenatal exposure to this ethanol regimen throughout gestation, including suppression of the hippocampal glutamate–NMDA receptor–NOS signaling system, decreased number of hippocampal CA1 pyramidal cells, increased spontaneous locomotor activity, and impaired performance in the Morris water maze.

The effects of chronic prenatal exposure to nicotine on the behavior of guinea pigs (Cavia porcellus).

Three groups of 15 offspring from guinea pig dams were injected twice daily throughout gestation with one of three doses (0.5, 1.5 or 2.5 mg/kg) of nicotine-hydrogen tartrate. These offspring and 15 saline-exposed offspring were tested on several behavioral measures. Offspring of nicotine-treated dams had significantly lower rates of spontaneous alternation as neonates. The 1.5 and 2.5 mg/kg nicotine-exposed offspring also alternated less at puberty than control offspring and would not enter an unfamiliar stimulus alley that a majority of controls entered. Nicotine offspring, as adults, performed significantly poorer than their controls on errors and trials to criterion on a discrimination and reversal task. Prenatal nicotine treatment resulted in performance deficits on both learned and innate behavioral measures throughout development and adulthood.

Postnatal Functional Analysis of Prenatal Exposure of Rats to 915 MHz Microwave Radiation

Thirty pregnant Wistar strain albino rats were used to determine the effects of chronic prenatal exposure to 915 MHz microwave radiation at a continuous wave power density level of 10 mW/cm2 on postnatal growth and neurobehavioral development. Eleven rats were irradiated in a fully characterized anechoic chamber from days 1 to 21 of gestation. Mean total exposure time was 6544 min. Nineteen rats were used as control animals. All animals delivered and raised their offspring (F1a) until weaning at 30 days of age Ten days later females were rebred and a standard teratologic evaluation was completed on the resultant F1b fetuses. Maternal brain, liver, kidneys, and ovaries were removed, weighed, examined, and fixed in formalin. The F1a (irradiated) neonates were given four perinatal reflex tests (surface righting, air righting, auditory startle, visual placing). One physiological parameter, eye opening, was also observed. Weekly weights were recorded throughout the study period. At 60 days of age the offspring were randomly given 3 of 6 tests (conditioned avoidance response, water T-maze, open field, activity wheel, forelimb hanging, swimming). At 90 days of age reproductive capability was evaluated and a standard teratologic analysis performed on the resultant F2 offspring. The brain, liver, kidneys, and gonads of all F1a offspring were removed, weighed, examined, and fixed in formalin. No significant morphologic or neurobehavioral alterations were observed due to chronic prenatal exposure to 915 MHz microwave radiation at a continuous wave power density level of 10 mW/cm2.

Results of prenatal alcohol exposure on the dimensions and binucleation of cardiac myocytes in neonatal and weanling rats

Sprague-Dawley rats were exposed to ethyl alcohol in utero. The effect of chronic prenatal exposure was examined by giving mature females alcohol in isocaloric liquid diets which served as the sole source of liquid and caloric intake before mating and throughout gestation. Controls consisted of females maintained on laboratory chow or an isocaloric liquid diet minus alcohol before and during gestation. The offspring were sacrificed at 21 days of age (weanlings) and the hearts dissociated enzymatically to give purified cardiac myocytes. The effects of daily acute prenatal alcohol exposure were studied by gastric intubation of alcohol to chow-fed females for the duration of pregnancy. The doses used approximated 4 and 5 shots of 80 proof liquor per day by a person weighing 150 lb. These offspring were sacrificed at 2, 6, and 21 days postnatal and cardiac myocytes prepared as above. Heart weights were determined and cardiac myocytes were analyzed for cell length, volume, cross-sectional area, and percent binucleation. Additionally, nuclear DNA content was measured in all of the 21 day offspring. Statistical analysis of the data showed no significant differences between hearts exposed to prenatal alcohol and nonexposed controls with either regimen with the exception of percent binucleation which was significantly but only slightly higher in the 6-day-old hearts. These findings are discussed in relation to anatomical heart defects found in patients with full fetal alcohol syndrome.

The effects of chronic prenatal exposure to dietary msg on later development, behavior and brain histology of rat offspring

International Journal of Developmental NeuroscienceVolume 3, Issue 4 p. 459-459 Neurotrophic Factor and Metabolic Aspect The effects of chronic prenatal exposure to dietary msg on later development, behavior and brain histology of rat offspring V.E. Grimm, V.E. GrimmSearch for more papers by this authorB. Frieder, B. FriederSearch for more papers by this author V.E. Grimm, V.E. GrimmSearch for more papers by this authorB. Frieder, B. FriederSearch for more papers by this author First published: 1985 https://doi.org/10.1016/0736-5748(85)90189-3AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume3, Issue41985Pages 459-459 RelatedInformation