ascorbic-acid and Fetal-Growth-Retardation

Vitamin C supplementation may help reduce the risk of pregnancy complications such as pre-eclampsia, intrauterine growth restriction and maternal anaemia. There is a need to evaluate the efficacy and safety of vitamin C supplementation in pregnancy.. To evaluate the effects of vitamin C supplementation, alone or in combination with other separate supplements on pregnancy outcomes, adverse events, side effects and use of health resources.. We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (31 March 2015) and reference lists of retrieved studies.. All randomised or quasi-randomised controlled trials evaluating vitamin C supplementation in pregnant women. Interventions using a multivitamin supplement containing vitamin C or where the primary supplement was iron were excluded.. Two review authors independently assessed trials for inclusion and risk of bias, extracted data and checked them for accuracy.. Twenty-nine trials involving 24,300 women are included in this review. Overall, 11 trials were judged to be of low risk of bias, eight were high risk of bias and for 10 trials it was unclear. No clear differences were seen between women supplemented with vitamin C alone or in combination with other supplements compared with placebo or no control for the risk of stillbirth (risk ratio (RR) 1.15, 95% confidence intervals (CI) 0.89 to 1.49; 20,038 participants; 11 studies; I² = 0%; moderate quality evidence), neonatal death (RR 0.79, 95% CI 0.58 to 1.08; 19,575 participants; 11 studies; I² = 0%), perinatal death (average RR 1.07, 95% CI 0.77 to 1.49; 17,105 participants; seven studies; I² = 35%), birthweight (mean difference (MD) 26.88 g, 95% CI -18.81 to 72.58; 17,326 participants; 13 studies; I² = 69%), intrauterine growth restriction (RR 0.98, 95% CI 0.91 to 1.06; 20,361 participants; 12 studies; I² = 15%; high quality evidence), preterm birth (average RR 0.99, 95% CI 0.90 to 1.10; 22,250 participants; 16 studies; I² = 49%; high quality evidence), preterm PROM (prelabour rupture of membranes) (average RR 0.98, 95% CI 0.70 to 1.36; 16,825 participants; 10 studies; I² = 70%; low quality evidence), term PROM (average RR 1.26, 95% CI 0.62 to 2.56; 2674 participants; three studies; I² = 87%), and clinical pre-eclampsia (average RR 0.92, 95% CI 0.80 to 1.05; 21,956 participants; 16 studies; I² = 41%; high quality evidence).Women supplemented with vitamin C alone or in combination with other supplements compared with placebo or no control were at decreased risk of having a placental abruption (RR 0.64, 95% CI 0.44 to 0.92; 15,755 participants; eight studies; I² = 0%; high quality evidence) and had a small increase in gestational age at birth (MD 0.31, 95% CI 0.01 to 0.61; 14,062 participants; nine studies; I² = 65%), however they were also more likely to self-report abdominal pain (RR 1.66, 95% CI 1.16 to 2.37; 1877 participants; one study). In the subgroup analyses based on the type of supplement, vitamin C supplementation alone was associated with a reduced risk of preterm PROM (average RR 0.66, 95% CI 0.48 to 0.91; 1282 participants; five studies; I² = 0%) and term PROM (average RR 0.55, 95% CI 0.32 to 0.94; 170 participants; one study). Conversely, the risk of term PROM was increased when supplementation included vitamin C and vitamin E (average RR 1.73, 95% CI 1.34 to 2.23; 3060 participants; two studies; I² = 0%). There were no differences in the effects o. The data do not support routine vitamin C supplementation alone or in combination with other supplements for the prevention of fetal or neonatal death, poor fetal growth, preterm birth or pre-eclampsia. Further research is required to elucidate the possible role of vitamin C in the prevention of placental abruption and prelabour rupture of membranes. There was no convincing evidence that vitamin C supplementation alone or in combination with other supplements results in other important benefits or harms.

Topics: Anemia; Ascorbic Acid; Dietary Supplements; Female; Fetal Growth Retardation; Humans; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Pregnancy Complications, Hematologic; Randomized Controlled Trials as Topic; Vitamins

Preeclampsia, intrauterine growth restriction (IUGR), and placental abruption are obstetrical conditions that constitute the syndrome of ischemic placental disease or IPD, the leading cause of indicated preterm birth and an important cause of neonatal morbidity and mortality. While the phenotypic manifestations vary significantly for preeclampsia, IUGR, and abruption, these conditions may share a common underlying etiology as evidenced by: (1) shared clinical risk factors, (2) increased recurrence risk across pregnancies as well as increased co-occurrence of IPD conditions within a pregnancy, and (3) findings that suggest the underlying pathophysiologic processes may be similar. IPD is of major clinical importance and accounts for a large proportion of indicated preterm delivery ranging from the periviable to late preterm period. Successful prevention of IPD and resultant preterm delivery could substantially improve neonatal and maternal outcomes. This article will review the following topics: (1) The complicated research literature on aspirin and the prevention of preeclampsia and IUGR. (2) Research evidence on other medical interventions to prevent IPD. (3) New clinical interventions currently under investigations, including statins. (4) Current clinical recommendations for prevention of ischemic placental disease.

Topics: Abruptio Placentae; Anticoagulants; Ascorbic Acid; Aspirin; Calcium, Dietary; Dietary Supplements; Fatty Acids, Omega-3; Female; Fetal Growth Retardation; Fibrinolytic Agents; Humans; Ischemia; Placenta; Placenta Diseases; Pre-Eclampsia; Pregnancy; Premature Birth; Risk Factors; Vitamin E

Epidemiological studies have suggested that metabolic programming begins during fetal life and adverse events in utero are a critical factor in the etiology of chronic diseases and overall health. While the underlying molecular mechanisms linking impaired fetal development to these adult diseases are being elucidated, little is known about how we can intervene early in life to diminish the incidence and severity of these long-term diseases. This paper highlights the latest clinical and pharmaceutical studies addressing how dietary intervention in fetal and neonatal life may be able to prevent aspects of the metabolic syndrome associated with IUGR pregnancies.

Topics: Antioxidants; Ascorbic Acid; Diet Therapy; Dietary Supplements; Exenatide; Fatty Acids, Omega-3; Female; Fetal Growth Retardation; Folic Acid; Humans; Hypoglycemic Agents; Melatonin; Metabolic Syndrome; Micronutrients; Peptides; Pregnancy; Prenatal Exposure Delayed Effects; Prenatal Nutritional Physiological Phenomena; Resveratrol; Stilbenes; Venoms

Topics: Acidosis; Animals; Ascorbic Acid; Blood Glucose; Brain; Dogs; Drug Therapy, Combination; Embryonic and Fetal Development; Female; Fetal Blood; Fetal Growth Retardation; Fetal Hypoxia; Glucose; Humans; Insulin; Insulin Secretion; Maltose; Maternal-Fetal Exchange; Oxygen Inhalation Therapy; Placenta; Placental Lactogen; Pregnancy; Sheep; Thiamine Pyrophosphate

Supplementation with antioxidant vitamins has been proposed to reduce the risk of preeclampsia and perinatal complications, but the effects of this intervention are uncertain.. We conducted a multicenter, randomized trial of nulliparous women between 14 and 22 weeks of gestation. Women were assigned to daily supplementation with 1000 mg of vitamin C and 400 IU of vitamin E or placebo (microcrystalline cellulose) until delivery. Primary outcomes were the risks of maternal preeclampsia, death or serious outcomes in the infants (on the basis of definitions used by the Australian and New Zealand Neonatal Network), and delivering an infant whose birth weight was below the 10th percentile for gestational age.. Of the 1877 women enrolled in the study, 935 were randomly assigned to the vitamin group and 942 to the placebo group. Baseline characteristics of the two groups were similar. There were no significant differences between the vitamin and placebo groups in the risk of preeclampsia (6.0 percent and 5.0 percent, respectively; relative risk, 1.20; 95 percent confidence interval, 0.82 to 1.75), death or serious outcomes in the infant (9.5 percent and 12.1 percent; relative risk, 0.79; 95 percent confidence interval, 0.61 to 1.02), or having an infant with a birth weight below the 10th percentile for gestational age (8.7 percent and 9.9 percent; relative risk, 0.87; 95 percent confidence interval, 0.66 to 1.16).. Supplementation with vitamins C and E during pregnancy does not reduce the risk of preeclampsia in nulliparous women, the risk of intrauterine growth restriction, or the risk of death or other serious outcomes in their infants. (Controlledtrials.com number, ISRCTN00416244.).

Topics: Adult; Antioxidants; Ascorbic Acid; Dietary Supplements; Female; Fetal Death; Fetal Growth Retardation; Humans; Hypertension; Infant Mortality; Infant, Newborn; Infant, Small for Gestational Age; Parity; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Respiratory Distress Syndrome, Newborn; Risk; Vitamin E

Aldehyde reductase encoded by the Akr1a gene catalyzes the NADPH-dependent reduction of a variety of aldehyde compounds, and it plays a role in the biosynthesis of ascorbic acid (AsA) by converting D-glucuronate to L-gulonate. Although supplementing drinking water with AsA (1.5 mg/mL) ameliorates the fertility of Akr1a

Topics: Aldehyde Reductase; Animals; Animals, Newborn; Ascorbic Acid; Blood Cell Count; Corticosterone; Female; Fetal Growth Retardation; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Pregnancy

Chronic fetal hypoxia is one of the most common outcomes in complicated pregnancy in humans. Despite this, its effects on the long-term health of the brain in offspring are largely unknown. Here, we investigated in rats whether hypoxic pregnancy affects brain structure and function in the adult offspring and explored underlying mechanisms with maternal antioxidant intervention. Pregnant rats were randomly chosen for normoxic or hypoxic (13% oxygen) pregnancy with or without maternal supplementation with vitamin C in their drinking water. In one cohort, the placenta and fetal tissues were collected at the end of gestation. In another, dams were allowed to deliver naturally, and offspring were reared under normoxic conditions until 4 months of age (young adult). Between 3.5 and 4 months, the behavior, cognition and brains of the adult offspring were studied. We demonstrated that prenatal hypoxia reduced neuronal number, as well as vascular and synaptic density, in the hippocampus, significantly impairing memory function in the adult offspring. These adverse effects of prenatal hypoxia were independent of the hypoxic pregnancy inducing fetal growth restriction or elevations in maternal or fetal plasma glucocorticoid levels. Maternal vitamin C supplementation during hypoxic pregnancy protected against oxidative stress in the placenta and prevented the adverse effects of prenatal hypoxia on hippocampal atrophy and memory loss in the adult offspring. Therefore, these data provide a link between prenatal hypoxia, placental oxidative stress, and offspring brain health in later life, providing insight into mechanism and identifying a therapeutic strategy.

Topics: Animals; Animals, Newborn; Antioxidants; Ascorbic Acid; Atrophy; Dietary Supplements; Disease Models, Animal; Female; Fetal Growth Retardation; Fetal Hypoxia; Hippocampus; Male; Memory Disorders; Pregnancy; Pregnancy Complications; Prenatal Exposure Delayed Effects; Rats; Rats, Wistar

Evidence derived from human clinical studies and experimental animal models shows a causal relationship between adverse pregnancy and increased cardiovascular disease in the adult offspring. However, translational studies isolating mechanisms to design intervention are lacking. Sheep and humans share similar precocial developmental milestones in cardiovascular anatomy and physiology. We tested the hypothesis in sheep that maternal treatment with antioxidants protects against fetal growth restriction and programmed hypertension in adulthood in gestation complicated by chronic fetal hypoxia, the most common adverse consequence in human pregnancy. Using bespoke isobaric chambers, chronically catheterized sheep carrying singletons underwent normoxia or hypoxia (10% oxygen [O2]) ± vitamin C treatment (maternal 200 mg.kg-1 IV daily) for the last third of gestation. In one cohort, the maternal arterial blood gas status, the value at which 50% of the maternal hemoglobin is saturated with oxygen (P50), nitric oxide (NO) bioavailability, oxidative stress, and antioxidant capacity were determined. In another, naturally delivered offspring were raised under normoxia until early adulthood (9 months). Lambs were chronically instrumented and cardiovascular function tested in vivo. Following euthanasia, femoral arterial segments were isolated and endothelial function determined by wire myography. Hypoxic pregnancy induced fetal growth restriction and fetal oxidative stress. At adulthood, it programmed hypertension by enhancing vasoconstrictor reactivity and impairing NO-independent endothelial function. Maternal vitamin C in hypoxic pregnancy improved transplacental oxygenation and enhanced fetal antioxidant capacity while increasing NO bioavailability, offsetting constrictor hyper-reactivity and replenishing endothelial function in the adult offspring. These discoveries provide novel insight into mechanisms and interventions against fetal growth restriction and adult-onset programmed hypertension in an animal model of complicated pregnancy in a species of similar temporal developmental milestones to humans.

Topics: Animals; Antioxidants; Ascorbic Acid; Female; Fetal Growth Retardation; Fetal Hypoxia; Hypertension; Hypoxia; Nitric Oxide; Oxidative Stress; Pregnancy; Pregnancy Complications; Prenatal Exposure Delayed Effects; Sheep

The weight of the infant at birth is a powerful predictor of infant growth and survival and is dependent on maternal health and nutrition during pregnancy. Pregnant women have a defense mechanism against increased oxidative stress composed of antioxidant enzymes and natural antioxidant vitamins like vitamin C and E. Therefore, we evaluated whether differences exist in serum levels of vitamin C and E in pregnant women complicated with intrauterine growth restriction (IUGR).. This study was done in 180 pregnant women admitted in hospital for delivery. Blood samples were collected and stored at -70°C until analysis. Among 180 pregnant women 150 were identified as IUGR pregnant women according to the weight of the infant and the remaining 30 normal healthy pregnant women as controls. Blood hemoglobin and serum vitamin C and E levels were measured in both groups.. The mean hemoglobin concentration was significantly decreased (p< 0.001) in IUGR pregnant women (8.92 ± 1.35 g/dL) as compared to the normal healthy pregnant women (10.51 ± 1.04 g/dL) in our study. The serum concentration of vitamin C in the group of pregnant women with IUGR was 0.54 ± 0.15 mg/dL, whereas in the group of normal healthy pregnant women it was 0.91 ± 0.23 mg/dL. The serum vitamin E level in the normal healthy pregnant women group was 1.22 ± 0.35 mg/dL and 0.65 ± 0.24 mg/dL in IUGR pregnant women group. The serum vitamin C and E level in IUGR pregnant women group was found to be significantly decreased as compared to the normal healthy pregnant women group.. The study indicates the importance of natural antioxidants vitamin C and E against increased oxidative stress in pregnancies complicated with IUGR. Therefore, it may be useful to measure serum vitamin C and E levels in IUGR pregnant women. This study suggests further research to investigate the role of these natural antioxidant vitamins in fetal growth at various gestation stages.

Topics: Adult; Antioxidants; Ascorbic Acid; Female; Fetal Growth Retardation; Humans; Oxidative Stress; Pregnancy; Vitamin E; Vitamins

Recently, we reported that preferential maternal-fetal vitamin C (vitC) transport across the placenta is likely to be impaired by prolonged maternal vitC deficiency. Maintenance of a basal maternal vitC supply at the expense of the fetus may impair fetal development; however, the knowledge of vitC's impact on intrauterine development is sparse. The aim of this study was to explore the effect of maternal vitC status on fetal and placental development in guinea pigs.. Twenty pregnant Dunkin Hartley guinea pigs were randomized into four groups to receive diets either sufficient (918 mg/kg CTRL) or deficient (100 mg/kg DEF) in vitC. Cesarean sections at gestational day (GD) 45 or 56 allowed for fetal and placental measurements.. At GD45, body, brain and placental weights were significantly reduced in DEF pups compared with CTRL (p < 0.05, p < 0.001 and p < 0.05, respectively). DEF plasma vitC levels were ~6% of those of CTRL (p < 0.0001), and the fetal/maternal plasma vitC ratio was significantly reduced at GD56 in the DEF animals compared with controls (p = 0.035). Placental vitC levels were reduced in DEF animals (p < 0.0001) and the ascorbate oxidation ratio and glutathione elevated compared with controls (p < 0.0001).. Although no clinical differences between CTRL and DEF pups were observed at GD56, the present data suggest that vitC plays a role in early fetal development. Although no clinical differences between CTRL and DEF pups were observed at GD56, the present data suggest that vitC plays a role in early fetal development. Low maternal vitC intake during pregnancy may compromise maternal weight gain, placental function and intrauterine development.

Topics: Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Diet; Disease Models, Animal; Euthanasia; Female; Fetal Development; Fetal Growth Retardation; Fetus; Guinea Pigs; Linear Models; Maternal Nutritional Physiological Phenomena; Maternal-Fetal Exchange; Placenta; Pregnancy; Sodium-Coupled Vitamin C Transporters

Sheep pregnancy in high-altitude environments frequently involves hypoxia and oxidative stress and causes intrauterine growth retardation. The adverse effects of altitude on fetal growth can be prevented by the administration of antioxidant vitamins, but the mechanisms responsible are not well known. The maintenance of a viable pregnancy depends largely on adequate placental steroidogenesis, especially in the last two-thirds of pregnancy. Thus, in the present study we evaluated the effect of antioxidant vitamins (C and E) on plasma concentrations of progesterone and 17β-oestradiol during the last two-thirds of high-altitude pregnancies in ewes both native and naïve to the high-altitude environment. In addition, pregnancy outcomes were evaluated by determining the bodyweight of newborn lambs. Sex steroid patterns differed between ewes with and without vitamin supplementation. Concentrations of plasma progesterone and 17β-oestradiol were significantly higher in the supplemented groups from approximately 40 days before parturition until near term. Newborn weights were significantly lower in animals not adapted to the higher altitude, and vitamin supplementation prevented this decrease. In conclusion, the administration of antioxidant vitamins in the present study enhanced placental steroidogenesis, thus favouring fetal development in pregnancies developing at high altitudes.

Topics: Altitude; Animals; Ascorbic Acid; Body Weight; Estradiol; Female; Fetal Growth Retardation; Hypoxia; Linear Models; Pregnancy; Progesterone; Sheep; Sheep Diseases; Steroids; Vitamin E

Fetal growth restriction (FGR) describes newborns that were born small for gestational age. The etiology of FGR is unknown, but it is assumed that it is the consequences of both genetic and environmental factors, and that one of the important environmental factors is oxidative stress. In this study we used the Cohen diabetic (CD) rats (sensitive and resistant strains) and the original Sabra strain fed either high sucrose low copper diet-HSD or regular diet-RD to evaluate the genetic and environmental factors contributing to FGR. In addition, we treated the pregnant rats with antioxidants (vitamins C and E added to their food) to evaluate the effects of antioxidants in the prevention of FGR and in changing the redox state of the fetuses.. The study was performed on term 21-day-old fetuses of the three strains fed RD or HSD. Fetal and placental weight and fetal crown rump length were measured. Heart, kidneys, brain and liver were also weighted and studied. The fetal and placental redox status was investigated by studying the levels of Malondialdehyde (MDA) to determine the lipid peroxidation damage and by measuring the activity of catalase (CAT) and superoxide dismutase (SOD) enzymes. Similar studies were performed following the addition of 0.1% of vitamins C and E to the diet.. FGR in the Cohen diabetic rats is a consequence of genetic (6-20% reduction in fetal weight in the CDr and CDs compared to Sabra) and environmental (11-36% reduction in fetal weight while on HSD) factors, with greater susceptibility in the CDs diabetic rats. Increased lipid peroxidation was observed in some of the organs only in HSD, however not only in the sensitive strain. In each organ, different patterns of anti oxidant capacity were observed. The addition of antioxidants to the food significantly reduced the signs of enhanced oxidative stress in all animals but partially restored normal fetal growth only in the diabetic CDs rats. This may imply that in this model oxidative stress is apparently not a major contributor to FGR.. Cohen diabetic rats are a good model for the study of the interaction of genetic and environmental factors in the development of FGR. Maternal nutrition can influence the antioxidant capacity of the fetal organs which is modified by antioxidants. However, FGR in our model does not seem to result primarily from enhanced oxidative stress, as it is only partially affected by the antioxidant treatment. Thus, the repeated observations of oxidative stress in SGA infants may be a resulting metabolic alteration of FGR and not the main cause.

Topics: Animals; Animals, Outbred Strains; Antioxidants; Ascorbic Acid; Catalase; Copper; Diabetes Mellitus, Experimental; Diet; Female; Fetal Growth Retardation; Lipid Peroxidation; Malondialdehyde; Models, Animal; Organ Size; Oxidation-Reduction; Oxidative Stress; Rats; Rats, Inbred Strains; Rats, Wistar; Sucrose; Superoxide Dismutase; Vitamin E

The aim of this study is to determine the oxidant and antioxidant status in Algerian mothers and their newborns according to birth weight.. Subjects for the study were consecutively recruited from Tlemcen hospital. 139 pregnant women and their newborns were included. The plasma total antioxidant activity (ORAC), vitamins A, C, E, hydroperoxides, carbonyl proteins, and erythrocyte antioxidant enzyme activities (catalase, glutathione peroxidase, glutathione reductase and superoxide dismutase) were measured on mothers and their newborns. Lipid and lipoprotein parameters were also determined. The results were assessed in accordance with small for gestational age (SGA), appropriate (AGA) and large (LGA) birth weight of the newborn.. SGA newborns and their mothers had low ORAC, vitamin C and E values (P<0.01) and high plasma hydroperoxide and carbonyl protein levels (P<0.01) compared to AGA groups. The SGA group showed also altered erythrocyte antioxidant enzyme activities and several lipid and lipoprotein changes. In LGA compared to control newborns, hydroperoxide, carbonyl protein levels and SOD activity were enhanced while ORAC, vitamin A and E levels were reduced. However, oxidant and antioxidant status in their mothers was similar to that in control mothers.. Oxidative stress is present in both SGA and LGA newborns, with a concomitant alteration in maternal oxidant and antioxidant status only in intrauterine growth restriction.

Topics: Adult; Antioxidants; Ascorbic Acid; Birth Weight; Catalase; Erythrocytes; Female; Fetal Growth Retardation; Glutathione Peroxidase; Glutathione Reductase; Humans; Infant, Newborn; Infant, Small for Gestational Age; Lipids; Lipoproteins; Male; Oxidants; Oxidative Stress; Pregnancy; Superoxide Dismutase; Vitamin A; Vitamin E

Lipopolysaccharide (LPS) has been associated with adverse developmental outcomes including embryonic resorption, intra-uterine fetal death (IUFD), intra-uterine growth retardation (IUGR) and preterm labor. Reactive oxygen species (ROS) mediate LPS-induced developmental toxicity. Ascorbic acid is an antioxidant. In the present study, we investigated the effect of ascorbic acid on LPS-induced IUFD and IUGR in mice. All ICR pregnant mice except controls received an intraperitoneal (75 microg/kg, i.p.) injection of LPS daily on gd 15-17. The experiment was carried out in three different modes. In mode A, the pregnant mice were pretreated with a single dose (500 mg/kg, i.p.) of ascorbic acid before LPS. In mode B, the pregnant mice were administered with a single dose (500 mg/kg, i.p.) of ascorbic acid at 3h after LPS. In mode C, the pregnant mice were administered with 500 mg/kg (i.p.) of ascorbic acid at 30 min before LPS, followed by additional dose (500 mg/kg, i.p.) of ascorbic acid at 3h after LPS. The number of live fetuses, dead fetuses and resorption sites was counted on gd 18. Live fetuses in each litter were weighed. Crown-rump and tail lengths were examined and skeletal development was evaluated. Results showed that maternally administered LPS significantly increased fetal mortality, decreased fetal weight and crown-rump and tail lengths of live fetuses, and retarded skeletal ossification in caudal vertebrae, anterior and posterior phalanges, and supraoccipital bone. LPS-induced IUFD and IUGR were associated with lipid peroxidation and GSH depletion in maternal liver, placenta and fetal liver. Pre-treatment with ascorbic acid significantly attenuated LPS-induced lipid peroxidation, decreased fetal mortality, and reversed LPS-induced fetal growth and skeletal development retardation. By contrast to pre-treatment, post-treatment with ascorbic acid had less effect on LPS-induced IUFD, although post-treatment significantly attenuated LPS-induced lipid peroxidation and reversed LPS-induced fetal growth and skeletal development retardation. Furthermore, post-treatment with ascorbic acid reduced the protective effects of pre-treatment on LPS-induced IUFD. All these results suggest that pre-treatment with ascorbic acid protected against LPS-induced fetal death and reversed LPS-induced growth and skeletal development retardation via counteracting LPS-induced oxidative stress, whereas post-treatment had less effect on LPS-induced IUFD.

Topics: Animals; Antioxidants; Ascorbic Acid; Bone and Bones; Bone Development; Crown-Rump Length; Female; Fetal Death; Fetal Growth Retardation; Fetal Weight; Glutathione; Injections, Intraperitoneal; Lipid Peroxidation; Lipopolysaccharides; Liver; Male; Mice; Mice, Inbred ICR; Odds Ratio; Placenta; Pregnancy; Thiobarbituric Acid Reactive Substances

In this study, we established an embryo model to study the effects of ethanol on fetal development. When embryos of Xenopus laevis (the African clawed frog) were exposed to ethanol, the resultant tadpoles had significantly reduced brain sizes (microencephaly) and retarded growth rates. These effects, similar to those observed in human fetal alcohol syndrome (FAS), were dose- and time-dependent. We further showed that the antioxidant ascorbic acid (vitamin C) could inhibit the ethanol-induced reactive oxygen species (ROS) production and NF-kappaB activation and protect the ethanol-treated embryos against microencephaly and growth retardation. These results suggest the involvement of NF-kappaB and oxidative stress in ethanol-mediated developmental defects, and the potential use of ascorbic acid as a new and effective protective agent for FAS.

Topics: Animals; Ascorbic Acid; Ethanol; Fetal Growth Retardation; Microcephaly; NF-kappa B; Reactive Oxygen Species; Xenopus laevis

We investigated treatment-related changes in oxidative stress indices in intrauterine growth retardation (IUGR) during pregnancy. Four parameters of cell membrane destruction were measured: malondialdehyde, Schiff bases, lipid peroxides, and conjugated dienes.. The study population included pregnant women under treatment in the Department of Obstetrics and Gynecology at the Medical University of Łódź in 1997-1999, divided into two groups: (I) - 30 healthy pregnant women, (II) - 31 pregnant women with a clinical and ultrasound diagnosis of IUGR. The course of treatment consisted of ten days of intravenous injections of cocarboxylase, Vitamin C, and solcoseryl as antioxidant factors. The parameters of oxidative stress were measured on the first day of hospitalization, after five days of treatment, and on the 10th day of treatment.. The mean value of MDA concentration in Group I was 2.03, vs. 2.39 in Group II. The mean value of conjugated dienes was 2.40 in Group I and 2.41 in Group II. The Schiff bases concentration in Group I was 8.03, as opposed to 8.83 in Group II. The concentration of lipid peroxides was 0.113 in Group I and 0.134 in Group II. We found that all the parameters of oxidative stress were higher in IUGR than in normal pregnancy. At the end of treatment a decrease was observed in all oxidative stress parameters.. IUGR is correlated with an increase in membrane damage parameters. Therapy for IUGR decreased the values of all indices of oxidative stress.

Topics: Actihaemyl; Adult; Ascorbic Acid; Female; Fetal Growth Retardation; Humans; Lipid Peroxidation; Oxidative Stress; Pregnancy; Thiamine Pyrophosphate

This article describes a study of the relationship between diet and smoking in a group of 821 Norwegian pregnant women. The study is part of a multi-centre project, examining risk factors for intrauterine growth retardation. Two 3-day dietary records were collected during the 17th and 33rd week of pregnancy. Information on smoking habits and other relevant parameters were collected through an extensive questionnaire. The results showed that the smokers consumed significantly less than the non-smokers of bread, cakes and cookies, vegetables, fruits and berries, cheese, yoghurt, low fat milk, juice and tea. The smokers also consumed significantly more meat, margarine, whole milk, soft drinks and coffee than the non-smokers on both occasions. The diet of the smokers contained significantly less protein, carbohydrate, dietary fibre, thiamin, riboflavin, vitamin C, calcium and iron as compared with the non-smokers. Fat contributed significantly more to the energy content of the diet of the smokers and it is concluded that their diet was less nutritious than that of the non-smokers throughout pregnancy.

Topics: Adult; Ascorbic Acid; Birth Weight; Chi-Square Distribution; Diet; Dietary Fats; Dietary Fiber; Female; Fetal Growth Retardation; Food Preferences; Humans; Iron; Linear Models; Logistic Models; Norway; Nutrition Surveys; Pregnancy; Risk Factors; Smoking

Trimethylamine (TMA) is an aliphatic amine, and its blood levels can increase after ingestion of certain foods, such as fish, and during disease states, such as chronic renal failure. We recently reported that TMA can inhibit fetal development in vivo and in vitro in mice. The present studies were done to find out if the inhibitory effects of TMA on embryonic development are caused by a decrease in macromolecular synthesis, using mouse embryo cultures as the experimental model. At a submaximally toxic concentration (0.75mM), TMA inhibited the growth of embryos to approximately 70% of control and caused neural-tube defects in 73% of embryos. By 42 h of culture, DNA, RNA, and protein content of TMA-treated embryos were approximately 50% of the control values. Embryotoxic effects of TMA were not caused by changes in pH and osmolarity of the culture media. The inhibitory effects of TMA on embryonic growth were time dependent and apparent at 2-4 h of culture. The inhibition of growth was accompanied by a decrease in the incorporation of tritium-labeled thymidine, uridine, and leucine into DNA, RNA, and proteins, respectively. Thiols (L- and D-cysteine, glutathione) and the antioxidant L-ascorbic acid did not cause significant antagonism of embryotoxic effects of TMA. It is concluded that TMA exerts teratogenic effects on mouse embryos in culture and inhibits their growth by reducing macromolecular synthesis; these effects may not involve glutathione depletion or generation of free radicals.

Topics: Abnormalities, Drug-Induced; Animals; Ascorbic Acid; Culture Techniques; DNA; Embryo, Mammalian; Embryonic and Fetal Development; Female; Fetal Growth Retardation; Hydrogen-Ion Concentration; Leucine; Macromolecular Substances; Methylamines; Mice; Models, Biological; Osmolar Concentration; Pregnancy; Protein Biosynthesis; RNA; Sulfhydryl Compounds; Thymidine; Tritium; Uridine

1. Studies were carried out on the distribution of ascorbic acid in human fetal tissues with the progress of gestation. 2. Fetuses and stillborn babies varying in gestational age from 12 to 38 weeks were obtained from various Baroda hospitals. Ascorbic acid levels were determined in selected tissues: brain, adrenal, liver, kidney, lung, heart and placenta. 3. Ascorbic acid concentration in the brain was higher than that in the adrenal at all gestational ages, suggesting the importance of this vitamin in brain development. The concentrations of this vitamin in liver, kidney, lung and placenta were comparable, but that in the heart tended to be lower. In all the tissues, there was a fall in ascorbic acid during late gestation. However, the levels in tissues of stillborn babies were higher than those reported for adults.

Topics: Ascorbic Acid; Body Weight; Female; Fetal Growth Retardation; Fetus; Gestational Age; Humans; Placenta; Pregnancy; Tissue Distribution

The first section of this paper reviews some of the effects of fetal and postnatal nutritional status on central nervous system development. It is seen that early malnutrition can be an important determinant of visual performance in children. The second section described the key role of vitamin A in the visual process. The consequences of primary and secondary vitamin A deficiencies are considered. The third section discusses some effects of diet on vision, including the role of the B vitamins and vitamin C.

Topics: Ascorbic Acid; Child; Diet; Female; Fetal Growth Retardation; Galactosemias; Humans; Nutrition Disorders; Optometry; Placenta Diseases; Pregnancy; Vision, Ocular; Vitamin A; Vitamin A Deficiency; Vitamin B Complex