PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Maternal Exposure”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1989

A toxicology evaluation of postnatal maternal exposure to cesium.

The effect of postnatal maternal exposure to CsCl on the newborn was studied in the mouse. Maternal ingestion of 1 mEq CsCl solution as the only drinking fluid began immediately after birth and the offspring were breast-fed until weaning. They were then separated from the nursing dams and remained Cs free for a subsequent 2 weeks prior to sacrifice. Maternal Cs exposure decreased the weanling body weight from controls and they attained normal body weight after 2 weeks of Cs-free period during development. Maternal Cs ingestion caused a reduction in offspring brain weight of both sexes compared to controls. The kidney weight of the developing female, but not male, offspring was also decreased from controls as a consequence of maternal Cs exposure. The offspring's hepatic alcohol and aldehyde dehydrogenase were not altered from controls as a function of maternal exposure to Cs salt. Little changes occurred in offspring heart lactate dehydrogenase by the maternal Cs treatment. The results suggest that maternal Cs exposure during breast-feeding affected body weight and the CNS of the offspring. The change noted in weanling kidney weight was sex dependent. These gross pathological changes in weanling organ weight were not apparent when maternal breast-feeding was eliminated. The data indicates that Cs adversely affected the newborn which was eliminated after cessation of the Cs exposure.

Alcohol Dehydrogenase↗
PubMed1989

Analyses of transplacentally induced sister chromatid exchanges and micronuclei in mouse fetal liver cells following maternal exposure to cigarette smoke.

The effect of maternal exposure to cigarette smoke on the fetus was studied by analyses of sister chromatid exchange (SCE) and formation of micronuclei with fetal liver cells. Fetal tissues were obtained from pregnant ICR/Jcl mice at the 16th day of gestation. Mice were exposed to mainstream or sidestream cigarette smoke with or without passage through filter (gas phase smoke or whole smoke). Each stream of smoke was used for three exposure schedules, i.e., short-term (two exposures at 15th and 16th day of gestation), long-term (exposure started at 4 wk before mating and stopped at 16th day of gestation), and prepregnant term (exposed for 4 wk before mating). The number of SCEs of fetal liver cells was significantly increased in all exposed groups. In the mainstream experiments, the long-term group showed a significant increase in the number of SCEs in comparison with that in the short-term group. Exposure to sidestream smoke increased the number of SCEs more than in groups exposed to mainstream smoke. This tendency was also recognized in the experiments with filtered smoke. On the contrary, no significant changes were observed by the micronucleus test. The transplacental genotoxic effect of maternally inhaled cigarette smoke was accurately detected by analysis of SCEs with fetal liver cells.

Animals↗
PubMed1991

Effect of maternal exposure to nicotine in the rat on level and binding of somatostatin in brain of developing offspring.

The effect of maternal exposure to nicotine on the level of somatostatin and specific binding in frontoparietal cortex and hippocampus of developing offspring was investigated. Sprague-Dawley rats were injected subcutaneously, throughout the pregnancy and the nursing period, with either: 3 mg/kg nicotine base or saline vehicle. In the offspring of control rats, the level of somatostatin-like immunoreactivity peaked at day 10 in the frontoparietal cortex, whereas the level of immunoreactivity in the hippocampus was the highest on day 30. Maternal exposure to nicotine caused enhanced levels of immunoreactivity in the frontoparietal cortex, on the day of birth and in the hippocampus, up to day 10. The maximum specific binding of somatostatin to the receptors in membranes from the frontoparietal cortex, peaked at 10 days of age in the offspring of control rats. The number of somatostatin receptors in cortical (but not in hippocampal) membranes was significantly decreased in the 0- to 10-day-old offspring of the nicotine-treated rats. Despite transient alterations in the number of somatostatin receptors, the affinity of the sites for somatostatin was consistently unchanged. The levels of somatostatin-like immunoreactivity and the number of somatostatin receptors in the frontoparietal cortex and hippocampus was comparable in the 30-day-old offspring of the control and nicotine-treated rats.

Aging↗
PubMed1989

Fetal lung growth: influence of maternal exposure to cold and exercise in rats.

The consequences of maternal exposure to low ambient temperature and exercise on maternal and fetal lung growth and in particular on the relationship between the three gas exchange organs (lungs and placenta) were studied in albino rats. Pregnant rats were subjected to 10 degrees C ambient temperature or to daily 10 min swimming exercise beginning at day 3 or day 11 of pregnancy till day 21 when they were sacrificed. Maternal lung growth was assessed by measuring the lung weight, lung air volume and lung DNA content, and the fetal lung growth by lung DNA content. Comparisons were made in rats with litter sizes of 9-14. The major findings were as follows. Cold increased: (1) the maternal lung, liver, kidney and heart size, and fetal body weight, in both groups, but to a greater degree in rats exposed to cold at day 3; and (2) fetal lung DNA content in rats subjected to cold at late gestation. It abolished the relationship between maternal and fetal lung DNA content which exists in large litter size pregnancies. Exercise did not enlarge the maternal lungs; it decreased the placental weight and fetal lung DNA content and abolished the relationship between maternal and fetal lung DNA content in rats subjected to exercise at early gestation. Neither cold nor exercise had an effect on fetal lung maturation. It is postulated that reduction in fetal lung DNA content with maternal exercise may result from the effects of hypoxemia which may be the consequence of reduced uterine blood flow; and that abolition of normally existing direct relationship between maternal and fetal lung DNA content may be the outcome of the effects of alterations in metabolic and endocrine functions, in both the mother and the fetus, in response to cold temperature and exercise, offsetting the influence the growing maternal lung may have on fetal lung growth.

Animals↗
PubMed1990

Cardiovascular malformations and maternal exposure to video display terminals during pregnancy.

The possible effects of working with video display terminals (VDTs) during pregnancy on the occurrence of cardiovascular malformations in the offspring was studied in 500 cases and 1055 controls. The cases represented all registered cardiovascular malformations reported in Finland during 1982-84, excluding those with chromosomal anomaly or known genetic syndrome. The controls were randomly selected from all babies born during the same period. Both the case and control mothers were interviewed by midwives using a structured questionnaire approximately three months after delivery. In this interview the mother's occupation, job description and employer during the first trimester were noted, as were large number of other exposures to chemical and physical factors. An industrial hygienist examined all these records for information indicating exposure to VDTs, unaware of case/control status. Work with VDTs during the first trimester of pregnancy was ascertained for 30 case mothers (6.0%, 30/500) and 53 control mothers (5.0%, 53/1055). In logistic regression analysis maternal exposure to VDTs for at least 20h a week during the first trimester of pregnancy showed a point estimate of odds ratio of 1.4 with 95% confidence limits of 0.5 and 3.8, when adjusted for age and alcohol use. Maternal exposure to VDTs was not associated with indicators of fetal growth such as birthweight, placental weight or length of gestation.

Computer Systems↗
PubMedDate not supplied

Developmental neurotoxicity following premating maternal exposure to hexachlorobenzene in rats.

The maternal transfer of hexachlorobenzene (HCB) may place the developing organism at risk. The present study assessed the developmental neurotoxicity of HCB using a battery of behavioral tests. Two weeks prior to breeding, maternal rats were exposed via gavage to either 10 or 100 mg HCB/kg body weight. Behaviors evaluated in pups exposed maternally to HCB included the negative geotaxic reflex on postnatal day (PND) 6, 8, and 10, olfactory discrimination (PND 9-11), and the development of exploratory behavior (PND 15-20). Significant effects in these three tests indicated hyperactivity in HCB-exposed pups. No significant effects on learning (swim T-maze) or motor activity were detected in older offspring (PND 40 and 50 respectively). The acoustic startle response (ASR) revealed apparent age-related effects of maternal HCB exposure. On PND 23 pups from the high treatment group demonstrated significantly reduced ASR amplitude, whereas these same animals, tested on PND 90 (using a reflex modification design), showed elevated ASR amplitude relative to the controls. This work demonstrates that HCB is a behavioral teratogen, and suggests that human fetuses and suckling infants may be at risk from the neurotoxic effects of HCB.

Animals↗
PubMed1992

Early changes in the development of dopaminergic neurotransmission after maternal exposure to cannabinoids.

Perinatal exposure to cannabinoid derivatives has been shown to affect brain development. In this work, we studied the changes induced by maternal exposure to cannabinoids during gestation and lactation on the dopaminergic activity in the prosencephalic area of offspring of several days of development. This brain area contains an increasing population of dopaminergic terminals from the different dopaminergic pathways that become differentiated in the adult rat. We measured the endogenous content of dopamine and its intraneuronal metabolite, L-3,4-dihydroxyphenylacetic acid, and the activity of tyrosine hydroxylase as indices of dopaminergic activity. Results showed that perinatal exposure to cannabinoids caused several changes in the evolution of the dopaminergic indices studied. These changes were mainly observed in males. The only alteration in females occurred on the tenth day of development: An increase in dopamine content was observed with no changes in either the content of L-3,4-dihydroxyphenylacetic acid or tyrosine hydroxylase activity. In males, the content of both dopamine and L-3,4-dihydroxyphenylacetic acid were decreased on the day previous to birth in the animals exposed to cannabinoids. Although the reduction in its metabolite disappeared on the fifth day, the decrease in dopamine was maintained and it was correlated with a decrease in tyrosine hydroxylase activity. However, this decrease in the activity of tyrosine hydroxylase was followed by an increase on the tenth day. These results allow us to conclude that perinatal exposure to cannabinoids produces changes in the normal development of several indices of the activity of dopaminergic neurons in the brain area containing the most important population of dopaminergic endings. These changes were mainly observed in males. They could be responsible for a long-term alteration in the neurological processes in which these neurons are involved in the adult.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Effects of maternal exposure to trioxane on postnatal development in rats.

Female rats were given by gavage every other day from days 2 to 20 of gestation an aqueous solution of trioxane at daily doses equal to 0.025; 0.075 and 0.15 LD50 (0.19: 0.58 and 1.16 g/kg). Maternal exposure to trioxane at the highest dose resulted in death of most neonates a few days after birth. Viability and postnatal growth of the offspring of dams that were given 0.19 and 0.58 g/kg were not affected. Transitional depression of exploratory locomotor activity in female offspring and a decrease of active avoidance acquisition were observed in adult male and female offspring from the 0.58 g/kg group, whereas a dose of 0.19 g trioxane /kg did not affect the behavioral performance of progeny.

Animals↗
PubMed1992

The toxicokinetics of mercury in mice offspring after maternal exposure to methylmercury--effect of selenomethionine.

Human evidence indicates fetotoxicity of methylmercury at exposure levels inducing only slight and reversible maternal toxicity, but experimental animal data demonstrate, that fetotoxicity may occur despite absence of noticeable maternal toxicity. However, in contrast to the long-term exposure in humans, the key point in the experimental design of the majority of experimental studies has been administration of few doses of methylmercury late in gestation. The present study in mice therefore used long-term maternal exposure to methylmercury (1 nmol/ml in drinking water) and a cross-fostering design to investigate separately in different offsprings the toxicokinetics of transplacentally absorbed mercury and mercury retained during lactation. Further, the influence of seleno-L-methionine (3 micrograms/ml in drinking water) on the toxicokinetics of methylmercury in these mice was studied. The present study demonstrated, that independent on seleno-L-methionine supplementation, offspring deposited equal amounts of mercury during lactation and during gestation. Moreover, the organ distribution and rate of excretion of mercury in transplacentally exposed mice were considerably different from those in mice exposed postnatally and from adult mice in studies using comparable dosages. Seleno-L-methionine only slightly affected the toxicokinetics of mercury in offspring.

Animals↗
PubMed1991

[Sexual dimorphism in the brain and drug actions: with special reference to the sex difference in the functional effects of maternal exposure to drugs in the littermate offspring].

It has long been known that in mammals there is a sex difference in the drug metabolizing enzyme activity that is reflected in the sex-related difference in the action of barbiturates and some other drugs. Recently, sex differences in the structure and function of the brain in humans and other primates have been demonstrated by many investigators. This review focused on the sex difference in the brain mainly of the rat studied with physiological, biochemical or even molecular endpoints. Our experimental results on the modulating effects of sex steroids for dopaminergic neurons were included. In addition, the findings that maternal exposure to various CNS acting drugs resulted in a marked sex difference in the brain function of the offspring when assessed with a number of measures such as open-field behavior, tolerance to the exposed drug itself, thermic responses to chlorpromazine, and the pituitary response to releasing hormones were presented and discussed.

Animals↗
PubMedDate not supplied

Maternal exposure to neighborhood carbon monoxide and risk of low infant birth weight.

This case-control study investigated the potential association between ambient levels of carbon monoxide in a pregnant woman's neighborhood of residence and her chance of delivering a low birth weight infant. Low birth weight infants and normal birth weight infants were contrasted with respect to ambient levels of CO during the 3 months prior to delivery in the neighborhoods where their mothers lived at birth. After adjustment for the confounding effects of maternal race and education, there was no association between higher CO exposure and higher odds of low birth weight. These data do not support a strong association between maternal exposure to neighborhood CO during pregnancy and odds of delivering a low birth weight infant. Further investigation of the effects of CO exposure on birth weight, with direct measurement of total CO exposure, is needed.

Air Pollutants↗
PubMed1991

Maternal exposure to chemical and physical factors during pregnancy and cardiovascular malformations in the offspring.

The possible effect of chemical and physical factors during pregnancy on the occurrence of cardiovascular malformations in the offspring was studied in 573 cases and 1,055 controls. The cases represented all verified cardiovascular malformations in Finland during 1982-1984. The controls were randomly selected from all babies born during the same period. Case and control mothers were interviewed by midwives approximately 3 months after delivery using a structured questionnaire. Maternal alcohol consumption during the first trimester of pregnancy was more common among the mothers of case infants (45.9%) than those of controls (39.6%). Exposure to organic solvents at work was slightly more prevalent among the ventricular septal defect group (12.1%) than the control mothers (7.8%). However, neither association was significant when adjusted for maternal age in logistic regression analysis. Moreover, one or both of these associations may be chance effects resulting from multiple comparisons. The risk of cardiovascular malformations was not associated with maternal smoking, or coffee, tea, or cola consumption, and was equal in urban and rural areas. Maternal exposures to anesthetic gases, pesticides, wood preservatives, microwave ovens, and video display terminals at work or home were not associated with the risk of cardiovascular malformations. It is concluded that some common environmental exposures during early pregnancy to physical and chemical factors should not necessarily be considered hazardous for the developing fetal heart. The causes of the majority of cardiovascular malformations remain unknown.

Alcohol Drinking↗
PubMed1991

Normal pregnancy outcome after early maternal exposure to gonadotropin releasing hormone agonist. A case report.

An infertile woman was treated with leuprolide acetate in preparation for in vitro fertilization and was found to be pregnant after exposure to the gonadotropin releasing hormone agonist (GNRHa) from days 21-38 after her last menstrual period. She delivered a healthy-appearing, male infant at term. We found reports of four other pregnancies with early maternal GNRHa exposure. While no malformations have been reported, patients are advised to use barrier contraception when GNRHa therapy is initiated.

Adult↗
PubMed1987

Abnormalities of the ear associated with exencephaly in mouse fetuses induced by maternal exposure to cadmium.

Exencephaly was induced in mouse fetuses by maternal injection of cadmium chloride (CdCl2) on day 7 of gestation. The heads of exencephalic, nonexencephalic experimental, and control fetuses were embedded in paraffin and sections were stained with hematoxylin and eosin. Compared to those of controls, the ears of the exencephalic fetuses were smaller (microtia) and low set. The meatal plug representing the external auditory canal was thick, variously branched, and often directed inferiorly. Usually, there were just two ossicles. The stapedial artery, facial nerve, and stapedius muscle were hypoplastic; the tensor tympani was small or absent. There were 1.0 to 2.0 turns of the cochlea in contrast to 2.5 turns in the controls. The organ of Corti was underdifferentiated; the spiral ganglion had fewer cells. In the control, the long axes of the anterior and posterior semicircular ducts were at right angles to each other and in vertical planes, but in the exencephalics, they tended more laterally towards the horizontal plane. The differentiation of the cristae ampullares and maculae was also severely affected. In several specimens, the entire membranous labyrinth had been distended; these labyrinths also had unusual epithelial infoldings. In cadmium-treated nonexencephalic fetuses, the external ears were normal and appropriate to the body size; five of them were examined histologically; in all, the five middle ear contents were hypoplastic; in three, the cochlea had a maximum of two turns and the organ of Corti, crista ampullaris, and macula were hypoplastic. By an analogy to abnormalities of mutants with neural tube defects, it is suggested that the exencephaly induced by cadmium might affect the differentiation of the ear. Partial involvement of the ear in nonexencephalic experimental embryos may be the result of direct action of cadmium during critical stages of development.

Abnormalities, Drug-Induced↗
PubMed1989

Embryotoxicity and in vivo cytogenetic changes following maternal exposure to cadmium chloride in mice.

Cadmium is a well-known teratogen in laboratory animals and a widespread environmental pollutant. The frequencies of sister chromatid exchanges (SCEs), nucleolar organizing regions (NORs) and chromosomal aberrations were analysed in maternal bone marrow and fetal liver and/or lung cells of mice, following maternal treatment with cadmium chloride, on gestational days 8 through 10. The embryotoxic effects and morphological changes on day 18 fetuses were also studied. Cadmium chloride is readily transferred across the placenta and significant levels were detected in both the placenta and fetus. No significant changes in the frequencies of SCEs or NORs in maternal and fetal cells were observed following exposure to cadmium chloride. Fetal tissues showed mitotic inhibition at the highest dose levels (8.4 and 11.4 mg/kg, b.w.). Maternal treatment with cadmium chloride increased embryonic resorptions and fetal lethality, as well as reduced placental weight; however, it did not produce significant chromosomal changes except at the highest dose level (11.4 mg/kg).

Abnormalities, Drug-Induced↗
PubMed1992

The effect of maternal exposure to dioxolane on prenatal and postnatal development in rats.

Female rats were given by gavage every other day from days 8-20 of gestation an aqueous solution of dioxolane at daily doses equal to 0.025, 0.1 and 0.2 LD50 (first series--prenatal development) or from days 2-20 of gestation at daily doses equal to 0.025, 0.075 and 0.15 LD50 (second series--postnatal development). At doses toxic or subtoxic to maternal rats (0.1 and 0.2 LD50) dioxolane did not cause increased embryo or fetus intrauterine death rates or congenital defects, it did cause, however, dose-related delays in fetal development. Dioxolane does not cause impairment of physical development or behavioral disturbances. Exposure to higher doses of the compound (0.2 LD50) leads to increased perinatal death rates in the offspring, without causing, however, disturbances in the maternal instinct. The exposure of pregnant rats to dioxolane decreased haemoglobin levels in 5-week-old offspring. At a dose 1.15 g/kg (0.2 LD50) the chemical significantly increased exploratory motor activity of female offspring at the age of 8 weeks, but did not affect significantly locomotor activity of males and the active avoidance acquisition of adult offspring.

Animals↗
PubMed1985

Perinatal induction of hepatic aminopyrine N-demethylase by maternal exposure to phenytoin.

Phenytoin is one of the most commonly used anticonvulsants in pregnant epileptic women. Unrelatedly, the drug is also an inducer of hepatic drug metabolizing enzymes. We report here that maternal treatment with therapeutic-like doses for the rat of phenytoin produces significant elevations in the Michaelis constants and maximal velocities of hepatic aminopyrine N-demethylase in the dams' 8-day-old offspring. Although the drug apparently had little, if any, adverse effects on the course of pregnancy or neonatal development, it appears that the maternally administered phenytoin was transferred to the perinates where it induced hepatic drug metabolizing enzymes.

Aminopyrine N-Demethylase↗