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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↗
PubMed1984

Differentation of rat embryo cells in culture: response following acute maternal exposure to teratogens and non-teratogens.

An in vivo-in vitro test system with high sensitivity to teratogens has been developed and validated. A single acute intra-peritoneal injection of teratogens (18) and non-teratogens (13) was administered to pregnant rats on the 12th day after fertilisation, and uteri were removed after 16 h by laparotomy. 34-36 Embryos somites were selected, and mid-brain (CNS) and fore-limb buds (LB) were dissected free and dispersed as single-cell suspensions in Ham's F12 culture medium. The cells were cultured as micromass cell islands for 5 days, and discrete foci of neuronal cells differentiated in CNS cultures and chondrocytes in LB cultures. After 5 days, differentiation as determined by number of stainable foci of differentiated cells and 3H-GABA incorporation in CNS or 35SO4 incorporation in LB and growth (as determined by total protein) were measured. Both differentiation and growth of CNS and LB cultures were markedly reduced following exposure of the dam to teratogens, whereas no significant effect was observed with non-teratogens. One teratogen (amaranth) and one non-teratogen (nitrilotriacetic acid) were classified as false negative and positive, respectively; the sensitivity of the test (proportion of teratogens correct) was therefore 92% and the specificity (proportion of non-teratogens correct) was 94%. Inhibition of growth and differentiation in the rat embryo cell cultures following maternal exposure forms the basis of a short-term in vitro test for teratogens.

Animals↗
PubMed2003

Increased expression of glial fibrillary acidic protein in cerebellum and hippocampus: differential effects on neonatal brain regional acetylcholinesterase following maternal exposure to combined chlorpyrifos and nicotine.

Cigarette smoking and environmental exposure to chlorpyrifos during pregnancy could lead to developmental toxicity in the offspring. In the present study, pregnant female Sprague-Dawley rats (300-350 g) were treated daily with nicotine (1 mg/kg, sc) or chlorpyrifos (0.1 mg/kg, dermal) or a combination of nicotine and chlorpyrifos from gestational days (GD) 4-20. Control animals were treated with saline and ethanol. Male offspring from the mothers treated with nicotine alone gained significantly less weight on postnatal day (PND) 30 as compared to control. On PND 7, there was a significant increase in brain acetylcholinesterase (AChE) activity in pups from nicotine- and chlorpyrifos-treated dams, whereas plasma butyrylcholinesterase (BChE) activity was significantly elevated in pups of mothers treated with either chlorpyrifos alone or pesticide combined with nicotine. On PND 30 there was a significant increase in AChE activity in brainstem and cerebellum in all treated male pups. In female pups on PND 30 there was a significant rise in AChE activity in brainstem of chlorpyrifos alone and in cerebellum of the combination nicotine and chlorpyrifos group. Histopathological evaluation demonstrated an increased neuronal cell death in the cerebellum granular cell layer of female offspring from nicotine or combined nicotine with chlorpyrifos group. A rise in glial fibrillary acidic protein (GFAP) immunostaining was observed in the CA1 subfield of hippocampus and cerebellum on PND 30 in female and male offspring of mothers treated with either nicotine or nicotine in combination with chlorpyrifos, but to a lesser extent in males. Data suggest that maternal exposure to nicotine and chlorpyrifos, alone or in combination, produces differential alterations in brain regional AChE activity and expression of GFAP in cerebellum and hippocampus in offspring on PND 30.

Acetylcholinesterase↗
PubMed1994

Fetal anemia following maternal exposure to 5-fluorouracil in the rat.

Previous studies from our laboratory have shown that maternal 5-fluorouracil (5-FU) exposure on day 14 of gestation (GD14) in the rat results in dose-dependent retardation of both cell cycle progression and growth of embryonic liver. At this developmental stage, hepatic erythropoiesis is the primary source of new circulating fetal erythrocytes. This study examined dose-dependent hematological changes in the fetus after maternal 5-FU exposure (0, 20, 30, 40 mg/kg on GD14) to assess 1) hematopoiesis as a potential target for 5-FU developmental toxicity and 2) the role of the observed 5-FU-induced fetal anemia in adverse developmental outcome. Standard clinical hematological parameters, including hematocrit, hemoglobin content, and erythrocyte counts, were measured in fetal blood drawn by cardiac puncture. Dose-related deficits were observed in all of these parameters within 48 hr of 5-FU administration. Calculation of various red cell indices revealed a concomitant increase in mean cell volume and mean cell hemoglobin. These changes were preceded by depletion of hepatic precursor populations which was evident by 24 hr after maternal exposure to 30 or 40 mg/kg. At doses of 20 and 30 mg/kg there was full and moderate recovery, respectively, in these endpoints by 72 hr after dosing, but persistent deficits were observed at 40 mg/kg. Fluorescence microscopy of Höechst-stained fetal blood smears revealed that at both 48 and 72 hr after dosing, the proportion of nucleated yolk sac-derived erythrocytes was increased relative to control.(ABSTRACT TRUNCATED AT 250 WORDS)

Anemia↗
PubMed2006

Infant acute leukemia and maternal exposures during pregnancy.

Infant acute leukemia (IAL) has a unique profile characterized by the high incidence of translocations involving the MLL gene located at the 11q23 region. To test the potential role of intrauterine and perinatal factors linked to the risk of IAL development, a hospital-based case-control study was conducted in different cities of Brazil. A total of 202 children (ages 0-21 months) with newly diagnosed IAL was enrolled (1999-2005), and 440 age-matched controls were selected from the same hospitals wherein IAL cases were treated. A statistically significant association between maternal use of hormones during pregnancy and IAL was observed [odds ratio (OR), 8.76; 95% confidence interval (95% CI), 2.85-26.93] in a multivariable analysis. The association of certain exposures during pregnancy (hormones, dipyrone, metronidazole, and misoprostol) and MLL gene rearrangements was tested using a case-case approach. Despite the lack of statistical significance, the magnitude of the OR for maternal exposure to dipyrone (OR, 1.45; 95% CI, 0.75-2.86), metronidazole (OR, 1.72; 95% CI, 0.64-4.58), quinolones (OR, 2.25; 95% CI, 0.70-25.70), and hormones (OR, 1.88; 95% CI, 0.50-7.01) may suggest the occurrence of interactions between such maternal exposures during pregnancy and MLL rearrangements, yielding into IAL development. The strong and statistically significant association between IAL and estrogen exposure during pregnancy observed in this study deserves further investigation to investigate its role in intrauterine leukemogenesis.

Acute Disease↗
PubMed2005

Maternal exposure to arsenic, cadmium, lead, and mercury and neural tube defects in offspring.

Arsenic, cadmium, lead, and mercury are neurotoxins, and some studies suggest that these elements might also be teratogens. Using a case-control study design, we investigated the relation between exposure to these heavy metals and neural tube defects (NTDs) in offspring of Mexican-American women living in 1 of the 14 Texas counties bordering Mexico. A total of 184 case-women with NTD-affected pregnancies and 225 control-women with normal live births were interviewed about their environmental and occupational exposures during the periconceptional period. Biologic samples for blood lead and urinary arsenic, cadmium, and mercury were also obtained for a subset of these women. Overall, the median levels of these biomarkers for heavy metal exposure did not differ significantly (P > 0.05) between case- and control-women. However, among women in the highest income group, case-women were nine times more likely (95% confidence interval (CI) 1.4-57) than control-women to have a urinary mercury 5.62 microg/L. Case-women were 4.2 times more likely (95% CI 1.1-16) to report burning treated wood during the periconceptional period than control-women. Elevated odds ratios (ORs) were observed for maternal and paternal occupational exposures to arsenic and mercury, but the 95% CIs were consistent with unity. The 95% CIs of the ORs were also consistent with unity for higher levels of arsenic, cadmium, lead, and mercury in drinking water and among women who lived within 2 miles at the time of conception to industrial facilities with reported emissions of any of these heavy metals. Our findings suggest that maternal exposures to arsenic, cadmium, or lead are probably not significant risk factors for NTDs in offspring. However, the elevated urinary mercury levels found in this population and exposures to the combustion of treated wood may warrant further investigation.

Adult↗
PubMed2002

Children's intellectual and emotional-behavioral adjustment at 4 years as a function of cocaine exposure, maternal characteristics, and environmental risk.

The authors examined 223 children at age 4 years for the effects of prenatal cocaine exposure, exposure to other substances, maternal and environmental risk factors, and neonatal medical problems on IQ, externalizing problems, and internalizing problems. Regression analyses showed that maternal verbal IQ and low environmental risk predicted child IQ. Cocaine exposure negatively predicted children's overall IQ and verbal reasoning scores, but only for boys. Cocaine exposure also predicted poorer short-term memory. Maternal harsh discipline, maternal depressive symptoms, and increased environmental risk predicted externalizing problems. In contrast, only maternal depressive symptoms predicted internalizing problems. These findings indicate that early exposure to substances is largely unrelated to subsequent IQ or adjustment, particularly for girls.

Adolescent↗
PubMed2005

Perinatal maternal exposure to picrotoxin: effects on sexual behavior in female rat offspring.

A previous study in our laboratory showed that perinatal maternal picrotoxin exposure (0.75 mg/kg) in rats improved heterosexual behavior in male offspring. In the present study, we examined the effects of this maternal treatment on sexual behavior in the female offspring. The dams received 0.75 mg/kg picrotoxin treatment (PT) once a day on the 18th and 21st day of pregnancy, 2 h after parturition and once a day during the first 4 days of lactation. The results showed that (1) at birth, the body weight and anogenital distance were not modified by treatment; (2) female sexual behavior was improved in experimental animals. These results demonstrate that perinatal picrotoxin exposure improves adult sexual behavior in female rat offspring as suggested by increase in the lordosis quotient.

Animals↗
PubMed2004

Fluctuating asymmetry in Bobwhite quail chicks (Colinus virginianus) does not follow a predictable dose-response relationship following maternal exposure to four different herbicides.

Most biomonitoring studies that have investigated the relationship between fluctuating asymmetry (FA) and anthropogenic stressors have measured organisms from polluted ecosystems and compared them to organisms at reference sites. What has received little attention is whether FA follows a dose-response relationship with stress, a key criterion of a useful biomarker. Using chicks from currently mandated avian reproductive tests we tested whether a composite index of FA (FAC), was related to the dose or duration of exposure of their parents to one of four different herbicides, and if FAC was indeed a more sensitive marker of stress than standard reproductive endpoints measured from this test. We found no consistent relationship between FAC and dose or duration of herbicide exposure in any of the four studies. Exposure to one of the four pesticides did result in significant reproductive toxicity but this was not accompanied or foreshadowed by higher levels of FAC. Our results do not support the hypothesis that FA is a reliable general biomarker of pesticide exposure.

Animals↗
PubMed1999

Maternal exposure to benzo[a]pyrene alters development of T lymphocytes in offspring.

Childhood cancer has been increasing significantly over the past two decades in the United States, suggesting that environmental exposures may be playing a causative role. One such cause may be maternal smoking during pregnancy. Suspected carcinogens in cigarette smoke and environmental pollution include N-nitrosamines and polycyclic aromatic hydrocarbons, which may be several micrograms per exposure. Previously, we have shown that mouse progeny of mothers exposed to benzo[a]pyrene (B[a]P) during midpregnancy had abnormalities in their humoral and cell-mediated immune response. Immunodeficiency was detectable during gestation, at one week after birth and persisted for 18 months. Tumor incidences in progeny were eight to 10-fold higher than in controls. The present study compared frequencies of CD4+, CD8+, V gamma 2+, and V beta 8+ T cells in progeny following in utero exposure to B[a]P. The significant reduction in newborn CD4+CD8+, CD4+CD8+V beta 8+ thymocytes and CD4+ splenocytes from 1-week-old progeny, suggests that B[a]P induces abnormal changes in developing T cells. These early alterations may lead to postnatal T cell suppression, thus providing a more suitable environment for the growth of tumors later in life. These results suggest that developmental immunosuppression mediated by B[a]P may play a critical role in the relationship between maternal exposures and childhood carcinogenesis.

Animals↗
PubMed2001

Maternal exposure to nitrate from drinking water and diet and risk for neural tube defects.

In this population-based case-control study conducted in California between June 1989 and May 1991, the authors investigated the association between maternal periconceptional exposure to nitrate from drinking water and diet and risk for neural tube defects. The mothers of 538 cases and 539 nonmalformed controls were interviewed regarding residential history, consumption of tap water at home, and dietary intake during the periconceptional period. Dietary nitrate exposure was not associated with increased risk for neural tube defects. Exposure to nitrate in drinking water at concentrations above the 45 mg/liter maximum contaminant level was associated with increased risk for anencephaly (odds ratio (OR) = 4.0, 95% confidence interval (CI): 1.0, 15.4), but not for spina bifida. Increased risks for anencephaly were observed at nitrate levels below the maximum contaminant level among groundwater drinkers only (OR = 2.1, 95% CI: 1.1,4.1 for 5-15 mg/liter; OR = 2.3, 95% CI: 1.1, 4.5 for 16-35 mg/liter; and OR = 6.9, 95% CI: 1.9, 24.9 for 36-67 mg/liter compared with <5 mg/liter). Adjustment for identified risk factors for anencephaly did not substantially alter these associations, nor did control for maternal dietary nitrate, total vitamin C intake, and quantity of tap water consumed. The lack of an observed elevation in risk for anencephaly in association with exposure to mixed water containing nitrate at levels comparable with the concentration in groundwater may indicate that something other than nitrate accounts for these findings.

Adolescent↗
PubMed2002

Maternal exposure to low-level air pollution and pregnancy outcomes: a population-based study.

BACKGROUND: Recent reports have shown that air pollution may increase the risk of adverse birth outcomes. We have evaluated the relationship between ambient air pollution and the occurrence of low birth weight and preterm delivery using routinely collected data in Lithuania. METHODS: This epidemiological study comprised all singleton newborns (N = 3,988), born to women in 1998, who resided in the City of Kaunas. Birth data and information on maternal characteristics were obtained from the Lithuanian National Birth Register. To estimate residential exposure levels, we used measurements of ambient nitrogen dioxide (NO2) and formaldehyde, which were collected at 12 monitoring posts. Multivariate logistic regression was used to estimate the effect that each pollutant would have on low birth weight (LBW) and premature birth while controlling for potential confounders. RESULTS: Adjusted odds ratios (OR) for LBW increased with increasing formaldehyde exposure (OR2nd tertile = 1.86, 95% CI 1.10-3.16; OR3rd tertile = 1.84, 95% CI 1.12-3.03). Adjusted ORs of preterm birth for the medium and high NO2 tertile exposures were OR = 1.14 (95% CI 0.77-1.68) and OR = 1.68 (95% CI 1.15-2.46), respectively. The risk of preterm birth increased by 25% (adjusted OR = 1.25, 95% CI 1.07-1.46) per 10 microg/m3 increase in NO2 concentrations. An analysis by trimester showed that pregnancy outcomes were associated with first-trimester exposure to air pollutants. However, there were no significant relationships in other pregnancy periods between preterm birth and exposure to formaldehyde or between LBW and NO2 exposure. CONCLUSION: Our findings suggest that in the City of Kaunas there might be a relationship between maternal exposure to ambient formaldehyde and the risk of LBW, as well as between NO2 exposure and the risk of preterm birth.

Adult↗
PubMed2001

Maternal exposure to a low dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) suppressed the development of reproductive organs of male rats: dose-dependent increase of mRNA levels of 5alpha-reductase type 2 in contrast to decrease of androgen receptor in the pubertal ventral prostate.

To assess the health risks associated with exposure to 2,3,7,8-tetrachlorodebenzo-p-dioxin (TCDD), we studied the effects of a relatively low dose of TCDD on the male reproductive system of rats, using the experimental protocol of T. A. Mably et al. (1992, Toxicol. Appl. Pharmacol. 114, 97-107, 108-117, 118-126), and searched for the most sensitive and reliable among several indices of TCDD toxicity. Pregnant Holtzman rats were given a single oral dose of 0, 12.5, 50, 200, or 800 ng TCDD/kg body weight on gestational day (GD) 15, and male offspring were sacrificed on postnatal day (PND) 49 or 120. GC-MS analysis of the abdominal fat tissue and testis clearly showed increased amounts of TCDD in these offspring. However, there was no TCDD effect on body weight of offspring. There were no changes on testicular or epididymal weights by TCDD administration, even at the 800-ng/kg dose in rats sacrificed on either PND 49 or 120. In addition, TCDD administration resulted in no changes in daily sperm production or sperm reserve at any of the doses used. However, the weight of the urogenital complex, including the ventral prostate, was significantly reduced at doses of 200 and 800 ng TCDD/kg in rats sacrificed on PND 120. Moreover, the anogenital distance (AGD) of male rats sacrificed on PND 120 showed a significant decrease in the groups receiving doses greater than 50 ng TCDD/kg. TCDD administration resulted in no apparent dose-dependent changes in levels of either serum testosterone or luteinizing hormone. Interestingly, reverse transcription-polymerase chain reaction (RT-PCR) analysis revealed that, in the ventral prostates of the PND 49 group, TCDD administration resulted in both a dose-dependent increase in 5alpha-reductase type 2 (5alphaR-II) mRNA level and a dose-dependent decrease in androgen receptor (AR) mRNA level. These results suggest that low-dose TCDD administration had a greater effect on the development of the external genital organs and ventral prostate than on development of the testis and other internal genital organs. Moreover, it is highly suggested that the decrease in the size of the ventral prostate by maternal TCDD exposure might be due to decreased responsiveness of the prostate to androgen due to an insufficient expression level of androgen receptor during puberty.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed2006

Transgenerational priming of immunity: maternal exposure to a bacterial antigen enhances offspring humoral immunity.

Young vertebrates have limited capacity to synthesize antibodies and are dependent on the protection of maternally transmitted antibodies for humoral disease resistance early in life. However, mothers may enhance fitness by priming their offspring's immune systems to elevate disease resistance. Transgenerational induced defences have been documented in plants and invertebrates, but maternal priming of offspring immunity in vertebrates has been essentially neglected. To test the ability of mothers to stimulate the immune systems of offspring, we manipulated maternal and offspring antigen exposure in a wild population of birds, pied flycatchers (Ficedula hypoleuca). We show that immunization of the mother before egg laying apparently stimulates a transgenerational defence against pathogens by elevating endogenous offspring antibody production. If the disease environments encountered by mothers and offspring are similar, this transgenerational immune priming may allow young to better cope with the local pathogen fauna.

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↗
PubMed2002

Maternal exposure to diethylene glycol monomethyl ether: a possible role in the etiology of retrocaval ureter.

Retrocaval ureter is a very rare condition. In light of the experimental studies, one of the etiologic factors seems to be maternal contact with diethylene glycol monomethyl ether or ethylene glycol monomethyl ether. A case of cardiovascular, skeletal, and retrocaval ureter anomalies caused by possible maternal contact while pregnant with these materials at her work in a textile factory is presented.

Abnormalities, Multiple↗