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Results for “Maternal Exposure”

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PubMed2005

Maternal exposure to toxoplasmosis and risk of schizophrenia in adult offspring.

OBJECTIVE: The authors examined the relationship between maternal antibody to toxoplasmosis and the risk of schizophrenia and other schizophrenia spectrum disorders in offspring. Toxoplasmosis is known to adversely affect fetal brain development. METHOD: In a nested case-control design of a large birth cohort born between 1959 and 1967, the authors conducted serological assays for Toxoplasma antibody on maternal serum specimens from pregnancies giving rise to 63 cases of schizophrenia and other schizophrenia spectrum disorders and 123 matched comparison subjects. Toxoplasma immunoglobulin (Ig)G antibody was quantified by using the Sabin-Feldman dye test. The Ig titers were classified into three groups: negative (<1:16) (reference), moderate (1:16-1:64), and high (> or =1:128). RESULTS: The adjusted odds ratio of schizophrenia/schizophrenia spectrum disorders for subjects with high maternal Toxoplasma IgG antibody titers was 2.61 (95% confidence interval=1.00-6.82). There was no association between moderate Toxoplasma Ig antibody titers and the risk of schizophrenia/spectrum disorders. CONCLUSIONS: These findings suggest that maternal exposure to toxoplasmosis may be a risk factor for schizophrenia. The findings may be explained by reactivated infection or an effect of the antibody on the developing fetus. Given that toxoplasmosis is a preventable infection, the findings, if replicated, may have implications for reducing the incidence of schizophrenia.

Adult↗

PubMed2005

Maternal exposure of rats to nicotine via infusion during gestation produces neurobehavioral deficits and elevated expression of glial fibrillary acidic protein in the cerebellum and CA1 subfield in the offspring at puberty.

Maternal smoking during pregnancy is known to be a significant contributor to developmental neurological health problems in the offspring. In animal studies, nicotine treatment via injection during gestation has been shown to produce episodic hypoxia in the developing fetus. Nicotine delivery via mini osmotic pump, while avoiding effects due to hypoxia-ischemia, it also provides a steady level of nicotine in the plasma. In the present study timed-pregnant Sprague-Dawley rats (300-350 g) were treated with nicotine (3.3 mg/kg, in bacteriostatic water via s.c. implantation of mini osmotic pump) from gestational days (GD) 4-20. Control animals were treated with bacteriostatic water via s.c. implantation of mini osmotic pump. Offspring on postnatal day (PND) 30 and 60, were evaluated for changes in the ligand binding for various types of nicotinic acetylcholine receptors and neuropathological alterations. Neurobehavioral evaluations for sensorimotor functions, beam-walk score, beam-walk time, incline plane and grip time response were carried out on PND 60 offspring. Beam-walk time and forepaw grip time showed significant impairments in both male and female offspring. Ligand binding densities for [3H]epibatidine, [3H]cytisine and [3H]alpha-bungarotoxin did not show any significant changes in nicotinic acetylcholine receptors subtypes in the cortex at PND 30 and 60. Histopathological evaluation using cresyl violet staining showed significant decrease in surviving Purkinje neurons in the cerebellum and a decrease in surviving neurons in the CA1 subfield of hippocampus on PND 30 and 60. An increase in glial fibrillary acidic protein (GFAP) immuno-staining was observed in cerebellum white matter as well as granular cell layer of cerebellum and the CA1 subfield of hippocampus on PND 30 and 60 of both male and female offspring. These results indicate that maternal exposure to nicotine produces significant neurobehavioral deficits, a decrease in the surviving neurons and an increased expression of GFAP in cerebellum and CA1 subfield of hippocampus of the offspring on PND 30 and 60. The results show that although 60-day-old male and female rat offspring of mothers exposed to nicotine during gestation did not differ from control in body weight gain or nicotinic acetylcholine receptors ligand binding, they exhibited significant sensorimotor deficits that were consistent with the neuropathological alterations seen in the brain. These neurobehavioral and pathological deficits indicate that maternal nicotine exposure may produce long-term adverse health effects in the offspring.

Animals↗

PubMed1998

Maternal exposure to environmental tobacco smoke alters Clara cell secretory protein expression in fetal rat lung.

We have previously demonstrated that aged and diluted sidestream cigarette smoke (ADSS) alters the development of bronchiolar epithelial cells in postnatal animals (C. M. Ji, C. G. Plopper, H. P. Witschi, and K. E. Pinkerton. Am. J. Respir. Cell Mol. Biol. 11: 312-320, 1994). This study was designed to examine the effects of maternal exposure to ADSS on the development of fetal Clara cells in rats with Clara cell 10-kDa protein (CC10; also designated Clara cell secretory protein) and CC10 mRNA as differentiation markers. Immunohistochemistry, Northern blots, and in situ hybridization were used to determine the abundance and distribution of CC10 at gestational days 14, 18, and 21. CC10 and CC10 mRNA were absent at gestational day 14 but were detectable at gestational day 18 and further increased by gestational day 21. Maternal exposure to ADSS was found to significantly increase fetal expression of CC10 and CC10 mRNA by gestational day 21 but not by gestational day 14 or 18. These findings demonstrate that in utero exposure to ADSS alters the normal developmental expression of CC10 in the fetal rat lung.

Animals↗

PubMed2006

The effects of maternal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin on testicular steroidogenesis in infantile male rats.

Exposure of adult male animals to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) decreases serum androgen concentrations. Reduction in androgen levels after maternal exposure has also been reported, but these results have not been reproduced. We have earlier shown that TCDD stimulates rather than inhibits testosterone synthesis in the prenatal rat testis. The aim of the present study was to elucidate in utero-induced effects of TCDD on testicular steroidogenesis in the 14-day-old infant rats. At that time the foetal Leydig cell population is still the prevailing source of androgens. Pregnant Sprague-Dawley dams were given a single oral dose of TCDD (0, 0.04, 0.2, or 1.0 microg/kg) on day 13 of pregnancy. On postnatal day 14, the body weight of male offspring was reduced after exposure to 1.0 microg/kg TCDD (from 33.9 +/- 1.66 g to 31.6 +/- 2.67 g). Relative testis weight, plasma testosterone, luteinizing hormone and follicle-stimulating hormone levels remained unaltered in all exposure groups. Moreover, in ex vivo incubations, testosterone and cAMP production was not affected. StAR protein level in the freshly isolated testes was increased in the 0.2 microg/kg group, and seminiferous cord diameter in the 0.04 microg/kg group. The present study confirms our earlier findings in in utero TCDD-exposed foetal testis indicating that maternal TCDD exposure does not negatively influence the developmental testosterone production of foetal type Leydig cells in rats.

Animals↗

PubMed2000

Maternal exposure to tamoxifen during pregnancy increases carcinogen-induced mammary tumorigenesis among female rat offspring.

Tamoxifen is under investigation as a potential chemopreventive agent in women of child-bearing age who are at an increased risk to develop breast cancer. However, because tamoxifen may act as an estrogen in the fetus and high fetal estrogenic activity, in turn, may increase subsequent breast cancer risk, we wanted to determine the effects of a maternal exposure to tamoxifen during pregnancy on offspring's susceptibility to mammary tumorigenesis. Pregnant rats were injected s.c. with 20 microg of tamoxifen or oil vehicle daily during days 15 and 20 of gestation. In utero exposure to tamoxifen caused abnormalities in the development and function of the reproductive track, including a delayed puberty onset and changes in uterine wet weights. The tamoxifen-exposed offspring, treated with 7,12-dimethylbenz[a]antracene (DMBA) at the age of 45 days, developed an increased incidence of mammary tumors. In week 18 after DMBA administration, 50% of the vehicle-controls had developed mammary tumors, whereas tumor incidence in the tamoxifen group was 95%. In addition, a significantly higher number of tumors in the tamoxifen-exposed group kept growing (rather than stopped growing or regressed) than in the control group. Furthermore, histopathological examination revealed that the mammary tumors in the tamoxifen offspring were less differentiated and exhibited a more aggressive phenotype, compared with the tumors growing in the controls. These results suggest that a maternal exposure to tamoxifen during pregnancy acts as an estrogen in the fetal mammary gland and increases the susceptibility to breast cancer among female offspring.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed2006

No evidence of relation between maternal exposure to herpes simplex virus type 2 and risk of schizophrenia?

OBJECTIVE: The authors examined whether maternal exposure to herpes virus type 2 is associated with risk for adult schizophrenia. METHOD: The authors studied a large birth cohort, born 1959-1967, with follow-up for schizophrenia from 1981 through 1997. Sixty patients were diagnosed with schizophrenia and other spectrum disorders; 110 comparison subjects had no schizophrenia spectrum or major affective disorders and were matched to patients by date of birth, gender, time in the cohort, and availability of maternal sera. Archived maternal sera of patients and comparison subjects from late pregnancy were assayed by enzyme-linked immunosorbent assay for immunoglobulin (IgG) antibody to herpes simplex virus type 2. RESULTS: The authors found no associations between maternal IgG seropositivity or antibody levels to herpes simplex virus type 2 and risk of schizophrenia. CONCLUSIONS: The authors found no support for a relationship between prenatal herpes simplex virus 2 type exposure and risk of schizophrenia.

Adult↗

PubMed2006

Maternal hair--an appropriate matrix for detecting maternal exposure to pesticides during pregnancy.

The detection of exposure of pregnant women to toxicants in the environment is important because these compounds can be harmful to the health of the woman and her fetus. The aim of this study was to analyze for pesticides/herbicides in paired maternal hair and blood samples to determine the most appropriate matrix for detecting maternal exposure to these compounds. A total of 449 pregnant women were prospectively recruited at midgestation from an agricultural site in the Philippines where a preliminary survey indicated significant use at home and on the farm of the following compounds: propoxur, cyfluthrin, chlorpyrifos, cypermethrin, pretilachlor, bioallethrin, malathion, diazinon, and transfluthrin. Paired maternal hair and blood samples were obtained from each subject upon recruitment into the study (midgestation) and at birth and were analyzed for the above compounds, as well as lindane and DDT [1,1,1-trichloro-2-2-bis(p-chlorophenyl) ethane], and some of their known metabolites by gas chromatography/mass spectrometry. The highest exposure rate was seen for propoxur and bioallethrin and maternal hair analysis provided the highest detection rate for these two compounds, compared to blood, at both time periods: (1) At midgestation, 10.5% positive for propoxur in hair compared to 0.7% in blood (P<0.001) and for bioallethrin, 11.9% positive in hair compared to 0% in blood (P < or = 0.001), and (2) at birth, 11.8% positive for propoxur in hair compared to 4% in blood (P < or = 0.001) and for bioallethrin, 7.8% in hair compared to 0% in blood (P < or = 0.001). A small number of maternal hair samples were also positive for malathion, chlorpyrifos, pretilachlor, and DDT. Only a few of the pesticide metabolites were detected, principally 3-phenoxybenzoic acid, malathion monocarboxylic acid, and DDE [1,1,dichloro-2-2-bis(p-chlorophenyl)ethylene], and they were mostly found in maternal blood. There was a significant association between the use of the home spray pesticide, Baygon, and propoxur in maternal hair at birth (P=0.001) and between the use of a slow-burning mosquito coil and the presence of bioallethrin in maternal hair at midgestation and at birth (P=0.001, P < or = 0.041, respectively). There is significant exposure of the pregnant woman to pesticides, particularly to pesticides that are used at home. Our study demonstrates the advantages of analyzing maternal hair as a readily available biologic matrix for studying maternal exposure to toxicants in the environment, compared to blood. For propoxur, there was a 3- to 15-fold higher detection rate of the pesticide in maternal hair as compared to blood. As for the other pesticides, bioallethrin, malathion, chlorpyrifos, and DDT were exclusively found in maternal hair compared to blood. On the other hand, pesticide metabolites were infrequently found in maternal hair or maternal blood. Pesticides in blood most likely represent acute exposure, whereas pesticides in hair represent past and/or concurrent exposure. The high sensitivity, wide window of exposure, availability, and ease of hair collection are distinct advantages in using hair to detect exposure to pesticides among pregnant women. However, pesticides in maternal hair may also be secondary to passive exposure and therefore not truly representative of the internal pesticide dose. Finally, the analysis of maternal hair for pesticides as an index of maternal exposure to pesticides in the environment allows the institution of measures to prevent further exposure during pregnancy.

Adult↗

PubMed2006

Maternal exposure to second-hand tobacco smoke and pregnancy outcome among couples undergoing assisted reproduction.

BACKGROUND: Exposure to second-hand tobacco smoke is preventable, yet common. This study assessed relationships between maternal exposure to second-hand tobacco smoke and adverse pregnancy outcomes. METHODS: We measured cotinine (a biomarker of tobacco smoke) in urine from 921 women undergoing assisted reproductive technologies (ARTs) between 1994 and 1998. We also collected information on self-reported exposure to second-hand smoke at home or at work, in addition to parental smoking during the women's childhood. RESULTS: In crude analysis, creatinine-adjusted cotinine levels were associated with a slight decrease in implantation rate among non-smoking women (11.1% in the lowest cotinine quintile versus 8.2% in the highest cotinine quintile; P=0.13). However, in multivariate logistic regression, cotinine levels above the median were not associated with failed fertilization, failed implantation or spontaneous abortion, nor was there evidence of a dose-response relationship among cotinine quintiles. After excluding women in couples diagnosed with male factor infertility, there were increased odds of having a spontaneous abortion among non-smoking women who reported that both parents smoked while they were children growing up compared with women reporting that neither parent smoked [adjusted odds ratio (OR) = 4.35; 95% confidence interval (CI) = 1.04-18.1]. CONCLUSIONS: Female exposure to second-hand smoke as a child or in utero may be associated with an increased risk of spontaneous abortion in adulthood. However, this may be a chance finding due to multiple comparisons. Similar associations should be explored in additional studies with more refined estimates of childhood and in utero exposure to tobacco smoke.

Abortion, Spontaneous↗

PubMedDate not supplied

Behavioral effects following single and combined maternal exposure to PCB 77 (3,4,3',4'-tetrachlorobiphenyl) and PCB 47 (2,4,2',4'-tetrachlorobiphenyl) in rats.

The present study has compared the neurobehavioral effects of two structurally different PCB congeners or their combination in rats. Time-mated Long-Evans rats received daily injections of the coplanar PCB 77 (3,4 3',4'-TCB: 0.5 or 1.5 mg/kg), the di-ortho-chlorinated PCB 47 (2,4,2',4'-TCB: 1.5 mg/kg) or a congener mixture (0.5 mg/kg PCB 77 + 1.0 mg/kg PCB 47) from day 7 to 18 of gestation. The PCB exposure levels in brain and perirenal fat of dams and offspring were determined by GC/ECD on gestational day 19 (GD 19), postnatal day 21 (PND 21), and PND 45. PCB 77 was accumulated to a smaller degree than PCB 47. On GD 19, PCB 77 was found to a greater extent in the brains of the offspring than in the brains of the dams, whereas the level of PCB 47 was almost the same in dams and offspring. The testing of open-field behavior in male rats on PND 18 and PND 70 revealed an altered distribution of activity with enhanced activity in the inner zone in PCB 77-treated rats compared to all other groups, while the overall activity was not changed. Distance traveled and rearing behavior on PND 340 were elevated relative to controls in all PCB-treated groups, indicating age-related effects of maternal exposure. A step-down passive avoidance task revealed decreased latencies in the PCB 77 and combined exposure groups on PND 80. Only PCB 77-treated animals showed increased latencies on PND 100 on the haloperidol-induced catalepsy test. These results indicate long-term effects of maternal exposure to PCB 77 on emotional and motor functions. At the dose levels used in the present experiments, the two congeners given in combination did not cause additive or synergistic effects. Instead, concurrent exposure to PCB 47 seemed to counteract PCB 77-induced changes in the pattern of activity.

Adipose Tissue↗

PubMed2000

Maternal exposure to respiratory infections and adult schizophrenia spectrum disorders: a prospective birth cohort study.

We sought to examine the relationship between maternal exposure to adult respiratory infections and schizophrenia spectrum disorder (SSD) in the Prenatal Determinants of Schizophrenia (PDS) Study, a large birth cohort investigation. Previous work suggests that second trimester exposure to respiratory infection may be a risk factor for SSD. We therefore examined whether this class of infection was associated with adult SSD. For this purpose, we capitalized on several design advantages of the PDS Study, including a comprehensive, prospective data base on physician-diagnosed infections and a continuous followup in which diagnoses of SSD were made, in the majority, by face-to-face interview. Second trimester exposure to respiratory infections was associated with a significantly increased risk of SSD, adjusting for maternal smoking, education, and race (rate ratio [RR] = 2.13 [1.05-4.35], chi2 = 4.36, df= 1,p = 0.04); no associations were shown for first trimester and third trimester exposure to these respiratory infections. These findings support-and extend-previous studies suggesting that second trimester respiratory infections are risk factors for SSD. This study therefore has implications toward uncovering the etiology of schizophrenia and developing preventive strategies.

Adult↗

PubMedDate not supplied

Micronucleus formation in 3-day mouse embryos associated with maternal exposure to chlorpyrifos during the early preimplantation period.

Chlorpyrifos, an organophosphate pesticide, was evaluated for its ability to induce cytogenetic damage in preimplantation embryos after maternal exposure. Pregnant female mice were intraperitoneally (i.p.) administered a single dose of chlorpyrifos (40 or 80 mg/kg) at 10:00 h on Day 0 of pregnancy. On Day 3 of gestation, blastocysts were collected and evaluated for gross morphology, micronucleus (MN) frequency, and cell number. A significant increase in MN frequency indicating cytogenetic damage was observed in the treatment groups in comparison to control. The MN frequency revealed a clear dose-dependent increase. There was also a significant decrease in the embryo cell number in the 80 mg/kg treated group. A simultaneous decrease in the cell number and increase in MN frequency may reflect an embryonic developmental disadvantage resulting from maternal treatment with chlorpyrifos.

Animals↗

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↗

PubMedDate not supplied

Maternal exposure to bacterial endotoxin during pregnancy enhances amphetamine-induced locomotion and startle responses in adult rat offspring.

An increased incidence of schizophrenia has been associated with several perinatal insults, most notably maternal infection during pregnancy and perinatal hypoxia. This study used a rat model to directly test if maternal exposure to bacterial endotoxin (lipopolysaccharide, LPS) during pregnancy alters behaviors relevant to schizophrenia, in offspring at adulthood. The study also tested if postnatal anoxia interacted with gestational LPS exposure to affect behavior. At adulthood, offspring from dams administered LPS on days 18 and 19 of pregnancy showed significantly increased amphetamine-induced locomotion, compared to offspring from saline-treated dams. A period of anoxia on postnatal day 7 had no effect on amphetamine-induced locomotion and there was no interaction between effects of gestational LPS and postnatal anoxia on this behavior. Offspring from LPS-treated dams also showed enhanced acoustic startle responses as adults, compared to offspring from saline-treated dams. In offspring tested for pre-pulse inhibition (PPI) of acoustic startle and for apomorphine modulation of PPI, no effects of either gestational LPS or of postnatal anoxia and no interactions between LPS and anoxia were observed. It is concluded that maternal LPS exposure during pregnancy in the rat may be a useful model to study mechanisms responsible for effects of maternal infection on behaviors relevant to schizophrenia, in offspring.

Amphetamines↗

PubMed2004

Association between maternal exposure to elevated ambient sulfur dioxide during pregnancy and term low birth weight.

This retrospective cohort study investigated whether the risk of delivering full term (37-44 completed weeks of gestation) low birth weight (LBW) infants is associated with differences in exposure to air pollutants in different trimesters. Full-term infants (37 completed weeks of gestation) with a birth weight below 2500 g were classified as term LBW infants. The study infants comprised 92,288 full-term live singletons identified from the Taiwan birth registry and born in the city of Taipei or Kaoshiung in Taiwan between 1995 and 1997. Maternal exposures to various air pollutants including CO, SO2, O3, NO2, and PM10 in each trimester of pregnancy was estimated as the arithmetic means of all daily measurements taken by the air quality monitoring station nearest to the district of residence of the mother at birth. The multivariable logistic regression model with adjustment for potential confounders was used to assess the independent effect of specific air pollutants on the risk of term LBW. This study suggested a 26% increase in term LBW risk given maternal ambient exposure to SO2 concentration exceeding 11.4 ppb during pregnancy compared to low exposure (<7.1 ppb) (OR=1.26, 95% CI=1.04-1.53). Since the relative risk of term LBW was reassessed according to exposure level in each trimester, mothers exposed to >12.4 ppb of SO2 in the last trimester showed 20% higher risk (OR=1.20, 95% CI=1.01-1.41) of term LBW delivery than mothers with lower exposure (<6.8 ppb). No significant elevation ORs was observed for other air pollutants.

Adult↗

PubMed2005

Influences of maternal exposure on the tolerance and physiological performance of Daphnia magna under mercury stress.

We examined the tolerance development to mercury (Hg) by a population of freshwater zooplankton (Daphnia magna) with different pre-exposure histories to Hg. The growth and reproductive performance of the F1 offspring as affected by the maternal (F0) and offspring (F1) exposures was quantified. The F0 daphnids exposed to 2.5 and 25 nM of Hg for 4 d and followed by 4 d of depuration had elevated levels of Hg and metallothionein-like proteins (MTLPs), as well as higher tolerance to Hg toxicity than the control daphnids. The higher Hg tolerance may be attributed to the higher proportion of Hg partitioned to the MTLPs. Moreover, significant enhancement of Hg tolerance also was found in the F1 offspring originating from the F0 mothers exposed to 25 nM of Hg, but there was no significant induction of MTLPs in these F1 offspring when compared to the offspring from the control mothers. The Hg tissue concentrations in the F1 neonates were approximately 25% of those in the F0 adults. However, there was similar Hg tolerance in the F2 offspring originating from both the control and Hg-exposed F0 mothers, indicating that the Hg tolerance in the daphnids disappeared two generations after Hg contamination. Further exposure of the F1 offspring to different Hg concentrations (1.5 and 15 nM for 28 d) indicated that maternal exposure history did not affect their growth and reproductive performance, which solely were influenced by the offspring exposure. Unexpectedly, the F1 offspring exposed to Hg had significantly higher final wet weights and reproductive rates than the control groups, suggesting the possibility of Hg hormesis. Furthermore, the maternal exposure had no effect on the Hg accumulation and the MTLP concentrations in the F1 offspring. Therefore, we concluded that the Hg tolerance might disappear quickly once the Hg contamination was removed and the maternal exposure history was not important in determining the physiological performance and Hg accumulation of the subsequent generations.

Animals↗

PubMed2003

Community diagnosis of maternal exposure to risk factors for congenital defects.

OBJECTIVES: This paper describes a community diagnosis of maternal exposure to risk factors for congenital defects in the population of Pelotas, RS, Brazil (400000 inhabitants). The authors investigated biological and demographic factors (maternal age, alcohol ingestion and smoking), social and economic factors (family income and type of work), and welfare factors (prenatal care, illnesses during pregnancy, drug therapy, and vaccinations). These factors were matched up with the Decalogue for Prevention of Congenital Defects recommended by the Latin American Collaborative Study of Congenital Malformations. METHODS: Data were collected in a population-based study in which mothers were interviewed in the hospitals of Pelotas, RS, during 1995. On each day, the first 3 women to give birth were interviewed in every city hospital. The sample resulted in a total of 3219 interviewed women. RESULTS AND CONCLUSIONS: Low-income groups are most exposed. They present the following potential risk factors: (a). outside the ideal age range for pregnancy; (b). fewer prenatal care appointments; (c). no prevention against rubella through vaccinations, and (d). more cigarette smoking. In the high-income groups, the potential risk factors were: (a). drug therapy (more common) and (b). more women working outside the home. We did not find any difference among social classes concerning: (a). illnesses during pregnancy and (b). ingestion of alcohol. When a general risk score was used, this figure was higher in the group of women who were not within ideal age for pregnancy. However, there was no difference among social classes. This has led us to conclude that delayed childbearing is a global risk whereas each social class has its own risks.

Adolescent↗

PubMed2004

Effect of maternal exposure to tributyltin on reproduction of the pearl oyster (Pinctada fucata martensii).

We examined the effect of tributyltin (TBT) on reproduction of the pearl oyster (Pinctada fucata martensii). In a maternal exposure test, five female pearl oysters were exposed to TBT at measured concentrations of 0 (control), 0.092, or 0.191 microg/L at 25 degreesC for one week, and the embryo developmental success (the ratio of normal D-larvae to all larvae) was measured. The embryo developmental success was significantly decreased in the 0.191-microg/L treatment group (65.5%) compared to that in the control group (82.5%; p = 0.031). Concentrations of TBT in the ovary reached 0.088 microg/g in the 0.191-microg/L treatment group. In a waterborne exposure test, inseminated eggs were exposed to TBT at measured concentrations of 0 (control), 0.020, 0.045, 0.091, 0.192, or 0.374 microg/L for 24 h. The embryo developmental success also was significantly decreased in the 0.192-microg/L treatment group (78.3%; p = 0.020) and no development at all was observed in the 0.374-microg/L treatment group compared with that in the control group (95.4%). These results clearly demonstrate that TBT accumulating in the bodies of bivalves has the potential to inhibit reproduction.

Animals↗

PubMed2003

Effects of maternal exposure to picrotoxin during lactation on physical and reflex development, square crossing and sexual behavior of rat offspring.

The effects of maternal exposure during the first 10 days of lactation to picrotoxin (0.75 mg/kg sc) on maternal behavior, offspring physical and neurobehavioral development as well as sexual behavior were studied. Results showed that (1) dam food and water consumption, maternal behavior and body weight were not different between control and experimental animals, (2) male and female pup body weight and the development of physical landmarks did no differ between control and experimental groups, (3) negative geotaxis was improved in female experimental offspring and palmar grasp reflex did not differ between groups, (4) at 75 days of age the square crossing by female rats of the experimental group was increased in relation to the control group; no differences were observed between male control and experimental animals, (5) male experimental rats exhibited a significant increase in the number of mounts, intromissions and ejaculations parallel to a decrease in latency to first mount, intromissions and ejaculation as well as in the latencies of first postejaculatory mount and intromission and (6) the intromission frequency per minute (hit rate) was increased in these animals. These results suggest that postnatal exposure to picrotoxin improved the sexual behavior of rats. Three hypotheses were proposed to explain the mechanisms underlying this effect: (1) the development of subsensitivity of GABAergic receptors, (2) an interference with early receptor development or (3) with neurotransmitter balance, mainly involving the dopaminergic system.

Animals↗