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PubMed2005

Pregnancy outcomes after maternal exposure to simvastatin and lovastatin.

BACKGROUND: Our objective was to determine the frequency of adverse outcomes after maternal exposure to simvastatin and/or lovastatin during pregnancy in postmarketing experience. METHODS: We reviewed the Merck & Co., Inc. (West Point, PA) pharmacovigilance database for reports of exposure to simvastatin or lovastatin during pregnancy. The reports were classified as prospective (reported prior to pregnancy outcome) or retrospective (reported after pregnancy outcome) and were evaluated for timing of exposure, outcome, congenital anomalies, and other events. Outcome rates were calculated for prospective pregnancies. RESULTS: We identified 477 reports (386 prospective and 91 retrospective) with 225 prospective outcomes reported: 154 live born infants, 49 elective abortions, 18 spontaneous abortions, and 4 fetal deaths. Six congenital anomalies were reported: chromosomal translocation, trisomy 18, hypospadias, duodenal atresia, cleft lip, and skin tag. The rate of congenital anomalies (congenital anomalies/live births plus fetal deaths) was 3.8%, which is similar to the background population rate (3.2%; relative ratio, 1.21; 95% 1-sided upper confidence interval [CI], 2.02). There were 13 retrospective reports describing a range of congenital anomalies. No specific pattern of anomalies was identified in either the prospective or retrospective reports. Rates for other outcomes were similar to background rates. CONCLUSIONS: Although the number of reports was relatively small, there was no evidence of a notable increase in congenital anomalies in women exposed to simvastatin or lovastatin versus the general population. Greater reporting of congenital abnormalities in the retrospective cohort is not unexpected and may reflect a reporting bias. Drugs should be used during pregnancy only if the benefits outweigh the risks. Simvastatin and lovastatin remain contraindicated during pregnancy.

Abnormalities, Drug-Induced↗

PubMed1996

Schizotypy and maternal exposure to influenza and to cold temperature: the Mauritius study.

A topic of current controversy is that maternal exposure to influenza in the 2nd trimester of pregnancy may place the offspring at increased risk for schizophrenia. However, exposure to cold and to influenza may be confounded in existing studies, and case finding and identification may introduce error. Use of measures of schizotypy that are dimensional may be used to overcome some of the difficulties of case identification. Data are derived from the longitudinal study in Mauritius, an island in the southern hemisphere, where, in the case of the 1968-1972 Hong Kong/A2 influenza virus epidemic, influenza and low temperature were not confounded. The results suggest that women's exposure to influenza in pregnancy is associated with an elevation of positive schizotypy scores, whereas exposure to low environmental temperatures is associated with an elevation of anhedonia scores in their offspring.

Adolescent↗

PubMed2006

Di-(2-ethylhexyl)-phthalate affects lipid profiling in fetal rat brain upon maternal exposure.

Lipids, especially essential fatty acids (EFAs), play critical roles in guiding proper fetal development. Exposure to xenobiotics that may alter the fetal supply of EFAs/lipids could potentially lead to fetotoxicity. In this study, we investigated the effects of the peroxisome proliferator chemical, di-(2-ethylhexyl)-phthalate (DEHP), on the lipid metabolomic profile of the rat fetal brain upon maternal exposure during gestation. Female Sprague-Dawley rats were orally gavaged with a control vehicle or DEHP (1,500 mg/kg) from gestational day (GD) 0 to GD 19 and fetal brain tissue was isolated at GD 20. The concentrations of 11 lipid classes [free fatty acid, free cholesterol (FC), cholesterol ester (CE), diacylglycerol (DAG), triacylglyceride, phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine (PS), lysophosphatidylcholine (LYPC), cardiolipin, and sphingomyelin (SM)] were determined, as well as the differences in the composition of individual fatty acids. The total lipid concentration decreased with DEHP exposure, particularly for FC and SM, by 33 and 54%, respectively. The same trend was observed in the fatty acid compositions, particularly the unsaturated fatty acids, where a greater decrease was observed with longer fatty acid chain length. The compositions of docosahexaenoic acid decreased significantly in five lipid classes (P < 0.05), including CE (43%), DAG (60%), PS (33%), LYPC (35%), and SM (40%). In contrast, the most remarkable reduction of arachidonic acid presented in two lipid classes, CE and LYPC, with a decrease of up to 33%. These results suggest that in utero exposure to DEHP alters the lipid metabolome in the fetal brain, which may lead to aberrant neurodevelopment.

Analysis of Variance↗

PubMedDate not supplied

Maternal exposure to exogenous nitrogen compounds and complications of pregnancy.

Increased lipid peroxidation and reduced antioxidant activity have been reported with pregnancy complications. Given that exogenous oxidants stimulate formation of lipid peroxides, the authors investigated the relationship between exposure to nitrogen-oxidizing species and pregnancy complications and took into account markers of antioxidant and oxidant status. The study sample included pregnant women who were from an area polluted by oxidized nitrogen compounds. Methemoglobin, a biomarker of individual exposure, was determined, as were measures of oxidant/antioxidant status, including glutathione balance and lipid peroxide levels. Only 10 women experienced normal pregnancies. The most common complications were anemia (67%), threatened abortion/premature labor (33%), and signs of preeclampsia (23%). Methemoglobin was elevated significantly in all three conditions, compared with normal pregnancies. Reduced:total glutathione decreased, whereas lipid peroxide levels increased. These results suggest that maternal exposure to environmental oxidants can increase the risk of pregnancy complications through stimulation of the formation of cell-damaging lipid peroxides and from a decrease in maternal antioxidant reserves.

Adult↗

PubMed1994

[Effects of maternal exposure to a single dose of kainic acid on the functional development of the brain in the rat].

Effects of maternal exposure to a single and small dose of kainic acid (KA) on the functional development of the offspring were studied in the rat. A single dose of KA at 3 mg/kg or distilled water (DW) was injected on one day during days 11-14 (G11KA-G14KA, G11DW-G14DW) or 17-19 (G17KA-G19KA, G17DW-G19DW) of gestation. The body growth of G14KA-G18KA was significantly larger than that of the controls. In an open-field, alterations observed in the KA-exposed rats were 1) a reduction of the latent time to the first line crossing at 15 days of age, 2) a decrease in ambulation score at 17 days of age and 3) early appearance of rearing behavior at 15 days of age. Frequencies of spontaneous head shakes, grooming and urination during the open-field test were in the normal range. The frequency of 9 mg/kg KA-induced wet-dog shakes increased only in the G17KA male rats when tested in the 5-week-old G12KA, G14KA and G17KA groups. The results indicated that prenatal exposure to a single dose of KA affects the body growth and behavior development during the infantile period in rats. The alterations in the growth and behavior appear to correlate with the exposure time to KA, days 13-18 of fetal life, which is the principal time of neurogenesis in the hippocampus, cerebral cortex and hypothalamus.

Animals↗

PubMedDate not supplied

Maternal exposure to Cd(II) causes malformations of Xenopus laevis embryos.

The FETAX (Frog Embryo Teratogenesis Assay: Xenopus) protocol was adapted to determine whether or not exposure of mature female Xenopus to CdCl2 causes malformed embryos. Twelve females (Group A) were exposed to 18 microM Cd(II) for 11 wk; eight females (Group B) were exposed to 90 microM Cd(II) for 4 wk; controls were also tested. The females were induced to ovulate; their eggs were fertilized with sperm from unexposed males; the embryos were scored for malformations at 101 h post-fertilization, and some were analyzed for Cd and metallothionein. The incidence of malformations was increased in embryos from Group A (median 14 percent, p < 0.05 vs 6 percent in controls), but not from Group B (7 percent). At the blastula stage, Cd content averaged 7.0 (SD +/- 2.8) pmol/embryo (Group A), 6.0 +/- 2.6 (Group B), and < 0.2 (controls); the Cd content was correlated with the malformation incidence in progeny of Group A. At the blastula stage, metallothionein averaged 8.1 +/- 2.9 pmol/embryo (Group A), 8.4 +/- 2.5 (Group B), and 6.3 +/- 1.7 (controls, p < 0.05 vs A or B). This study shows that prolonged maternal exposure to Cd(II) can induce malformations in Xenopus embryos. This study also shows that cadmium is transferred from dam to embryo, probably by Cd(II)-binding to yolk proteins and metallothionein, and suggests that Cd(II)-induced embryotoxicity is influenced by the timing of Cd(II) exposure during oogenesis.

Animals↗

PubMed2005

Effects of long-term maternal exposure to low doses of PCB126 and PCB153 on the reproductive system and related hormones of young male goats.

In this study, female goats were orally exposed to PCB126 or PCB153, at 49 ng/kg body weight per day and 98 microg/kg body weight per day respectively, from gestational day 60 until delivery at approximately day 150. Exposure of the offspring continued via lactation until postnatal day 40. Reproductive toxicity in the male offspring was studied by the evaluation of conventional reproductive endpoints as well as flow cytometric analyses of spermatogenesis and sperm chromatin structure. PCB153-treated animals showed a significant smaller testis diameter in comparison to the control group. Neither of the treated groups showed differences for plasma FSH in comparison to controls. PCB153-treated animals differed significantly from the control group with respect to plasma LH and testosterone levels, whereas PCB126-treated animals only differed from the controls in plasma testosterone concentrations. Neither the PCB126 nor the PCB153 group differed from the controls with respect to the conventional sperm parameters or testis histology. A significant lower ratio of interstitium area to seminiferous tubules area and proportion of diploid testis cells were observed for the PCB153 group. Sperm from PCB153-treated animals showed a significantly higher percentage of sperm with damaged DNA. From the results of the present study it was concluded that PCB153 was able to induce alterations in reproductive endpoints related to the hypothalamic-pituitary-axis as well as to the testis. The effects observed in male kids after a long-term maternal exposure to PCB153 support the concept that exposure to endocrine-disrupting compounds during foetal development may lead to adverse reproductive effects in adult life.

Androgens↗

PubMed2003

Effects of the GSTM1 and GSTT1 polymorphisms on the relationship between maternal exposure to environmental tobacco smoke and neonatal birth weight.

The purpose of the investigation was to determine whether genetic polymorphisms in enzymes that metabolize exogenous chemicals modulate the effects of environmental tobacco smoke (ETS) exposure on birth weight. A survey was conducted from 2000 to 2001 among 266 pregnant women who were hospitalized for delivery and on their singleton live births. We determined maternal GSTM1 and GSTT1 polymorphisms by polymerase chain reaction and measured the urinary cotinine of pregnant women at delivery by radioimmunoassay. Birth weight was found to decrease significantly with increasing concentrations of maternal urinary cotinine (P < 0.05). The interactive effect of exposure to ETS and the presence of the GSTT1 polymorphism was found to be significant by multivariate analysis (P < 0.01), whereas the interactive effect of exposure to ETS and the presence of GSTM1 polymorphism did not reach statistical significance (P = 0.21). A combination of the GSTM1-null and the GSTT1 null-genotypes was found to exacerbate the effect of maternal exposure to ETS on birth weight more than the presence of either genotype alone. Our data indicate that maternal exposure to ETS negatively affects neonatal birth weight, and the adverse effect of maternal exposure to ETS on neonatal birth weight could be modified by the maternal metabolic genotypes, GSTM1 and GSTT1.

Adult↗

PubMed1984

Neonatal cytomegalovirus infections: the relative role of neonatal blood transfusion and maternal exposure.

A prospective study of premature infants admitted to an intensive care neonatal unit was undertaken to evaluate the relative role of blood transfusions and maternal exposure in infections caused by cytomegalovirus (CMV), varicella zoster virus (VZV) and herpes simplex virus (HSV). During the first year of life, 13.7%, 4.8% and 4% of the infants became infected with CMV, VZV and HSV, respectively, as determined by virus isolation or seroconversion. Transfusion in the newborn period did not influence the rates of VZV or HSV infections. A higher rate of CMV infections occurred in transfused (18.8%) than in non-transfused (11%) infants but the difference was not statistically significant. A significant correlation was found between maternal antibody titers and the rate of CMV infection in infants whether or not transfusion occurred. An even stronger association was found between breast feeding and CMV infections. The risk of alloimmunization to erythrocyte and leucocyte antigens was also assessed; no evidence of increased alloimmunization to these antigens was associated with transfusion.

Antibodies, Viral↗

PubMed1998

Gene mutations with characteristic deletions in cord blood T lymphocytes associated with passive maternal exposure to tobacco smoke.

We have investigated the molecular effects of passive maternal cigarette exposure in a newborn population and consider the possible implications of the observed genetic changes in the development of neoplastic diseases in children. We present a distribution analysis of somatic mutational events in a reporter gene, HPRT, in cord blood T lymphocytes from newborns after transplacental exposure to cigarette smoke. Analysis of 30 HPRT mutant isolates from 12 newborn infants born to mothers with no evidence of environmental exposure to cigarette smoke and 37 HPRT mutant isolates from 12 infants born to mothers exposed to passive cigarette smoke showed a significant difference in the HPRT mutational spectrum in those exposed in utero to cigarette smoke. The most notable change was an increase in 'illegitimate' genomic deletions mediated by V(D)J recombinase, a recombination event associated with hematopoietic malignancies in early childhood. Recent epidemiological studies of maternal and paternal cigarette smoke exposure and childhood cancers may need to be re-interpreted, given these results.

Base Sequence↗

PubMed2002

Effects of maternal exposure to a reconstituted mixture of polychlorinated biphenyls on sex-dependent behaviors and steroid hormone concentrations in rats: dose-response relationship.

In a previous experiment, maternal exposure to a polychlorinated biphenyl (PCB) mixture reconstituted according to the congener pattern found in human breast milk resulted in decreased aromatase activity in the brain of newborn male rats, together with feminization of sweet preference behavior in adult male littermates. Both mixtures led to similar reductions of serum testosterone and testes weights. The purpose of the present study was (1) to examine the dose-response relationship for the reconstituted mixture and (2) to study if the rewarding properties of testosterone are affected at levels sufficient to alter sweet preference behavior. Female rats were fed diets with 0, 5, 20, or 40 mg PCBs/kg diet, resulting in an average daily intake of 0, 0.5, 2, or 4 mg/kg body wt. Exposure started 50 days prior to mating and was continued until birth of the offspring. A dose-dependent elevation of sweet preference was found in adult male offspring, indicating feminization of this sexually dimorphic behavior. Examination of conditioned place preference revealed a preference for the testosterone-paired side at the highest exposure condition. In weanling female offspring, dose-dependent reductions of serum testosterone and estradiol concentrations were detected. In addition, testosterone concentrations were reduced in a dose-dependent manner in adult male littermates long after termination of exposure. PCB concentrations in adipose tissue from offspring of the low dose group (0.5 mg/kg body wt) were approximately 10 times higher than values at the upper margin of current human exposure. Taken together, results indicate long-lasting and dose-dependent changes in sex-dependent behaviors and levels of sex steroid hormones in rats following developmental exposure to a PCB mixture that resembles the breast milk pattern.

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↗

PubMed1997

Effects of maternal exposure to chlorinated diphenyl ethers on thyroid hormone concentrations in maternal and juvenile rats.

Polychlorinated diphenyl ethers (PCDEs) are industrial byproducts and widespread environmental contaminants. Their structural similarity to PCBs suggests that they may exhibit subtle effects on both adult and juvenile mammals. We examined the effects of 3 PCDEs (2,2',4,5,6'-pentachlorodiphenyl ether, 2',3,4,6'-tetrachlorodiphenyl ether, and 2,2',4,4',5,5'-hexachlorodiphenyl ether) on maternal rat thyroid levels shortly after exposure, and on the thyroid levels of 16 day old juvenile rats that had been prenatally exposed. Both 2,2',4,5, 6'-pentachlorodiphenyl ether and 2',3,4,6'-tetrachlorodiphenyl ether depressed thyroxine (T4) levels in the maternal females as well as in both sexes of juvenile rats. 2,2',4,4',5,5'-hexachlorodiphenyl ether did not alter T4 levels in the pregnant females, but depressed juvenile T4 levels. None of the congeners studied significantly altered T3 levels. Effects on thyroid hormones did not correlate with the congeners' induction of cytochrome P450.

Analysis of Variance↗

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↗

PubMed2005

Maternal exposure to occupational solvents and childhood leukemia.

Many organic solvents are considered probable carcinogens. We carried out a population-based case-control study including 790 incident cases of childhood acute lymphoblastic leukemia and as many healthy controls, matched on age and sex. Maternal occupational exposure to solvents before and during pregnancy was estimated using the expert method, which involves chemists coding each individual's job for specific contaminants. Home exposure to solvents was also evaluated. The frequency of exposure to specific agents or mixtures was generally low. Results were generally similar for the period ranging from 2 years before pregnancy up to birth and for the pregnancy period alone. For the former period, the odds ratio (OR), adjusted for maternal age and sex, for any exposure to all solvents together was 1.11 [95% confidence interval (CI), 0.88-1.40]. Increased risks were observed for specific exposures, such as to 1,1,1-trichloroethane (OR = 7.55; 95% CI, 0.92-61.97), toluene (OR = 1.88; 95% CI, 1.01-3.47), and mineral spirits (OR = 1.82; 95% CI, 1.05-3.14). There were stronger indications of moderately increased risks associated with exposure to alkanes (C5-C17; OR = 1.78; 95% CI, 1.11-2.86) and mononuclear aromatic hydrocarbons (OR = 1.64; 95% CI, 1.12-2.41). Risk did not increase with increasing exposure, except for alkanes, where a significant trend (p = 0.04) was observed. Home exposure was not associated with increased risk. Using an elaborate exposure coding method, this study shows that maternal exposure to solvents in the workplace does not seem to play a major role in childhood leukemia.

Adolescent↗

PubMed1996

Expression of cytochrome P450 17alpha-hydroxylase/C17-20 lyase in the fetal rat testis is reduced by maternal exposure to exogenous estrogens.

Testosterone is required for normal development of the male reproductive tract. Synthesis of testosterone occurs in the Leydig cells and is dependent upon the expression of several enzymes, including cytochrome P450 17alpha-hydroxylase/C17-20-lyase (P450c17), which is highly regulated within the testis. The aim of the present study was to investigate whether maternal exposure to estrogenic chemicals was able to affect Leydig cell function in the developing male fetus at the time of masculinization. Pregnant rats were injected sc with diethylstilbestrol (DES; 100 or 500 micrograms/kg), 4-octylphenol (OP; 100 or 600 mg/kg), or vehicle (oil, control) on days 11.5 and 15.5 postcoitum. Doses were chosen to reflect the reported estrogenic potency of the chemicals in vitro. On day 17.5, fetal testes were fixed before performing in situ hybridization and immunocytochemistry, used for extraction of RNA, or homogenized in phosphate buffer for determination of 17alpha-hydroxylase enzyme activity. There was no difference between fetuses from control and treated mothers in either the overall histology of the testes or the apparent number of Leydig cells, as determined by immunocytochemistry with an antibody directed against 3beta-hydroxysteroid dehydrogenase. However, there was a consistent and striking reduction in the amount of P450c17 detected by immunocytochemistry in testes from the groups given the higher dose of DES or OP. These observations were supported by measurement of 17alpha-hydroxylase activity, which was significantly reduced compared with that in controls (6.25 +/- 0.65 pmol/testis x min) in fetuses from animals treated with 100 micrograms/kg DES (4.27 +/- 0.39; P < 0.05), 500 micrograms/kg DES (1.4 +/- 0.47; P < 0.001), or 600 micrograms/kg OP (4.25 +/- 0.33; P < 0.05). RT-PCR and in situ hybridization revealed that these changes were mirrored by reductions in P450c17 messenger RNA in testes from fetuses from treated mothers compared with control levels. In conclusion, maternal treatment with either a potent sythetic estrogen (DES) or a putative environmental estrogen (OP) results in reduced expression of the messenger RNA and protein for P450c17 in fetal Leydig cells. These results, therefore, provide a mechanism by which inappropriate exposure of the fetus to estrogenic chemicals might have an adverse effect on fetal steroid synthesis and masculinization.

Aldehyde-Lyases↗

PubMed2002

Effect of maternal exposure to the environmental estrogen, octylphenol, during fetal and/or postnatal life on onset of puberty, endocrine status, and ovarian follicular dynamics in ewe lambs.

Octylphenol (OP) is one of a number of compounds found in the environment that has estrogen-mimicking actions in vivo. Our objective was to determine if maternal exposure to octylphenol during fetal and/or postnatal life would affect the onset of puberty, endocrine status, and subsequent ovarian follicular dynamics of ewe lambs. Lambs were born in March to ewes that received twice weekly s.c. injections of octylphenol (1000 micro g/kg/day) from Day 70 of gestation to weaning (n = 6); Day 70 of gestation to birth (n = 3); birth to weaning (n = 5; gestation = 145 days); or corn oil from Day 70 of gestation to weaning (control; n = 5). Blood samples were collected twice weekly to determine progesterone and FSH concentrations from 20 wk of age throughout the first breeding season. Onset of puberty and interestrous intervals were determined from 20 wk of age by twice daily observation for estrus in the presence of a vasectomized ram. During January the ovaries of each lamb were examined using transrectal ultrasonography from the day of estrus for 15 days. Blood samples were collected every 8 h to examine FSH concentrations and every 2 h to detect the preovulatory gonadotropin surge throughout this estrous cycle. The onset of puberty and first progesterone rise was advanced and the FSH preovulatory surge was elevated for longer in the OP-treated lambs compared with the control lambs (P < 0.05). Interestrous intervals, FSH profiles, and ovarian follicular dynamics were not affected (P > 0.05) by exposure to octylphenol. In conclusion, octylphenol exposure advanced the onset of puberty but it did not disrupt FSH concentrations or the dynamics of ovarian follicular growth.

Animals↗