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At least 235 records · Page 13Linked to original sources
PubMed1994

Developmental effects of endothelin-1 on the pulmonary circulation in sheep.

Endothelin-1 (ET-1) is a polypeptide that has potent hemodynamic effects on the pulmonary circulation. To determine whether there are changes in these effects with increasing postnatal age, we investigated the effects of ET-1 (250 ng/kg) at rest and during pulmonary hypertension in eight lambs (< 1 wk old) and 11 juvenile sheep (6-12 mo old). At rest, ET-1 did not change pulmonary arterial pressure in lambs, but increased pulmonary arterial pressure by 64.0 +/- 37.5% (p < 0.05) in sheep. During pulmonary hypertension, ET-1 produced greater decreases in pulmonary arterial pressure in lambs than in sheep (26.6 +/- 3.4% versus 18.7 +/- 8.3%, p < 0.05). In juvenile sheep, the increase in resting pulmonary arterial pressure produced by ET-1 was inhibited by meclofenamic acid, an inhibitor of prostaglandin synthesis (40.3 +/- 9.9% versus 2.3 +/- 4.7%, p < 0.05); during pulmonary hypertension, the decrease in pulmonary arterial pressure produced by ET-1 was inhibited by N omega-nitro-L-arginine, an inhibitor of endothelium-derived nitric oxide synthesis (21.4 +/- 10.7% versus 8.0 +/- 3.6%, p < 0.05) and by glybenclamide, an ATP-dependent potassium-channel blocker (18.8 +/- 8.4% versus 4.0 +/- 4.4%, p < 0.05). The hemodynamic effects of ET-1 on the pulmonary circulation are dependent on postnatal age. Pulmonary vasoconstriction is mediated by prostaglandin production, and pulmonary vasodilation is mediated, in part, by release of endothelium-derived nitric oxide and activation of ATP-dependent potassium channels.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1986

17 beta-estradiol 2- and 4-hydroxylation catalyzed by rat hepatic cytochrome P-450: roles of individual forms, inductive effects, developmental patterns, and alterations by gonadectomy and hormone replacement.

The participation of rat hepatic P-450 in the conversion of 17 beta-estradiol to catechol estrogens was examined by means of enzyme reconstitution and immunoinhibition studies. It was thus demonstrated that three rat liver microsomal cytochrome P-450 forms, designated P-450UT-A, P-450PCN-E, and P-450ISF-G, each contribute to the 2- and 4-hydroxylation of 17 beta-estradiol catalyzed by hepatic microsomal preparations. Two of these enzymes, P-450UT-A and P-450PCN-E, are expressed constitutively, are male-specific, and are regulated by testosterone as well as influenced by the administration of various chemicals. Consistent with these observations, 17 beta-estradiol 2- and 4-hydroxylation activities both increased rapidly during puberty in male rats and were induced by treatment of rats with phenobarbital or pregnenolone 16 alpha-carbonitrile. Castration of male rats at birth or at 5 weeks of age suppressed the levels of 17 beta-estradiol 2- and 4-hydroxylase activities measured at 10 weeks of age. This suppression of activity was reversed upon administration of testosterone during the neonatal period (days 1 and 3 of life) or by capsule implantation at 5 weeks of age. These patterns of 17 beta-estradiol 2- and 4-hydroxylation are discussed in terms of the previously characterized response of the multiple rat hepatic P-450 forms to ontogenic, hormonal, and xenobiotic factors.

Aging↗
PubMed1984

Developmental effects after inhalation exposure of gravid rabbits and rats to ethylene glycol monoethyl ether.

The effects of ethylene glycol monoethyl ether (EGEE) were determined on development in utero. Pregnant New Zealand White rabbits were exposed to air or 160 or 617 ppm EGEE for 7 hr/day from 1 to 18 days of gestation (dg). Virgin Wistar rats were exposed to 150 or 649 ppm EGEE or air 5 days/week for the 3 weeks immediately preceding their breeding. Sperm-positive rats were subsequently exposed to air or 202 or 767 ppm EGEE for 7 hr/day from 1 to 19 dg. Group sizes were 29 to 38 per concentration for both species. Pregestational exposure of rats had no effect on mating success, and there was no effect of EGEE exposure on establishment of pregnancy in either species. Rabbits exposed to the both concentrations had decreased food intake and depressed weight gain. Exposure-related mortality occurred in the 617 ppm EGEE group of rabbits. The only toxic sign seen in rats was reduced weight gain after exposure to 767 ppm EGEE. Exposure induced high embryomortality at maternal toxic concentrations in rats and rabbits, while lower levels induced fetal growth retardation in rats but not in rabbits. Gestational exposure increased the incidence of anomalies and variations; these were primarily of soft tissues in rabbits and of skeleton in rats. Thus, significant evidence of terata, fetal growth retardation and embryomortality were induced in rabbits and rats at levels that were below or similar to those that induced maternal manifestation of toxicity. These data implicate EGEE as a teratogen.

Abnormalities, Drug-Induced↗
PubMed1993

Developmental effects of endocrine-disrupting chemicals in wildlife and humans.

Large numbers and large quantities of endocrine-disrupting chemicals have been released into the environment since World War II. Many of these chemicals can disturb development of the endocrine system and of the organs that respond to endocrine signals in organisms indirectly exposed during prenatal and/or early postnatal life; effects of exposure during development are permanent and irreversible. The risk to the developing organism can also stem from direct exposure of the offspring after birth or hatching. In addition, transgenerational exposure can result from the exposure of the mother to a chemical at any time throughout her life before producing offspring due to persistence of endocrine-disrupting chemicals in body fat, which is mobilized during egg laying or pregnancy and lactation. Mechanisms underlying the disruption of the development of vital systems, such as the endocrine, reproductive, and immune systems, are discussed with reference to wildlife, laboratory animals, and humans.

Animals↗
PubMed1977

Developmental effects of the uterine environment: dependence on fetal sex in rats.

Body weight was recorded as a function of intrauterine position for 20-day-old male and female rat fetuses from 83 normal litters. Male fetuses located in the middle of the uterine horn were invariably heavier than males located at the extreme ovarian or cervical positions, those at intermediate positions being intermediate in size. The mean body weight of male fetuses was inversely related to the number of fetuses present in the ipsilateral uterine horn. The body weight of female fetuses appeared independent of both intrauterine position and ipsilateral uterine occupancy. For both sexes, fetal body weight was inversely related to the number of littermates in the contralateral horn. Male fetuses were significantly larger than female fetuses under all but the most adverse intrauterine conditions. Therefore, random fluctuations in sex ratio may distort the true relationshp between mean fetal weight and intrauterine position, if the two sexes are not analysed separately.

Animals↗
PubMedDate not supplied

Developmental effects of prenatal exposure to bisphenol a on the uterus of rat offspring.

Exposure to estrogenic compounds during critical periods of fetal development could result in adverse effects on the development of reproductive organs that are not apparent until later in life. Bisphenol A (BPA), which is employed in the manufacture of a wide range of consumer products, is a prime candidate for endocrine disruption. We examined BPA to address the question of whether in utero exposure affects the uterus of the offspring and studied the expression and distribution of the estrogen receptors alpha (ERalpha) and beta (ERbeta), because estrogens influence the development, growth, and function of the uterus through both receptors. Gravid Sprague-Dawley dams were administered by gavage either 0.1 or 50 mg/kg per day BPA or 0.2 mg/kg per day 17alpha-ethinyl estradiol (EE2) as reference dose on gestation days 6 through 21. Female offspring were killed in estrus. Uterine morphologic changes as well as ERalpha and ERbeta distribution and expression were measured by immunohistochemistry and Western blot analysis. Striking morphologic changes were observed in the uterine epithelium of postpubertal offspring during estrus of the in utero BPA-treated animals (the thickness of the total epithelium was significantly reduced). ERalpha expression was increased in the 50-mg BPA and EE2-treated group. In contrast, we observed significantly decreased ERbeta expression in all BPA- and EE2-treated animals when compared with the control. In summary, these results clearly indicate that in utero exposure of rats to BPA promotes uterine disruption in offspring. We hypothesize that the uterine disruption could possibly be provoked by a dysregulation of ERalpha and ERbeta.

Animals↗
PubMed2006

Physiological and developmental effects of O3 on cottonwood growth in urban and rural sites.

Previously we found that cloned cottonwood saplings (Populus deltoides) grew twice as large in New York, New York, USA, compared to surrounding rural environments and that soils, temperature, CO2, nutrient deposition, and microclimatic variables could not account for the greater urban plant biomass. Correlations between final season biomass and cumulative O3 exposures, combined with twofold growth reductions in an open-top chamber experiment provided strong evidence that higher cumulative O3 exposures in rural sites reduced growth in the country. Here, we assess the field gas exchange, growth and development, and allocation responses underlying the observed growth differences and compare them with isolated O3 responses documented in the open-top chamber experiment. Cottonwoods showed no visible foliar injury, reduced photosynthesis of recently expanded foliage, early leaf senescence, protective reduction in stomatal conductance, or compensatory allocation to shoot relative to root biomass for either the chamber or field experiment. Instead, O3-impacted chamber plants had significantly higher conductance and reduced photosynthesis of older foliage that led to reduced leaf area production and a twofold biomass reduction in the absence of visible injury. Rural-grown field plants showed the same pattern of significantly higher conductance in the absence of concomitant increases in photosynthesis that was indicative of a loss of stomatal control. Incremental changes in foliar production were also significantly inversely related to fluctuations in ambient O3 exposures. The similarity in biomass, gas exchange, phenological, and allocation responses between chamber and field experiments indicate that mechanisms accounting for reduced growth at rural sites were consistent with those in the open-top chamber O3 experiment. This study shows the limitation of visible symptoms as a sole diagnostic factor for documenting detrimental O3 impacts and points toward a new approach to show O3 impacts when visible injury is not present. Namely, O3-impacted vegetation showed an unusual inverse relationship of increased conductance with lower photosynthesis of older foliage that was indicative of a loss of stomatal control. This increased stomatal conductance of O3-impacted vegetation accentuates pollutant flux into affected foliage and has important implications for system water balance during warm, dry portions of the growing season when O3 concentrations are highest.

Air Pollutants↗
PubMed2006

Teratogenic and developmental effects of lithium.

A review is presented on the effects of lithium in therapeutic doses on the outcome of human pregnancy. The results of various studies including cohort, prospective, retrospective and small number case reports indicate that lithium is a "weak" teratogen in humans. The main effects attributable to lithium are, cardiac malformations and babies with increased birth weight. There is a possibility that, in particular, lithium may be associated with the Ebstein anomaly but present evidence cannot definitely affirm or deny this association. Animal studies with lithium using doses comparable to human therapeutic serum levels have not reported any abnormalities. However, higher doses have produced exencephaly, skeletal and craniofacial defects and abnormalities of blood vessel development. Experiments with other vertebrates have shown that lithium affects dorsoventral specification and inhibition of vasculogenesis. Both these effects can be prevented by pretreatment with myo-inositol indicating that lithium interferes with the phosphatidyl inositol cycle. More recent findings have shown that the effects of lithium on invertebrates may be mediated through inhibition of GSK-3beta in the Wnt-GSK-3 pathway.

Animals↗
PubMed1985

Developmental effects associated with exposure to xylene: a review.

Data obtained from rodents indicates that maternal exposure to mixed xylenes or individual xylene isomers can have adverse effects on the conceptus. Fetotoxic effects were reported following maternal inhalation exposure to mixed xylenes; altered enzyme activities were also found in rat pups. Dermal application resulted in apparent changes in fetal enzyme activities, while oral treatment was followed by prenatal mortality, growth inhibition, and malformations, primarily cleft palate. Maternal inhalation of individual isomers was associated with all of the above mentioned effects, with the exception of cleft palate. The o- and p-isomers appeared more hazardous to offspring than did the m-isomer. Malformations (i.e., cleft palate) associated with mixed or individual isomers were primarily reported at maternally toxic doses. Thus, a clear case for a selective teratogenic effect due to exposure to xylene has yet to be presented.

Animals↗
PubMed1997

Maternal substance use: epidemiology, treatment outcome, and developmental effects: an annotated bibliography, 1995.

Understanding the effects of substance misuse by pregnant women and mothers of young children requires a knowledge of the epidemiology of women's drug and alcohol use and misuse, the treatment of pregnant and postpartum chemically dependent women, the impact of prenatal exposure on the offspring outcome and later development, and, finally, methodological issues related to these fields. This bibliography provides a list of recent and classic articles in these areas as well as information about the research in these areas.

Female↗
PubMed1976

Developmental effects of seizures: role of malnutrition.

Eighty-eight rats were paired at birth according to sex and weight. One member of each pair received two electroconvulsive seizures a day during the neonatal period (days 2 to 11). Access of its control littermate to the mother was restricted so that the body weights of any two paired rats never diverged by more than 2 gm on any day of life, and were usually within one half gram of each other. This guaranteed that the nutritional status of seizure-treated and control animals was similar throughout development. On day 30 of life, seizure-treated rats had smaller brains (-56 mg, P less than .05) and reduced numbers of brain cells (-13.10(6), P less than .05) compared to their control littermates. It was concluded that the reduction of brain DNA brought about by neonatal seizures was not simply caused by malnutrition of seizure-treated animals.

Animals↗
PubMed2003

Salivary testosterone diurnal variation and psychopathology in adolescent males and females: individual differences and developmental effects.

Individual differences in salivary testosterone were examined in 213 adolescents (106 boys, 107 girls; mean age = 13.66 years) in relation to externalizing and internalizing psychopathology. Self- and parent-report measures of behavior problems and psychiatric symptoms were obtained. Latent anxiety-depression, disruptive behavior, and attention problem constructs were developed using multitrait, multimethod procedures. Saliva samples were collected in the morning, midday, and late afternoon on multiple days and were later assayed for testosterone. Latent constructs were derived for testosterone level and diurnal variation across the six sampling occasions. Structural equations modeled relationships between problem behavior and intra- and interindividual differences in testosterone separately by gender. For boys, lower levels of testosterone and testosterone levels that decreased more slowly across the day were related to higher levels of anxiety-depression and attention problems. These associations were not moderated by pubertal development. For girls, steep declines in testosterone production across the day related to higher levels of disruptive behavior problems, but this association was only evident after including pubertal development as a moderator in the model. These findings raise novel questions regarding the nature and magnitude of links between testosterone and problem behavior in youth.

Adolescent↗