The Role of the Placenta in Developmental Toxicology

Juchau, Mont R.

doi:10.1007/978-1-4615-9790-2_7

Cited by 13 publications

(2 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The majority of teratology experiments have explored such problems as the identification of agents that cause developmental toxicity; the characterization of the role that is played by the stage of embryonic development at the time a teratogen is applied; the role that embryonic cell death may play in the genesis of malformation; or how interference with such processes as morphogenetic movements or tissue interactions affect the outcome development. The efficiency of maternal-embryonic exchange via the placenta has been recognized as being potentially important in developmental toxicity [2,3]. However, except for experiments examining the capability of the placenta to modulate the transfer of substances to and from the developing organism, the role of the placenta in developmental toxicity remains relatively unexplored.…”

Section: Introductionmentioning

confidence: 99%

Maternal factors in developmental toxicity

DeSesso

1987

Teratog Carcinog Mutagen

View full text Add to dashboard Cite

The maternal organism provides the developing embryo with its physical environment, nutrients, and a mechanism for eliminating metabolic wastes. Since the physiological state of the pregnant female affects her ability to provide those requirements for the developing embryo, it is not surprising that there are maternal factors that can affect the wellbeing of the embryo. Extremes of maternal age in both humans and animals have been implicated in growth retardation, as well as autosomal trisomies. The influence of maternal size on fetal size is more pronounced among larger species with longer gestation periods such as humans and domestic animals. A clear relationship between the parity of the mother and potential developmental toxicity in humans has not been established due to the confounding influences of maternal age. Among laboratory rodents, however, it appears that offspring of multiparous animals are at increased risk of developmental toxicity. A variety of infectious agents, particularly viruses, have either been demonstrated or implicated as causes of developmental toxicity. In addition, hyperthermia is a possible confounding factor inherent with maternal infection. Although under experimental conditions hyperthermia is teratogenic in laboratory animals, a causative role for transient hyperthermia, which occurs during febrile states concomitant with infections, cannot be clearly established. Chronic maternal vascular disease states including essential hypertension, heart disease, or diabetes mellitus are likely to contribute to uteroplacental insufficiency and developmental toxicity. Poor maternal nutrition among humans contributes to growth retardation, but not to malformations. The production of "abnormal" maternal antibodies, such as are present in Rh incompatibility, can cause fetal wastage. An important maternal factor in humans is uteroplacental insufficiency, which can occur in normal states like twinning, as well as in abnormal conditions including reduced placental size, chronic maternal hypoxia, or uterine ischemia. Although all these maternal factors can contribute to developmental toxicity, they do not necessarily occur as isolated events. Some developmental toxicants exert deleterious effects within both the embryo and the maternal system.

show abstract

Section: Introductionmentioning

confidence: 99%

Maternal factors in developmental toxicity

DeSesso

1987

Teratog Carcinog Mutagen

View full text Add to dashboard Cite

show abstract

“…The potential of chemicals to induce placental injury, thereby compromising placental function, has been described (Juchau 1982;Miller et al 1983). Since the placenta plays a central role in maintaining pregnancy, it seems evident that toxic agents interacting with this organ could have an adverse effect on prenatal development.…”

Section: Introductionmentioning

confidence: 99%

Secretion of human chorionic gonadotropin in superfused young placental tissue exposed to cadmium

et al. 1992

View full text Add to dashboard Cite

The effect of various concentrations of cadmium (Cd) in levels ranging from 0.75 to 12 micrograms/ml medium, on the secretion of human chorionic gonadotropin (hCG) in first-trimester placental explants, after 6 or 24 h incubation, employing both static and dynamic systems was examined. Later the unbound Cd was washed for 45 min with fresh medium devoid of Cd, followed by superfusion with the latter medium for 75 min, during which time samples were collected for hCG assay. For the superfusion experiments the parameters used for evaluating the hCG secretion pattern were: mean peak amplitude (MPA), pulse frequency (PF) and the area under the hCG secretion curve (AUC). The results indicate that in the dynamic system the hCG secretion increased significantly, and this increase was dose dependent. There was also a dose-related increase in mean total hCG secreted by the explants exposed to Cd. Maximal hCG secretion was observed after 24 h exposure of explants to 6 micrograms of the metal/ml. Both the MPA and AUC parameters showed a statistically significant increase for this dose level. At 12 micrograms/ml, the pulsatile secretion of hCG decreased, the value for the mean hCG secretion being comparable to that observed for 0.75 micrograms/ml. After 6 h incubation, however, there were no significant changes from the control, as judged by all of the above parameters. The levels of hCG secreted by the explants into the media in the static system were not significantly different from their respective controls, for both incubation periods and Cd levels. These results indicate that Cd may affect the normal placental function, as reflected in its hCG secretion pattern.

show abstract

Perinatal Toxicology: Its Recognition and Fundamentals

Miller

1983

American J Industrial Med

View full text Add to dashboard Cite

Perinatal toxicology is the study of aberrant or toxic responses to environmental agents when exposure occurs from conception through the neonatal period. The current increased interest in perinatal toxicology reflects the concern of both society and the individual in the resultant deficits induced by exposure to agents in the workplace, home, environment and by therapeutic intervention during early development. Not only is differentiation during organogenesis (the first eight weeks in human gestation) a highly susceptible period to the induction of malformations, but the fetal/neonatal developmental phases are just as sensitive for certain developmental deficits. Long-term postnatal evaluations are in most instances critical for the documentation of fetal/neonatal functional defects, which include carcinogenesis, behavioral impairment, endocrine and immune dysfunction. Ethylnitrosourea, estrogens (diethylstilbestrol), and cadmium are discussed in relationship to specificity of their fetal effects, long-term follow-up, and possible mechanisms of toxic action.

show abstract

The Role of the Placenta in Developmental Toxicology

Cited by 13 publications

References 72 publications

Maternal factors in developmental toxicity

Maternal factors in developmental toxicity

Secretion of human chorionic gonadotropin in superfused young placental tissue exposed to cadmium

Perinatal Toxicology: Its Recognition and Fundamentals

Contact Info

Product

Resources

About