Prenatal hamster development following maternal administration of PGE2 at midterm

Liebgott, B.; Wiley, Michael J.

doi:10.1016/0262-1746(85)90120-9

Cited by 14 publications

(1 citation statement)

References 15 publications

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“…Our data suggest that these APOs are associated with increases in host-derived PGE2 and TNF-ot produced following bacterial challenge. The embryotoxic effects of PGE2 in the absence of infection were demonstrated by Liebgott and Wiley (12). By using the hamster model with a similar design, it was shown that PGE2 delivered in a single intraperitoneal bolus on day 8 of gestation produced teratogenic effects comparable with the results of this study.…”

Section: Discussionsupporting

confidence: 81%

Effects of a Porphyromonas gingivalis infection on inflammatory mediator response and pregnancy outcome in hamsters

et al. 1994

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This study examines the effects of various localized, nondissemination challenges ofPorphyromonas gingivalis on inflammatory mediator production and pregnancy outcome in the golden hamster. Live or heat-killed (HK) organisms were inoculated into a previously implanted subcutaneous tissue chamber on the 8th day of gestation to determine the effects on fetal weight, viability, and resorption. In one group of animals, HK organisms were inoculated prior to mating to determine the effects of previous exposure on day-8 gestational challenges. Chamber contents were assayed at 1 and 5 days after challenge for prostaglandin E2 (PGE2) and tumor necrosis factor alpha (TNF-a). All P. gingivalis challenges caused a significant increase in chamber PGE2 and TNF-a at P < 0.01 in the following order of potency: HK < Live < HK+Live. For example, following the HK+Live challenge, PGE2 levels increased from 4.7 pg/ml at baseline to 362 pg/ml at day 5 and TNF-a increased from 26.4 pg/ml to 724 pg/ml at day 5. The same order of potency of the various challenges was maintained with regard to the toxic effects of P. gingivalis on pregnancy outcome. For the HK+Live challenge, fetal weight was decreased 24%; embryolethality increased to 26.5% and the percent fetal resorption increased to 10.6% compared with control animal levels. There was a statistically significant association between increasing levels of both PGE2 and TNF-ot and fetal growth retardation and embryolethality at P < 0.001. These data suggest that infections with gram-negative periodontal pathogens can elicit adverse pregnancy outcomes and that the levels of PGE2 and TNF-at produced as a result of challenge are associated with the severity of fetal effect.

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Section: Discussionsupporting

confidence: 81%

Effects of a Porphyromonas gingivalis infection on inflammatory mediator response and pregnancy outcome in hamsters

et al. 1994

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Dinoprostone 363‐24‐6

2004

Sax's Dangerous Properties of Industrial Materials

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Effects of N‐acetylcysteine on fetal development and on phenytoin teratogenicity in mice

Wong

Wells

1988

Teratog Carcinog Mutagen

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The teratogenicity of phenytoin may result from its enzymatic bioactivation to a reactive intermediate, which interacts irreversibly with fetal tissues. Since glutathione (GSH) is involved in the detoxification of many reactive intermediates, N-acetylcysteine (NAC), a glutathione precursor, was evaluated for its effects on murine fetal development and phenytoin teratogenicity. NAC, 100 to 275 mg/kg, was given intraperitoneally (ip) or per os (po), or as 266 to 410 mg/kg in the drinking water, at various times before or after phenytoin, 65 to 75 mg/kg ip, on gestational days 12 and 13. Dams were killed on gestational day 19, fetal resorptions were noted, and fetuses were examined for anomalies. Significant reductions in phenytoin-induced fetal weight loss and cleft palates were observed when NAC was given by gavage 6 hours after phenytoin or in the drinking water with the lower dose of phenytoin. NAC administered in the drinking water also reduced the incidence of resorptions produced by the higher dose of phenytoin and enhanced postpartum survival in fetuses exposed to 65 or 75 mg/kg phenytoin (P less than .05). Conversely, the incidence of resorptions increased when NAC was given by gavage at other times before or after phenytoin, by single or repetitive ip injections, or in high concentrations in the drinking water (P less than .05). When given with the higher dose of phenytoin, NAC administered via the drinking water significantly increased the incidence of phenytoin-induced cleft palates and fetal weight loss (P less than .05). Similar results were obtained with a single ip injection of NAC and a lower dose of phenytoin. Thus, when given orally, NAC can partially reduce phenytoin teratogenicity and embryopathy. However, altering the route of NAC administration, or increasing the dose of phenytoin and/or NAC, enhanced phenytoin embryotoxicity, and NAC alone at higher doses had embryopathic effects.

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Prenatal hamster development following maternal administration of PGE2 at midterm

Cited by 14 publications

References 15 publications

Effects of a Porphyromonas gingivalis infection on inflammatory mediator response and pregnancy outcome in hamsters

Effects of a Porphyromonas gingivalis infection on inflammatory mediator response and pregnancy outcome in hamsters

Dinoprostone 363‐24‐6

Effects of N‐acetylcysteine on fetal development and on phenytoin teratogenicity in mice

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