Effect of some therapeutic agents on the rabbit fetus

McColl, J. D.; Robinson, S.; Globus, Morton

doi:10.1016/0041-008x(67)90107-x

Cited by 47 publications

(15 citation statements)

References 20 publications

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“…McColl et al (1967) described an increased incidence of small auricles in the hearts from fetuses whose does had been administered 200 mg/kg a day of aspirin by gavage from GD 7 to GD 15. Schardein et al (1969) reported a marked reduction in litter size among does that received 200 mg/kg a day of aspirin from GD 6 to GD 18.…”

Section: Introductionmentioning

confidence: 99%

Analysis of the nonsteroidal anti‐inflammatory drug literature for potential developmental toxicity in rats and rabbits

Cook¹,

Jacobson²,

Gao³

et al. 2003

Birth Defects Research Pt B

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This analysis of the non-clinical NSAID literature demonstrated a possible association between exposure to NSAIDs and developmental anomalies. The anomalies were similar for aspirin and for other NSAIDs, but effects occurred at a much lower incidence with non-aspirin NSAIDs than previously reported with aspirin. Such a finding is consistent with the concept that reversible inhibition of COX-1 and/or COX-2 by other NSAIDs would produce weaker developmental toxicity signals than aspirin. However, there were limitations of the evaluated studies: (1) there were very few robust International Conference on Harmonization-compliant studies conducted with NSAIDs in the published literature; (2) many of the studies were conducted at doses well below the maximum tolerated dose (MTD), where effects are rarely seen; and (3) numerous studies were conducted above the MTD, where reduced numbers of fetuses hampered detection of low-incidence findings. Although weak associations were observed, these limitations prevented us from definitively determining the presence or absence of a developmental toxicity signal from the existing body of NSAID data. Further exploration of this hypothesis will require assessing the potential association in animal models by using dose levels centered around the MTD.

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Section: Introductionmentioning

confidence: 99%

Analysis of the nonsteroidal anti‐inflammatory drug literature for potential developmental toxicity in rats and rabbits

Cook¹,

Jacobson²,

Gao³

et al. 2003

Birth Defects Research Pt B

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“…2005) were found to be different from those of the skeletal anomalies in fetuses from the PB‐administered dams reported in the rat studies by Terada et al . (1987) and McColl et al . (1963, 1967) and in the present study, as well as in the mouse studies by Walker and Patterson (1974) and Sullivan and McElhatton (1975).…”

Section: Discussionmentioning

confidence: 97%

“…Teratologic studies with laboratory animals demonstrated PB‐induced cleft palate in mice (Walker & Patterson 1974; Sullivan & McElhatton 1975), skeletal malformation in rats (McColl et al . 1963) and skull defects in rabbits (McColl 1967). The types of retinoic acid‐induced skeletal anomalies (Shoji et al .…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular malformations induced by prenatal exposure to phenobarbital in rats

Okuda

Nagao

2006

Congenital Anomalies

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The effects of prenatal exposure to phenobarbital (PB) on the cardiovascular system were examined in rat fetuses and pups. PB was administered at a dose of 80 or 120 mg/kg/day by gavage to Sprague Dawley (SD) rats on two consecutive gestational days (GD): 7-8, 8-9, 9-10, or 10-11. Fetuses were examined for cardiovascular malformations on GD 20. In addition, pups were examined for PB-induced cardiovascular malformations. Incidences of ventricular septal defect (VSD), overriding aorta, double outlet right ventricle and transposition of great arteries were significantly increased in the fetuses whose dams were administered PB at 120 mg/kg on GD 8-9, 9-10 or 10-11. GD 8-11 was the critical period for the cardiovascular malformations associated with administration of PB in rats. Various types of cardiovascular malformations were detected in pups from the PB-administered dam. Severe cardiovascular malformations induced by PB caused deaths on early postnatal days. However, slight malformations such as isolated VSD persisted until weaning, and did not affect postnatal viability.

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“…Numerous investigators speculated that it is the malformed or defective offspring that are cannibalized. Published studies in both mice (Kalter, 1970) and rabbits (McColl, Robinson & Globus, 1967) implied that mutilation of presumably abnormal offspring by the mother was responsible for differences in the frequency of malformation in those killed at term compared to those allowed to deliver. Although this effect has not been demonstrated experimentally, the assumption has become a determining influence in rodent reproduction work and sacrifice at term has come into routine use to avoid cannibalism which could influence the analysis of reproductive effects (FDA, 1970).…”

Section: Discussionmentioning

confidence: 99%

Cannibalistic traits observed in rats treated with a teratogen

Schardein¹,

Petrere²,

Hentz³

et al. 1978

Lab Anim

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81 SummaryRat offspring malformed as a result of maternal exposure to a teratogen were cannibalized preferentially to apparently normal offspring. Lack of viability also appeared to be a factor in the cannibalistic tendency, since both normal and malformed dead pups were consumed more frequently than viable pups of either category. Of the 29 cannibalized pups observed, 86 % were cannibalized in the 1st 24 h.

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Effect of some therapeutic agents on the rabbit fetus

Cited by 47 publications

References 20 publications

Analysis of the nonsteroidal anti‐inflammatory drug literature for potential developmental toxicity in rats and rabbits

Analysis of the nonsteroidal anti‐inflammatory drug literature for potential developmental toxicity in rats and rabbits

Cardiovascular malformations induced by prenatal exposure to phenobarbital in rats

Cannibalistic traits observed in rats treated with a teratogen

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