Retinoic acid-induced stress protein synthesis in the mouse

LaBorde, James B.; Pipkin, James L.; Hinson, William G.; Anson, Jeanne F.; Sheehan, Daniel M.; Young, John F.; Hansen, Deborah K.

doi:10.1016/0024-3205(95)00148-y

Cited by 21 publications

(11 citation statements)

References 35 publications

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“…Hsp72 overexpression protects mouse embryos from the teratogenic effects of arsenite (Dix et al, 1998;Hunter and Dix, 2001). Maternal exposure of GD10 mice to retinoic acid results in abnormal forelimbs, hindlimbs, and tail, and accumulation of a 20-25 kD stress protein was seen in all of these tissues shortly after dosing (LaBord et al, 1995). In addition, accumulation of a 90-kD stress protein was observed in the forelimbs and tail, while an 84-kD protein accumulated in the forelimbs.…”

Section: Discussionmentioning

confidence: 92%

Mercury, cadmium, and arsenite enhance heat shock protein synthesis in chick embryos prior to embryotoxicity

Papaconstantinou

Brown

Noren

et al. 2003

Birth Defects Research Pt B

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Section: Discussionmentioning

confidence: 92%

Mercury, cadmium, and arsenite enhance heat shock protein synthesis in chick embryos prior to embryotoxicity

Papaconstantinou

Brown

Noren

et al. 2003

Birth Defects Research Pt B

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“…Fetal carcasses were skinned, fixed in ethanol, and double-stained (LaBorde et al, 1995); Test chemical and dose formulations. Fumonisin B 1 (Lot E12-47-2, skeletons were examined for cartilage and bone malformations.…”

Section: Methodsmentioning

confidence: 99%

Lack of Embryotoxicity of Fumonisin B1in New Zealand White Rabbits

LaBorde¹,

Terry

Howard

et al. 1997

Fundamental and Applied Toxicology

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Fumonisin B1 (FB1) is one of a number of mycotoxins produced by fungi, especially Fusarium sp. As a contaminant of many maize-derived products, this toxin is associated with a variety of animal diseases, including esophageal cancer and possibly neural tube defects in humans. We have investigated the embryotoxic potential of this compound in New Zealand White rabbits. Animals were dosed by gavage daily on GD 3-19 with purified FB1 at 0.10, 0.50, or 1.00 mg/kg/day. Maternal lethality occurred at the 0.50 and 1.00 mg/kg/day doses. When examined on GD 29, there were no differences in maternal body weight, maternal weight gain, maternal organ weights, number of nonlive implantations, and number of malformations. Fetal weight was decreased at 0.50 and 1.00 mg/kg/day (13 and 16%, respectively); this was true for male and female pups. Fetal liver and kidney weights were also decreased at these doses. Analysis of embryonic sphinganine to sphingosine ratios demonstrated no differences between control and treated embryos on GD 20, although these ratios were increased in maternal urine, serum, and kidney when compared to control animals. These data suggest that FB1 did not cross the placenta and that the observed decreased fetal weight was probably the result of maternal toxicity, rather than any developmental toxicity produced by FB1.

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“…Fetuses were examined for visceral abnormalities and sexed by internal exam employing the fresh tissue dissection technique (Stuckhardt and Poppe, 1984). Some fetal carcasses were stained with alizarin red S and alcian blue for subsequent examination of cartilage and bone in fetal skeletons (LaBorde et al, 1995). Outcome measures included gravid uterine weight, number of implantation sites per litter, number and percentage of non-live implants per litter, as well as number, percentage, and types of malformations per litter.…”

Section: Animals and Animal Carementioning

confidence: 99%