Skeletal Malformations Resulting from Cadmium Treatment in the Hamster

Gale, Thomas F.; Ferm, Vergil H.

doi:10.1159/000240596

Cited by 46 publications

(14 citation statements)

References 14 publications

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“…The effects of the metal on exencephaly, together with those on foetal weight ( Table 2), indicate that the post-implantation stage of pregnancy presents the QS mouse with a period of increased sensitivity to the adverse actions of cadmium. These findings are consistent with those of earlier studies which showed that susceptibility to the teratogenic effects of cadmium and other extraneous factors varies with the developmental stage at the time of exposure (Chiquoine 1965;Ferm 1971;Barr 1973;Gale and Ferm 1973;Wo1kowski 1974;Hall 1977). The rate of uptake and accumulation of cadmium in embryonic, placental, and ovarian tissues also depends on the day of pregnancy on which the metal is administered (Dencker 1975).…”

Section: Discussionsupporting

confidence: 91%

“…Thus, in males of several species cadmium induces deleterious effects on the vasculature of the testes and subsequently influences spermatogenesis and androgen production (Gunn and Gould 1970;Saksena et al 1977;Aoki and Hoffer 1978;Lau et al 1978;Niewenhuis and Fende 1978). In female mammals, cadmium may disturb maternal-embryonic relationships and cause placental necrosis, foetal resorption and embryonic developmental malformations (Parizek 1964;Ferm 1971;Schroeder and Mitchener 1971;Gale and Ferm 1973;Dencker 1975).…”

Section: Introductionmentioning

confidence: 99%

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Foetotoxicity of Cadmium in Quackenbush Strain Mice and the Effects of the Metal on Uterine Alkaline Phosphatase During Pseudopregnancy

Murdoch¹,

Cowen²

1981

Aust. Jnl. Of Bio. Sci.

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Experiments were conducted to determine the sensitivity of Quackenbush strain (QS) mice to the foetotoxic effects of single subcutaneous injections of CdClz (2, 4 and 8 mg of cadmium per kilogram body weight) on days 1, 2, 4 or 8 of pregnancy. Autopsies performed on day 16 of pregnancy revealed that cadmium was teratogenic and increased the incidence of malformed forelimbs and exencephaly and decreased foetal weight. The metal caused foetal weight changes and exencephaly only when it was administered on day 8 of pregnancy indicating that the post-implantation stage presents the QS mouse with a period of increased sensitivity to the foetotoxic effects of cadmium.Although injections of cadmium (8 mg per kilogram body weight) during early pseudopregnancy did not prevent the uterus from undergoing a decidual reaction in response to a peanut oil stimulus, they did in some cases prevent alkaline phosphatase from reaching maximal activity levels in decidualized uterine horns. Thus, inhibition of alkaline phosphatase occurred only in response to the metal injected on day 4 of pseudopregnancy and the enzyme was not affected when cadmium was administered on days 1,2, 3, 5 or 6 of pseudopregnancy.The results suggested that changes in either progesterone and oestrogen production by the ovary or the alkaline phosphatase activity of the uterus are unlikely to be responsible to any great extent for the teratogenic effects of single subcutaneous injections of cadmium in the QS mouse during early pregnancy.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Foetotoxicity of Cadmium in Quackenbush Strain Mice and the Effects of the Metal on Uterine Alkaline Phosphatase During Pseudopregnancy

Murdoch¹,

Cowen²

1981

Aust. Jnl. Of Bio. Sci.

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“…bone struc¬ tures (Gale & Ferm, 1973), is more difficult to explain on the basis of an endo¬ dermal accumulation. It seems possible, however, that long-term retention in the gut wall may affect intestinal function with secondary damage to all the organism.…”

Section: Micementioning

confidence: 99%

“…As the gut endoderm is derived from the visceral yolk-sac endoderm, it seems probable that these two structures develop the same role for the absorption of nutrients to the fetus (the yolk sac mainly in rodents) from the amniotic, and the uterine cavities, respectively. It is tempting to interpret the résorptions and malformations, especially facial ones, recorded by Ferm (1971) and Gale & Ferm (1973) (Langman, 1969). As the yolk sac is large (and probably functionally important) during the first weeks of pregnancy, these experimental findings may also have some relevance in man.…”

Section: Micementioning

confidence: 99%

“…In the golden hamster during early gestation (8th to 9th day), cadmium causes résorptions and embryonic structural defects, the character of which is dependent on the time of administration (Ferm & Carpenter, 1967;Ferm, 1971; Gale & Ferm, 1973). These authors thought that cadmium was an embryonic "site-specific teratogen" due to its interference with specific enzy¬ matic reactions.…”

Section: Introductionmentioning

confidence: 99%

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Possible Mechanisms of Cadmium Fetotoxicity in Golden Hamsters and Mice: Uptake by the Embryo, Placenta and Ovary

Dencker¹

1975

Reproduction

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Summary. Pregnant golden hamsters and mice of different gestational ages were injected intravenously with 109CdCl2. The whole animal or the uterus and embryos were submitted to autoradiography. Cadmium administered on the 8th day accumulated in the primitive gut of the embryos. No cadmium was detected in the embryos after administration on or after the 9th day (hamster) and 11th day (mouse). This finding can be explained by the ability of cadmium to pass from the yolk-sac cavity into the primitive gut (where it is absorbed) before the closure of the vitelline duct but not later. This uptake by the embryo might explain the severe malformations produced by cadmium given on the 8th day as compared with the 9th day in the hamster. Cadmium is also heavily accumulated in the decidua (mainly the antimesometrial part), the yolk sac, the ectoplacental cone, and later in the chorioallantoic placenta\p=m-\possiblydisturbing the maternal-embryonic relationship and fetal nutrition. A high accumulation in the CL and the follicles and in the pituitary may also disturb reproductive function.

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Induction and characterization of metallothionein in chicken epiphyseal growth plate cartilage chondrocytes

Sauer

Nie

et al. 1998

J. Cell. Biochem.

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Following exposure to cadmium or zinc, chickens were sacrificed and the liver, kidney, and bone epiphyseal growth plates harvested. When cytosolic extracts of the growth plate cartilage were fractionated by gel filtration chromatography, a protein with high metal-binding capacity and low ultraviolet (UV) absorbance eluted in the same position as liver metallothionein (MT) and a MT standard. Cd or Zn treatment resulted in a 25-fold or 5-fold induction in growth plate MT, respectively. In liver the greatest level of MT induction was seen with short-term Cd exposures. In contrast, MT levels in the growth plate increased as the duration of Cd exposure increased. Induction of MT in growth plate chondrocyte cell cultures was observed for media Cd concentrations of > or = 0.1 microM and Zn concentrations of > or = 100 microM. Basal and inducible levels of MT declined through the culture period and were lowest in the terminally differentiated mineralized late stages of the culture. Alkaline phosphatase activity was also lowest in the late-stage cultures, while total cellular protein increased throughout the culture period. Treatment of chondrocytes with Zn prior to Cd exposure resulted in a protective induction of MT. Pre-treatment of chondrocytes with dexamethasone resulted in suppressed synthesis of MT upon Cd exposure and greater Cd toxicity. Both Cd and Zn resulted in significantly increased levels of MT mRNA in chondrocyte cell cultures. Dexamethasone treatment resulted in an approximate 2- to 3-fold increase in MT mRNA. This is contrary to the finding that MT protein levels were decreased by dexamethasone. The findings suggest that an increased rate of MT degradation in dexamethasone-treated and late-stage chondrocyte cultures may be associated with the terminally differentiated phenotype.

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Skeletal Malformations Resulting from Cadmium Treatment in the Hamster

Cited by 46 publications

References 14 publications

Foetotoxicity of Cadmium in Quackenbush Strain Mice and the Effects of the Metal on Uterine Alkaline Phosphatase During Pseudopregnancy

Foetotoxicity of Cadmium in Quackenbush Strain Mice and the Effects of the Metal on Uterine Alkaline Phosphatase During Pseudopregnancy

Possible Mechanisms of Cadmium Fetotoxicity in Golden Hamsters and Mice: Uptake by the Embryo, Placenta and Ovary

Induction and characterization of metallothionein in chicken epiphyseal growth plate cartilage chondrocytes

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