Effect of oral cadmium administration to female rats during pregnancy on zinc, copper, and iron content in placenta, foetal liver, kidney, intestine, and brain

Sowa, Bogusław; Steibert, E

doi:10.1007/bf00295164

Cited by 44 publications

(22 citation statements)

References 24 publications

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“…In contrast to our observations, these authors observed deficits in the birth weight and growth of animals prenatally exposed to Cd, the latter being effects that could be responsible for a delayed sensorimotor development (Smart and Dobbing, 1971). Evidence from previous studies indicates that the oral administration of Cd results in a reduced absorption of trace elements such as Ca, Zn and Fe (Pond and Walker, 1975;Sowa and Steibert, 1985;Baranski, 1987). In this work, the Cd subcutaneously administered during organogenesis could therefore be responsible for alterations in the normal development of sensorimotor reflexes and motor coordination of the offspring which are reflected in the observed maturation deficits of the righting reflex and in the cliff aversion.…”

Section: Discussioncontrasting

confidence: 99%

Sensorimotor developmental delays and lower anxiety in rats prenatally exposed to cadmium

Minetti

Reale

2005

J. Appl. Toxicol.

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Pregnant rats were treated with 0.3 or 0.6 mg cadmium (CdCl2) kg(-1) injected subcutaneously on a daily basis from gestational day 7 to day 15 (organogenesis period). One control group was not injected and the other received saline. Offspring were tested for ontogeny of sensorimotor development and at 45 or 90 days of age for anxiety behavior. The study of sensorimotor development showed that gestational exposure to 0.6 mg Cd kg(-1) produced a delay in the development of the righting reflex and of the cliff aversion in the pups. No differences were observed in the development of the negative geotaxis, nor in the ages of eye and ear opening. Anxiety studies using an elevated plus maze showed a lower anxiety in all the offspring prenatally exposed to 0.6 mg Cd kg(-1) as these rats spent more time and entered the open arms more times compared with those of the other groups. The results demonstrate that exposure to low levels of Cd during organogenesis may modify some central nervous system functions.

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Section: Discussioncontrasting

confidence: 99%

Sensorimotor developmental delays and lower anxiety in rats prenatally exposed to cadmium

Minetti

Reale

2005

J. Appl. Toxicol.

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“…Also, our results show that Cd was accumulated in the placenta and in fetal liver but it was not detected in the fetal testis of Cd exposed-animals. These results suggest that placenta could deter most of Cd to passing from dams to fetus [32][33][34]. Importantly, exposure to Cd in utero did not impair fetus growth since the fetal weights and the craniocaudal length at the end of gestation (GD20) of the control and Cd group were not statistically different.…”

Section: Discussionmentioning

confidence: 77%

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

Chemek

Mimouna

Boughammoura

et al. 2016

Reproductive Toxicology

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Highlights Effects of Cd and Zn on testicular development were assessed. Cd accumulation and Zn depletion in testis during lactation were noted. Cd-induced abnormal seminiferous tubules and a plasmatic testosterone decrease. Zn supply induced a significant protection against Cd toxicity. Cd toxicity observed in pups is mediated by disruption of maternal Zn metabolism. *Research Highlights AbstractTo assess the effects of exposure to Cd and Zn on rat testicular development, offspring, from mothers receiving either tap water, Cd, Zn or Cd+Zn during gestation and lactation periods, were observed on gestational day (GD) 20 and on postnatal days (PND) 12, 21 and 35. During gestation, Cd induced maternal hypozincemia and less transfer of Zn to the fetus. During lactation, progressive Cd accumulation and Zn depletion in testis at PND12 and PND21 werenoted. An increase of abnormal seminiferous tubules and a decrease in testis weight and plasmatic testosterone concentration were also observed at PND21 and PND35 respectively. Interestingly, Zn supply induced a significant protection against Cd toxicity. These results suggest that the toxic effects of Cd observed during development are mediated by the disruption of Zn metabolism, which is established in mothers during pregnancy causing Zn deficiency in fetuses and continues to become more pronounced during lactation.

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“…Gestational exposure to oral cadmium resulted in decreased zinc, copper, iron, and metallothionein (MT) content in fetal liver as well as in reduced copper content in the placenta and fetal intestine (Sowa et al, 1982;Steibert et al, 1984;Sowa and Steibert, 1985).…”

Section: Introductionmentioning

confidence: 99%

Cadmium Interaction with Essential Metals (Zn, Cu, Fe), Metabolism Metallothionein, and Ceruloplasmin in Pregnant Rats and Fetuses

Chmielnicka

Sowa

1996

Ecotoxicology and Environmental Safety

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Effect of oral cadmium administration to female rats during pregnancy on zinc, copper, and iron content in placenta, foetal liver, kidney, intestine, and brain

Cited by 44 publications

References 24 publications

Sensorimotor developmental delays and lower anxiety in rats prenatally exposed to cadmium

Sensorimotor developmental delays and lower anxiety in rats prenatally exposed to cadmium

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

Cadmium Interaction with Essential Metals (Zn, Cu, Fe), Metabolism Metallothionein, and Ceruloplasmin in Pregnant Rats and Fetuses

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