1997
DOI: 10.1002/(sici)1096-9926(199711)56:5<327::aid-tera6>3.0.co;2-u
|View full text |Cite
|
Sign up to set email alerts
|

Repeated administration of α-hederin results in alterations in maternal zinc status and adverse developmental outcome in the rat

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

0
6
0

Year Published

2002
2002
2017
2017

Publication Types

Select...
5
2

Relationship

2
5

Authors

Journals

citations
Cited by 18 publications
(6 citation statements)
references
References 21 publications
0
6
0
Order By: Relevance
“…In this study, maternal dietary restriction of Zn resulted in cardiac malformations of the outflow tract and thin myocardium in the hearts of the conceptuses. As our group has previously demonstrated, primary or secondary Zn deficiency during pregnancy results in maternal unthriftiness and fetal deficiencies (Daston et al, 1994b; Taubeneck et al, 1994; Duffy et al, 1997). Maternal dietary Zn deficiency in this study reduced maternal weight gain during pregnancy, decreased the number of viable fetuses, and resulted in smaller live fetuses at the end of gestation.…”
Section: Discussionmentioning
confidence: 80%
See 1 more Smart Citation
“…In this study, maternal dietary restriction of Zn resulted in cardiac malformations of the outflow tract and thin myocardium in the hearts of the conceptuses. As our group has previously demonstrated, primary or secondary Zn deficiency during pregnancy results in maternal unthriftiness and fetal deficiencies (Daston et al, 1994b; Taubeneck et al, 1994; Duffy et al, 1997). Maternal dietary Zn deficiency in this study reduced maternal weight gain during pregnancy, decreased the number of viable fetuses, and resulted in smaller live fetuses at the end of gestation.…”
Section: Discussionmentioning
confidence: 80%
“…Our group has also previously demonstrated that fetal Zn deficiency can occur in the face of adequate maternal dietary Zn when the Zn‐binding protein metallothionein is upregulated in the liver, sequestering available Zn away from the fetus (Keen et al, 1993; Daston et al, 1994b; Taubeneck et al, 1994). Metallothionein induction can be triggered by stress and a diverse list of substances that are not themselves teratogenic (Daston et al, 1994a; Duffy et al, 1997). This secondary mechanism leading to fetal Zn deficiency and malformations might be a new consideration for mechanisms underlying congenital heart disease.…”
Section: Discussionmentioning
confidence: 99%
“…Several studies (e.g., Khera, 1987Khera, , 1991Keen et al, 2003a;DeSesso & Goeringer, 1990;Carey et al, 2000Carey et al, , 2003DeSesso, 1987;Daston, 1994;Taubeneck et al, 1994;Duffy et al, 1997) illustrate the necessity to consider maternal toxicity as a common contributing cause to abnormal fetal development or death. Similarly, maternal toxicity can, and does, influence the development of the young during the postnatal period (Keen et al, 2003b;Weaver et al, 2004).…”
Section: Discussionmentioning
confidence: 99%
“…Rats when treated with α-HN exhibited Zn depilation with a decreased fetal weight and increased the incidence of abnormal fetuses at high dose (300mM/kg) [57]. Duffy et al [58] suggested a secondary Zn deficiency in rats treated with α-HN at 20 or 30mM/kg for 10 days.…”
Section: Miscellaneousmentioning
confidence: 99%