2003
DOI: 10.1016/s1472-6483(10)62060-3
|View full text |Cite
|
Sign up to set email alerts
|

Oxygen, early embryonic metabolism and free radical-mediated embryopathies

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

2
134
0
6

Year Published

2008
2008
2015
2015

Publication Types

Select...
5
3

Relationship

0
8

Authors

Journals

citations
Cited by 226 publications
(142 citation statements)
references
References 100 publications
2
134
0
6
Order By: Relevance
“…31,32 In addition, it is widely recognized that placental and embryonic tissues are particularly sensitive to oxidative stress, as a consequence of the high cell proliferation rate and concomitant exposure of DNA. 33 For such reasons it has been proposed that the physiological hypoxia characterizing the first trimester of human gestation might be a way to protect the fetus from teratogenic effects of reactive oxygen species (ROS). 34 The presence of extensive vascular alterations and of thrombi in our model system ( Figure 3DÀG) led us to hypothesize that placental damage might be a consequence of oxidative stress.…”
Section: Articlementioning
confidence: 99%
“…31,32 In addition, it is widely recognized that placental and embryonic tissues are particularly sensitive to oxidative stress, as a consequence of the high cell proliferation rate and concomitant exposure of DNA. 33 For such reasons it has been proposed that the physiological hypoxia characterizing the first trimester of human gestation might be a way to protect the fetus from teratogenic effects of reactive oxygen species (ROS). 34 The presence of extensive vascular alterations and of thrombi in our model system ( Figure 3DÀG) led us to hypothesize that placental damage might be a consequence of oxidative stress.…”
Section: Articlementioning
confidence: 99%
“…Our findings, using a first trimester cytotrophoblast cell line, reveal that the protective activity of endogenous HBEGF is lost when O 2 levels are abruptly increased. The resulting cell death requires caspase activity and is accompanied by phosphatidylserine randomization, while cells remain intact and retain cytoplasmic LDH activity; all indicative of apoptosis (14) It has been suggested that excessive oxidative stress in the first trimester can compromise trophoblast function or survival (1)(2)(3)(4)(5)9). Trophoblast survival and extravillous differentiation required for remodeling of the uterine spiral arteries are deficient in both missed abortion and preeclampsia (1), perhaps due to elevated levels of oxidative stress.…”
Section: Commentmentioning
confidence: 99%
“…A role for H/R injury in early pregnancy loss has been advanced by several lines of molecular evidence, including morphological evidence of increased apoptosis and markers of cellular stress, expression of heat shock protein 70, protein nitrosylation and lipid peroxidation in tissues obtained from missed abortions with early onset placental perfusion (1)(2)(3)(4)(5). Xanthine dehydrogenase, which normally utilizes NAD as an electron acceptor, is converted under the conditions of ischemia/reperfusion into xanthine oxidase.…”
Section: Commentmentioning
confidence: 99%
See 1 more Smart Citation
“…As mentioned above, PO2 and ROS might be essential parameters at least in early embryogenesis [42]. The discrepancies in the results of the above-mentioned studies may be partially explained by differences in culture hardware as well as culture methods: for example, oxygen tension in droplets of medium under oil will be 1ess than those without an oil overlay [43].…”
Section: Delivery Of Human Babies By Assisted Reproductive Technologymentioning
confidence: 96%