2020
DOI: 10.1016/j.redox.2019.101329
| View full text |Cite
|
Sign up to set email alerts
|

Abstract: Pregnancy complications such as preeclampsia cause increased fetal oxidative stress and fetal growth restriction, and associate with a higher incidence of adult metabolic syndrome. However, the pathophysiological contribution of oxidative stress per se is experimentally difficult to discern and has not been investigated. This study determined, if increased intrauterine oxidative stress (IUOx) affects adiposity, glucose and cholesterol metabolism in adult Ldlr−/−xSod2+/+ offspring from crossing male Ldlr−/−xSod… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1

Citation Types

1
3
0

Year Published

2020
2020
2023
2023

Publication Types

Select...
4
1

Relationship

0
5

Authors

Journals

citations
Cited by 5 publications
(4 citation statements)
references
References 27 publications
1
3
0
Order By: Relevance
“…As hypoxia and oxidative stress stimulate growth and differentiation of the placenta ( Pringle et al, 2010 ), suppressing these protective pathways may explain the enhanced growth we observe. Further, early gestational exposures to transient oxidative stress induce a similar repertoire of metabolic outcomes as those we identified in the male offspring of alcohol-exposed sires ( Dimova et al, 2020 ). If our mouse studies directly translate to humans, gene-environment differences in oxidative stress responses may play an unappreciated role in the susceptibility to alcohol-induced teratogenesis and contribute to the wide variation in FASD phenotypes and prevalence observed in the clinics ( Schaefer and Deere, 2011 ; McCarthy and Eberhart, 2014 ).…”
Section: Resultssupporting
confidence: 58%
“…As hypoxia and oxidative stress stimulate growth and differentiation of the placenta ( Pringle et al, 2010 ), suppressing these protective pathways may explain the enhanced growth we observe. Further, early gestational exposures to transient oxidative stress induce a similar repertoire of metabolic outcomes as those we identified in the male offspring of alcohol-exposed sires ( Dimova et al, 2020 ). If our mouse studies directly translate to humans, gene-environment differences in oxidative stress responses may play an unappreciated role in the susceptibility to alcohol-induced teratogenesis and contribute to the wide variation in FASD phenotypes and prevalence observed in the clinics ( Schaefer and Deere, 2011 ; McCarthy and Eberhart, 2014 ).…”
Section: Resultssupporting
confidence: 58%
“…Moreover, some studies demonstrate that the increase in UCP subtype 2 (UCP2), in other organs, occurs due to the increase in mitochondrial ROS signalling, which works as a protective mechanism against oxidative stress 60 , 64 . Interestingly, Dimova et al 65 have shown that in addition to promoting intrauterine growth restriction, intrauterine oxidative stress promotes increased energy expenditure due to browning of WAT, as indicated by higher UCP1 expression, and protects the offspring against diet-induced adiposity, insulin resistance and hyperlipidaemia. Although in our study we did not evaluate the browning of WAT, increased UCP1 expression on BAT of the offspring of RYGB female rats may constitute a mechanism to attempt to control mitochondrial ROS production and the development of pathologies, since BS did not re-establish the expressions of CI and CIII, and our group has already showed 49 that maternal RYGB in rats can negatively affect the growth and insulin secretion of offspring, resulting in insulin resistance and β-cell dysfunction in adult life.…”
Section: Discussionmentioning
confidence: 99%
“…In worms, multiple reports can link transgenerational germline programming to early-life mitochondrial dysfunction and the epigenetic regulation of antioxidant pathways (Kishimoto et al, 2017;Zhang et al, 2021c). Significantly, similar pathways are also present in mammalian systems, and transient, intrauterine episodes of placental oxidative stress induce improvements in hepatic metabolism, priming of antioxidant pathways, and resistance to high-fat dietinduced obesity; a phenomenon broadly termed mitohormesis (Yun and Finkel, 2014;Cox et al, 2018;Dimova et al, 2020). Our data examining low-level paternal alcohol exposures also identify altered transcription of placental mitochondrial genes (Thomas et al, 2021;, and the male offspring of alcoholexposed sires exhibit resistance to the effects of a high-fat diet (Chang et al, 2019b).…”
Section: Sperm Noncoding Rnasmentioning
confidence: 99%