Oxidative stress in pre-eclampsia

Bowen, Robin S.; Moodley, J.; Dutton, Michael F.; Theron, Annette J.

doi:10.1080/j.1600-0412.2001.080008719.x

Cited by 27 publications

(44 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Serum MDA mainly results from the oxidation of cell membrane and lipoprotein lipid contents that are rich in polyunsaturated fatty acids [34]. Several authors [3,5,[12][13][14], but not all [45], reported increased serum MDA levels in preeclampsia. In a recent study [11] that was carried out in our laboratories, MDA level was determined by a spectrophotometric method, and in the present study, MDA level was determined by HPLC that has been accepted as a more specific technique for MDA measurements.…”

Section: Discussionmentioning

confidence: 99%

Oxidizability of apolipoprotein B-containing lipoproteins and serum paraoxonase/arylesterase activities in preeclampsia

Sarandöl

Şafak

Dirican

et al. 2004

Clinical Biochemistry

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Oxidizability of apolipoprotein B-containing lipoproteins and serum paraoxonase/arylesterase activities in preeclampsia

Sarandöl

Şafak

Dirican

et al. 2004

Clinical Biochemistry

View full text Add to dashboard Cite

“…These patients had significantly higher levels of thiobarbituric acid reactive substances (TBARS) than the control subjects (P Ͻ.001) and patients with preeclampsia (P Ͻ.01) (29). Bowen et al found significantly higher levels of cord blood MDA in patients with eclampsia (30). The studies by Diedrich et al and Bowen et al suggest that oxidative stress increases with the severity of HELPP syndrome and eclampsia.…”

Section: Lipid Peroxidation: Role In Preeclampsiamentioning

confidence: 95%

The Role of Placental Oxidative Stress and Lipid Peroxidation in Preeclampsia

Gupta

Agarwal²,

Sharma³

2005

Obstetrical & Gynecological Survey

152

View full text Add to dashboard Cite

show abstract

“…The resultant abnormal intrauterine milieu restricts the supply of crucial nutrients to the fetus, thereby limiting fetal growth. Multiple studies have shown that intrauterine growth retardation is associated with increased oxidative stress in the human fetus [73][74][75][76][77][78][79][80]. A major consequence of limited nutrient availability is an alteration in the redox state in susceptible fetal tissues leading to oxidative stress.…”

Section: Cellular Mechanisms: Mitochondrial Dysfunction and Oxidativementioning

confidence: 99%

Role of metabolic programming in the pathogenesis of β-cell failure in postnatal life

Simmons

2007

Rev Endocr Metab Disord

View full text Add to dashboard Cite

Intrauterine growth retardation (IUGR) has been linked to later development of type 2 diabetes in adulthood. Human studies indicate that individuals who were growth retarded at birth have impaired insulin secretion and insulin resistance. Multiple animal models of IUGR demonstrate impaired beta-cell function and development. We have developed a model of IUGR in the rat that leads to diabetes in adulthood with the salient features of most forms of type 2 diabetes in the human: progressive defects in insulin secretion and insulin action prior to the onset of overt hyperglycemia. Decreased beta-cell proliferation leads to a progressive decline in beta-cell mass. Using this model, we have tested the hypothesis that uteroplacental insufficiency disrupts the function of the electron transport chain in the fetal beta-cell and leads to a debilitating cascade of events: increased production of reactive oxygen species, which in turn damage mitochondrial (mt) mtDNA and causes further production of reactive oxygen species (ROS). The net result is progressive loss of beta-cell function and eventual development of type 2 diabetes in the adult. Studies in the IUGR rat also demonstrate that an abnormal intrauterine environment induces epigenetic modifications of key genes regulating beta-cell development; experiments directly link chromatin remodeling with suppression of transcription. Future research will be directed at elucidating the mechanisms underlying epigenetic modifications in offspring.

show abstract

Oxidative stress in pre-eclampsia

Cited by 27 publications

References 0 publications

Oxidizability of apolipoprotein B-containing lipoproteins and serum paraoxonase/arylesterase activities in preeclampsia

Oxidizability of apolipoprotein B-containing lipoproteins and serum paraoxonase/arylesterase activities in preeclampsia

The Role of Placental Oxidative Stress and Lipid Peroxidation in Preeclampsia

Role of metabolic programming in the pathogenesis of β-cell failure in postnatal life

Contact Info

Product

Resources

About