Maternal and fetal plasma adenosine deaminase, xanthine oxidase and malondialdehyde levels in pre-eclampsia

Karabulut, Aysun Bay; Kafkaslı, Ayşe; Burak, Feza; Gözükara, Engin M.

doi:10.1002/cbf.1152

Cited by 52 publications

(35 citation statements)

References 25 publications

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“…MDA is a marker of lipid peroxidation in ischemic tissues [30]. Intensity of MDA staining was the same in sham and infliximab + pringle groups and high in Pringle group.…”

Section: Discussionmentioning

confidence: 86%

Influence of infliximab pretreatment on ischemia/reperfusion injury in rat intestine

Akdoğan

Kalkan

Tümkaya

et al. 2014

Folia Histochem Cytobiol.

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Abstract. The Pringle maneuver is used in hepatic surgery to prevent blood loss but is associated with ischemia-reperfusion injury. To investigate the effect of infliximab on inflammation and apoptosis in rat intestinal mucosa during ischemia-reperfusion (IR) injury. A total of 30 male Wistar albino rats were equally divided into three groups to be subjected to (i) sham operation (sham), (ii) IR injury via Pringle maneuver (pringle) or (iii) infliximab (IFX) group (IFX was given at a dose 3 mg/kg for 3 days before IR injury). Following reperfusion period of 60 min., intestinal tissue and blood samples were taken and processed by standard histological methods. The Pringle maneuver and following reperfusion caused significant histopathological changes, increased serum transaminases' activity and the levels of oxidative stress markers and decreased glutathione peroxidase activity. IFX pretreatment partially prevented these changes. Infliximab pretreatment may protect intestinal mucosa against ischemia-reperfusion injury. Further studies are needed to investigate mechanism and evaluate safety and optimal dosing of IFX in humans exposed to the possible tissue damage by ischemia-reperfusion.

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“…MDA is a marker of lipid peroxidation in ischemic tissues [30]. Intensity of MDA staining was the same in sham and infliximab + pringle groups and high in Pringle group.…”

Section: Discussionmentioning

confidence: 86%

Influence of infliximab pretreatment on ischemia/reperfusion injury in rat intestine

Akdoğan

Kalkan

Tümkaya

et al. 2014

Folia Histochem Cytobiol.

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“…Considering that adenosine at high concentrations could have deleterious effects, and the fact that intracellular uptake is one of the main mechanisms for controlling the extracellular level of adenosine, those results were interpreted as a compensatory response, present in preeclampsia, to address the recovery of the physiological extracellular adenosine concentration in the feto-placental circulation. Compatible with this idea, Karabulut et al [29] have shown that elevation of adenosine levels triggers a compensatory elevation of adenosine deaminase activity in the umbilical circulation. Despite this latest evidence, the causes or consequences of high adenosine levels in the feto-placental circulation during preeclampsia are not well understood.…”

Section: Discussionmentioning

confidence: 99%

Impaired A2A adenosine receptor/nitric oxide/VEGF signaling pathway in fetal endothelium during late- and early-onset preeclampsia

Escudero

Bertoglia

Hernadez

et al. 2012

Purinergic Signalling

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To investigate whether fetal endothelial cell proliferation and migration are modulated by the A 2A adenosine receptor (A 2A AR), nitric oxide (NO) and the vascular endothelial growth factor (VEGF) signaling pathway, we isolated human umbilical vein endothelial cells from normal pregnancy (n023), preterm delivery (n04), and late-onset (LOPE, n010) and early-onset preeclampsia (EOPE, n08). We used the non-selective adenosine receptor agonist (NECA) and the selective agonist (CGS-21680) and/or selective antagonist (ZM-241385) for A 2A AR. Also, the nitric oxide synthase (NOS) inhibitor, L-NAME, was used in co-incubation with CGS-21680. Compared to normal pregnancy, EOPE exhibited low cell proliferation and migration associated with reduced expressions of A 2A AR and VEGF and NO synthesis (i.e., total and phosphorylated serine 1177 endothelial NOS and nitrite formation). In contrast, LOPE exhibited the opposite behavior in all these markers compared to normal pregnancy or EOPE. Cell proliferation and migration were increased by CGS-21680 (or NECA) in all analyzed groups (EOPE>LO-PE>normal pregnancy) compared to their respective basal conditions, an effect that was associated with high NO and VEGF synthesis and blocked by ZM-241385 with significantly different IC 50 for each group (EOPE>LOPE>normal pregnancy). The differences seem independent of gestational age.L-NAME blocked the CGS-21680-mediated cell proliferation and migration in normal pregnancy and LOPE (IC 50 036.2± 2.5 and 8.6±2.2 nM, respectively) as well as the VEGF expression in normal pregnancy. Therefore, the A 2A AR/NO/ VEGF signaling pathway exhibits a pro-angiogenic effect in normal pregnancies and LOPE, whereas impairment in this pathway seems related to the reduced angiogenic capacity of the fetal endothelium in EOPE.

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“…20 In the present study, we evaluated ADA activity in maternal and fetal plasma and in placental tissue and investigated possible correlations between the severity of pre-eclampsia and ADA activity in these three compartments.…”

Section: Discussionmentioning

confidence: 99%

Clinical Correlation between Adenosine Deaminase Activity and Pre-eclampsia Severity

Kafkaslı

Atmaca

et al. 2006

J Int Med Res

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This study evaluated the relationship between the activity of the inflammatory indicator adenosine deaminase (ADA) in placental tissue and maternal and fetal (umbilical cord) plasma and the severity of pre-eclampsia. Maternal and umbilical vein whole blood and placental tissue samples were collected from women with normal pregnancies (n = 33) and patients with mild (n = 12) or severe (n = 17) preeclampsia. ADA activity was measured spectrophotometrically. Significantly increased ADA activity was detected in maternal and fetal plasma, and placental tissue in patients with mild and severe preeclampsia compared with normal pregnancies; there were no significant differences between the mild and severe cases. The presence of increased ADA activity in pre-eclampsia is consistent with activation of the inflammatory system in this condition. The increased ADA activity was related to the presence of the disease but not the severity of clinical symptoms. Neonatal outcome did not significantly correlate with observed ADA activity.

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Maternal and fetal plasma adenosine deaminase, xanthine oxidase and malondialdehyde levels in pre-eclampsia

Cited by 52 publications

References 25 publications

Influence of infliximab pretreatment on ischemia/reperfusion injury in rat intestine

Influence of infliximab pretreatment on ischemia/reperfusion injury in rat intestine

Impaired A2A adenosine receptor/nitric oxide/VEGF signaling pathway in fetal endothelium during late- and early-onset preeclampsia

Clinical Correlation between Adenosine Deaminase Activity and Pre-eclampsia Severity

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