The Change of Oxidative Stress in Maternal Blood During Pregnancy

Author(s):  
Fukase Mika ◽  
Watanabe Norikazu ◽  
Yamanouchi Keiko ◽  
Tsutsumi Seiji ◽  
Nagase Satoru
Author(s):  
S. Vijaya ◽  
M. Mahalakshmi ◽  
I. Inbapriyanka

Background: Preeclampsia is a multi system disorder with placenta as the organ of origin and maternal endothelium being the organ of target.  According to recent studies, the cell free haemoglobin induces oxidative stress mediated damage to the blood placenta barrier with consequently elevated levels of HbF in maternal blood. Alpha 1 microglobulin is an endogenous protein with antioxidant property, present in elevated levels in maternal blood in response to oxidative stress. This fact forms the basis for our study. The objective of the present study was to establish association between high levels of fetal hemoglobin and alpha 1 microglobulin in plasma of pregnant women between 10 to 16 weeks of gestational age and subsequent development of preeclampsia.Methods: This was a prospective cohort study undertaken in the Department of Obstetrics and Gynaecology, ISO -KGH, between December 2016 to November 2017. A total of 100 pregnant women were included in the study after getting informed written consent. Both primigravida and multigravida, belonging to age group of 20 to 35 years (singleton/ multiple) between 10 to 16 weeks GA and with BMI between 16 to 35 kg/m2 were included in the study. A woman with Diabetes mellitus, Hypertension, Renal disease, Epilepsy and Vascular disorders were excluded from the study.Results: The cut off value for alpha 1 microglobulin was 1.86ng/ml and the cut off value of fetal haemoglobin was 1.92ng/ml above which the pregnant women develop preeclampsia.Conclusions: Higher values of fetal hemoglobin and alpha 1 microglobulin in pregnant women between 10 to 16 weeks gestational age positively correlates with development of preeclampsia in those women.


2011 ◽  
Vol 285 (2) ◽  
pp. 371-375 ◽  
Author(s):  
Meral Erdem ◽  
Muge Harma ◽  
Ibrahim Mehmet Harma ◽  
Ilker Arikan ◽  
Aykut Barut

2015 ◽  
Vol 308 (3) ◽  
pp. R163-R172 ◽  
Author(s):  
Jude S. Morton ◽  
Anita Quon ◽  
Po-Yin Cheung ◽  
Tatsuya Sawamura ◽  
Sandra T. Davidge

Preeclampsia is a disorder of pregnancy with a significant impact on maternal and fetal health. The complexity of this multifactorial condition has precluded development of effective therapies and, although many potential pathways have been investigated, the etiology still requires clarification. Our group has investigated the scavenger lectin-like oxidized LDL (LOX-1) receptor, which may respond to factors released from the distressed placenta that contribute to the vascular pathologies observed in preeclampsia. Given the known beneficial effects of sodium tanshinone IIA sulfonate (STS; a component of Salvia miltiorrhiza) on vasodilation, reduction of oxidative stress, and lipid profiles, we have investigated its role as a potential treatment strategy. We hypothesized that STS would improve vascular endothelial function and, combined with a reduction in oxidative stress, would improve pregnancy outcomes in a rat model of preeclampsia (reduced uteroplacental perfusion pressure, RUPP). We further hypothesized this may occur via the action of STS on the LOX-1 and/or platelet-activating factor (PAF) receptor axes. The RUPP model increased maternal blood pressure, vascular oxidative stress, and involvement of the vascular PAF receptor. Treatment with STS during pregnancy decreased both oxidative stress and involvement of the PAF receptor; however, it also increased involvement of the LOX-1 receptor, which is in line with the concept that scavenger receptors, such as LOX-1 and PAF, are upregulated in response to ligand binding and/or under pathological conditions. In this model of preeclampsia, however, the vascular actions of STS did not lead to improvements in pregnancy outcome such as fetal biometrics or maternal blood pressure.


2014 ◽  
Vol 21 (8) ◽  
pp. 973-977 ◽  
Author(s):  
Ana Paula Machado Spada ◽  
Débora Cristina Damasceno ◽  
Yuri Karen Sinzato ◽  
Kleber Eduardo Campos ◽  
Priscila Afonso Faria ◽  
...  

2010 ◽  
Vol 29 (5) ◽  
pp. 351-358 ◽  
Author(s):  
Rahul Pathak ◽  
Sanvidhan G Suke ◽  
Tanzeel Ahmed ◽  
Rafat S Ahmed ◽  
AK Tripathi ◽  
...  

A number of studies have focused attention on various biochemical abnormalities evoked due to exposure to organochlorine pesticides (OCPs). The aim of the present study was to analyze the OCP residues in maternal and cord blood of women and assess the levels of different non-enzymatic oxidative stress markers as well as to establish correlation with OCP levels, if any. Thirty women in each group of full-term delivery (FTD; ≥37 weeks of gestation) and preterm delivery (PTD; <37 weeks of gestation) were enrolled in this study. Levels of OCPs like Hexachlorocyclohexane (HCH), endosulfan, p,p′ Dichlorodiphenyldichloroethylene (DDE) and p,p’ Dichlorodiphenyltrichloroethane (DDT) were analyzed by gas chromatography. Non-enzymatic oxidative stress was measured by the quantification of malondialhyde (MDA), protein carbonyl, reduced glutathione (GSH) and ferric-reducing ability of plasma (FRAP). MDA and protein carbonyl levels were increased significantly, while the levels of GSH and FRAP were decreased in PTD in comparison to FTD cases. We have observed higher levels of β-HCH and α-endosulfan and increased oxidative stress in PTD than FTD cases. In PTD cases, a significant positive correlation was observed between maternal blood levels of β-HCH and MDA (r = .78), β-HCH and GSH (r = —.65), γ-HCH and MDA (r = .89), γ-HCH and GSH (r = —.74) and α-endosulfan and MDA (r = .54) in PTD cases. We also found significant correlations between cord blood levels of β-HCH and MDA (r = .59), β-HCH and GSH (r = —.69), γ-HCH and MDA (r = .62) and α-endosulfan and MDA (r = .54) in PTD cases. In conclusion, our results suggest that higher levels of some of the OCP residues may be associated with PTD and increased oxidative stress.


2020 ◽  
Vol 11 (10) ◽  
pp. 8547-8559
Author(s):  
Hongjing Zhao ◽  
Yu Wang ◽  
Mengyao Mu ◽  
Menghao Guo ◽  
Hongxian Yu ◽  
...  

Antibiotics are used worldwide to treat diseases in humans and other animals; most of them and their secondary metabolites are discharged into the aquatic environment, posing a serious threat to human health.


2019 ◽  
Vol 476 (24) ◽  
pp. 3705-3719 ◽  
Author(s):  
Avani Vyas ◽  
Umamaheswar Duvvuri ◽  
Kirill Kiselyov

Platinum-containing drugs such as cisplatin and carboplatin are routinely used for the treatment of many solid tumors including squamous cell carcinoma of the head and neck (SCCHN). However, SCCHN resistance to platinum compounds is well documented. The resistance to platinum has been linked to the activity of divalent transporter ATP7B, which pumps platinum from the cytoplasm into lysosomes, decreasing its concentration in the cytoplasm. Several cancer models show increased expression of ATP7B; however, the reason for such an increase is not known. Here we show a strong positive correlation between mRNA levels of TMEM16A and ATP7B in human SCCHN tumors. TMEM16A overexpression and depletion in SCCHN cell lines caused parallel changes in the ATP7B mRNA levels. The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS). Pretreatment with either chelator significantly increased cisplatin's sensitivity, particularly in the context of TMEM16A overexpression. We propose that increased oxidative stress in TMEM16A-overexpressing cells liberates the chelated copper in the cytoplasm, leading to the transcriptional activation of ATP7B expression. This, in turn, decreases the efficacy of platinum compounds by promoting their vesicular sequestration. We think that such a new explanation of the mechanism of SCCHN tumors’ platinum resistance identifies novel approach to treating these tumors.


2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.


2001 ◽  
Vol 120 (5) ◽  
pp. A217-A217
Author(s):  
C SPADA ◽  
S SANTINI ◽  
F FOSCHIA ◽  
M PANDOLFI ◽  
V PERRI ◽  
...  

2001 ◽  
Vol 120 (5) ◽  
pp. A116-A116
Author(s):  
S ALEYNIK ◽  
M ALEYNIK ◽  
C LIEBER
Keyword(s):  

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