Oxidative‐Nitrative Stress and Poly (ADP‐Ribose) Polymerase Activation 3 Years after Pregnancy

Abstract

Background Oxidative-nitrative stress and poly (ADP-ribose) polymerase activation have been previously observed in healthy and gestational diabetic pregnancies, and they were also linked to the development of metabolic diseases. The aim of the present study was to examine these parameters and their correlation to known metabolic risk factors following healthy and gestational diabetic pregnancies. Methods Fasting and 2 h postload plasma total peroxide level, protein tyrosine nitration, and poly (ADP-ribose) polymerase activation were measured in circulating leukocytes three years after delivery in women following healthy, “mild” (diet-treated) or “severe” (insulin-treated) gestational diabetic pregnancy during a standard 75 g OGTT. Nulliparous women and men served as control groups. Results Fasting plasma total peroxide level was significantly elevated in women with previous pregnancy (B = 0.52 ± 0.13; p < 0.001), with further increase in women with insulin-treated gestational diabetes (B = 0.36 ± 0.17; p < 0.05) (R2 = 0.419). Its level was independently related to previous pregnancy (B = 0.47 ± 0.14; p < 0.01) and current CRP levels (B = 0.06 ± 0.02; p < 0.05) (R2 = 0.306). Conclusions Elevated oxidative stress but not nitrative stress or poly (ADP-ribose) polymerase activation can be measured three years after pregnancy. The increased oxidative stress may reflect the cost of reproduction and possibly play a role in the increased metabolic risk observed in women with a history of severe gestational diabetes mellitus.

Evaluation of oxidative/nitrative stress and uterine artery pulsatility index in early pregnancy

“…We hypothesize that this lower LDH reflects the decreased trophoblast invasion. Additionally, it has been previously shown by our research group that even after a healthy pregnancy, the degree of oxidative stress is elevated after three years [16]. It is also conceivable that low-resistance pregnant women had higher oxidative stress levels because of their higher number of previous pregnancies.…”

“…According to this reaction pathway, the change in nitrotyrosine levels might be expected to follow the changes in PRX concentration. On the other hand, previous studies also failed to confirm to this relationship, especially in chronic disease and healthy conditions [16,25].…”

“…The study size was estimated according to earlier measurements of plasma total peroxide level in healthy women. With a pooled standard deviation of 269 mM, a 200-mM difference by unpaired Student's t-test may be detected with a 5 0.05 and a power of 0.8 by a sample size of 29 per group [16].…”

Urinary Biomarkers of Oxidative Stress in Aging: Implications for Prediction of Accelerated Biological Age in Prospective Cohort Studies

“…Accordingly, increased circulating levels of biomarkers of oxidative stress were shown to associate with multiple agerelated diseases, including cancer, diabetes mellitus [21], neurodegenerative diseases, and cardiovascular diseases, as Oxidative Medicine and Cellular Longevity well as pathological conditions characterized by ongoing inflammatory processes [37,38]. On another note, nitrative stress-imposed by reactive derivatives of NO-contributes to a plethora of pathophysiological processes as well as aging [7,[39][40][41]. This study also found that concentrations of urinary biomarkers of oxidative stress varied considerably in older individuals.…”

Fundamental Mechanisms of the Cell Death Caused by Nitrosative Stress

“…Under nitrosative stress, ONOO – not only induces DNA single-strand breaks but also activates PARP ( Buelow et al, 2009 ), which consumes a large amount of NAD + , resulting in energy depletion and necrotic cell death. One study showed that DNA nitration is upstream of PARP-1 activation ( Barany et al, 2017 ; Horvath et al, 2018 ). The initial signaling of PARP-1 in mitochondria is mediated by the downstream activation of JNK-1, a stress-activated protein kinase (SAPK).…”