Impairment of mitochondrial respiration in platelets and placentas: a pilot study in preeclamptic pregnancies

Bînă, Anca M.; Aburel, Oana Maria; Avram, Vlad Florian; Lelcu, Theia; Chiriac, Veronica Daniela; Mocanu, Adelina Geanina; Bernad, Elena; Borza, Claudia; Craina, Marius; Popa, Z.; Muntean, Daniela-Lucia; Creţu, Octavian

doi:10.1007/s11010-022-04415-2

Cited by 15 publications

(10 citation statements)

References 51 publications

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“…Complex I activity is then inhibited by rotenone to assess the ET capacity for CII. Finally, complex III is inhibited with antimycin A, allowing the measure the residual oxygen consumption (ROX) due to processes other than OXPHOS (which are subtracted from the other respiratory rates) [ 31 ].…”

Section: Introductionmentioning

confidence: 99%

Impairment of Mitochondrial Respiration in Metabolic Diseases: An Overview

Avram

Merce

Hâncu

et al. 2022

IJMS

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Mitochondrial dysfunction has emerged as a central pathomechanism in the setting of obesity and diabetes mellitus, linking these intertwined pathologies that share insulin resistance as a common denominator. High-resolution respirometry (HRR) is a state-of-the-art research method currently used to study mitochondrial respiration and its impairment in health and disease. Tissue samples, cells or isolated mitochondria are exposed to various substrate-uncoupler-inhibitor-titration protocols, which allows the measurement and calculation of several parameters of mitochondrial respiration. In this review, we discuss the alterations of mitochondrial bioenergetics in the main dysfunctional organs that contribute to the development of the obese and diabetic phenotypes in both animal models and human subjects. Herein we review data regarding the impairment of oxidative phosphorylation as integrated mitochondrial function assessed by means of HRR. We acknowledge the critical role of this method in determining the alterations in oxidative phosphorylation occurring in the early stages of metabolic pathologies. We conclude that there is a mutual two-way relationship between mitochondrial dysfunction and insulin insensitivity that characterizes these diseases.

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Section: Introductionmentioning

confidence: 99%

Impairment of Mitochondrial Respiration in Metabolic Diseases: An Overview

Avram

Merce

Hâncu

et al. 2022

IJMS

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“…Of note, we have also recently reported a dichotomous behavior in placental mitochondria respiration in relation to the fetal birth weight. PE pregnancies with fetal growth restriction were associated with decreased active respiration (OXPHOS capacity) and maximal uncoupled respiration, while an increase in both respiratory parameters was found in PE pregnancies with normal weight fetuses [24].…”

Section: Discussionmentioning

confidence: 93%

Placental oxidative stress and monoamine oxidase expression are increased in severe preeclampsia: a pilot study

et al. 2022

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Preeclampsia (PE) is the most severe complication of pregnancy with substantial burden of morbidity and mortality for mother and neonate. The increased placental oxidative stress (OS) has been involved as central pathomechanism, yet the sources of reactive oxygen species (ROS) are partially elucidated. Monoamine oxidase (MAO) with 2 isoforms, A and B, at the outer mitochondrial membrane has emerged as a constant source of ROS in cardiometabolic pathologies. The present pilot study was purported to assess as follows: (i) the magnitude of placental OS in relation to the site of sampling and (ii) the expression of placental MAO in the setting of PE. To this aim, central and placental samples were harvested during cesarean section from mild and severe PE versus healthy pregnancies. ROS generation (dihydroethidium staining) and MAO expression were assessed (confocal microscopy). MAO gene transcript was evaluated by RT-PCR. The main findings are as follows: (i) a significant increase in placental OS was found in severe (but not in mild) PE with no regional differences between central and peripheral areas and (ii) placental MAO-A and B (gene and protein) were significantly increased in severe preeclampsia. The signal transduction of the latter finding, particularly in relation with mitochondrial dysfunction, is worth further studying.

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“…It is a leading cause of neonatal mortality and long-term morbidity, with profound implications for families and healthcare systems [ 3 , 4 ]. Various risk factors have been identified in the etiology of preterm birth, including demographic, genetic, environmental, and, particularly, infectious contributors [ 5 , 6 , 7 , 8 , 9 , 10 , 11 ]. Among these, genital infections in pregnant women are recognized as critical factors that can disrupt the normal course of gestation and precipitate early labor [ 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

“…Genital infections, encompassing a range of bacterial, viral, and fungal pathogens, can ascend from the lower genital tract to affect the uterus, amniotic fluid, and fetus [ 8 , 9 ]. The inflammatory response triggered by these infections, as well as systemic inflammation are well-documented causes of preterm labor [ 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

Impact of Genital Infections and Antibiotic Use on Incidence of Preterm Birth: A Retrospective Observational Study

Marti,

Bratosin,

Rosca

et al. 2024

Antibiotics

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This study investigates the complex interplay among genital infections, antibiotic usage, and preterm birth. This study aims to identify common genital pathogens associated with preterm births, assess the impact of various antibiotic treatments on pregnancy outcomes, and understand antibiotic resistance patterns among these pathogens. This study included 71 pregnant women who experienced preterm birth and 94 women with genital infections who delivered at term. Various maternal characteristics, medical history, signs and symptoms, gestational weight, gestational age, type of birth, vaginal pH, Nugent scores, and vaginal flora were analyzed. Antibiotic resistance patterns of isolated microorganisms were also examined. The prevalence of sexually transmitted diseases (STDs) and genital herpes was significantly higher in the preterm group. Preterm births were associated with fever, pelvic pain, vaginal spotting, and fatigue. Vaginal pH levels and Nugent scores were significantly higher in the preterm group, indicating disturbed vaginal flora. The presence of Extended-Spectrum Beta-Lactamases (ESBLs) was a particularly strong risk factor, increasing by more than four times the odds of preterm birth (OR = 4.45, p = 0.001). Vancomycin-Resistant Enterococci (VRE) presence was another critical factor, with a four-fold increase in the odds of preterm birth (OR = 4.01, p = 0.034). The overall presence of Multidrug-Resistant (MDR) organisms significantly increased the odds of preterm birth (OR = 3.73, p = 0.001). Specific pathogens like Chlamydia trachomatis (OR = 3.12, p = 0.020) and Mycoplasma hominis (OR = 3.64, p = 0.006) were also identified as significant risk factors. Ureaplasma urealyticum also showed a significantly higher risk of preterm birth (OR = 2.76, p = 0.009). This study highlights the importance of screening for and treating genital infections during pregnancy, especially STDs and genital herpes, as they can significantly increase the risk of preterm birth. Additionally, the presence of specific microorganisms and antibiotic resistance patterns plays an essential role in preterm birth risk. Early detection and targeted antibiotic treatment may help mitigate this risk and improve pregnancy outcomes.

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Impairment of mitochondrial respiration in platelets and placentas: a pilot study in preeclamptic pregnancies

Cited by 15 publications

References 51 publications

Impairment of Mitochondrial Respiration in Metabolic Diseases: An Overview

Impairment of Mitochondrial Respiration in Metabolic Diseases: An Overview

Placental oxidative stress and monoamine oxidase expression are increased in severe preeclampsia: a pilot study

Impact of Genital Infections and Antibiotic Use on Incidence of Preterm Birth: A Retrospective Observational Study

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