Sergiu Dumitrescu

Sergiu Dumitrescu
Ludwig Boltzmann Institute for Experimental and Clinical Traumatology · Molecular Mechanisms

MSc

About

31
Publications
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113
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Introduction
I am currently a PhD fellow at the Ludwig Boltzmann Institute for Experimental and Clinical Traumatology in the group of molecular mechanisms. The aim of my PhD project is to determine the role of mitochondria and ROS/RONS in the mechanism underlying stem cell activation. My research area is cell biology, and the outcome of my project should enrich the field of stem cell therapy with new insights on the mechansim of stem cell activation. Our most recent publication is 'SEP-11: ANTI-ROS TREATMENT BY SPECIFIC MITOCHONDRIA-TARGETED ANTIOXIDANTS SKQ1 AND MITOTEMPO EXACERBATE MORTALITY IN THE ACUTE MURINE POLYMICROBIAL SEPSIS'.

Publications

Publications (31)
Article
Full-text available
Mitochondrial ROS (mitoROS) control many reactions in cells. Biological effects of mitoROS in vivo can be investigated by modulation via mitochondria-targeted antioxidants (mtAOX, mitoTEMPO). The aim of this study was to determine how mitoROS influence redox reactions in different body compartments in a rat model of endotoxemia. We induced inflamma...
Article
Full-text available
Background Cerebral ischemia and neuroinflammation following aneurysmal subarachnoid hemorrhage (SAH) are major contributors to poor neurological outcome. Our study set out to investigate in an exploratory approach the interaction between NO and energy metabolism following SAH as both hypoxia and inflammation are known to affect nitric oxide (NO) m...
Article
Full-text available
The human amniotic membrane (hAM) has been used for tissue regeneration for over a century. In vivo (in utero), cells of the hAM are exposed to low oxygen tension (1-4% oxygen), while the hAM is usually cultured in atmospheric, meaning high, oxygen tension (20% oxygen). We tested the influence of oxygen tensions on mitochondrial and inflammatory pa...
Article
Full-text available
Background and purpose: Based on the fact that traumatic brain injury is associated with mitochondrial dysfunction we aimed at localization of mitochondrial defect and attempted to correct it by thiamine. Experimental approach: Interventional controlled experimental animal study was used. Adult male Sprague-Dawley rats were subjected to lateral...
Conference Paper
Increased levels of nitric oxide (NO) and peroxynitrite (ONOO‒), mitochondrial dysfunction at complex I, and excessive accumulation of glutamate have been suggested as the key pathophysiological events leading to brain damage upon traumatic brain injury (TBI). The aim of this study was to delineate the relationship between these three events and to...
Conference Paper
Although mitochondrial dysfunction is commonly accepted to mediate organ failure induced by systemic inflammatory response (SIR) the data on impairment of mitochondrial respiration upon SIR are still controversial. The aim of this study was to understand the contribution of mitochondrial reactive oxygen species (mtROS) to liver failure induced by S...
Article
Full-text available
Inorganic nitrite (NO2⁻) can be reduced back to nitric oxide (NO) by several heme proteins called nitrite reductases (NR) which affect both the vascular tonus and hemodynamics. The objective of this study was to clarify the impact of several NRs on the regulation of hemodynamics, for which hemodynamic parameters such as heart rate, blood pressure,...
Article
Full-text available
Mitochondrial-derived reactive oxygen species have been deemed an important contributor in sepsis pathogenesis. We investigated whether two mitochondria-targeted antioxidants (mtAOX; SkQ1 and MitoTEMPO) improved long-term outcome, lessened inflammation, and improved organ homeostasis in polymicrobial murine sepsis. 3-month-old female CD-1 mice ( n=...
Data
Supplementary Fig. 1. Score sheet for a custom-developed mouse clinical assessment scoring system. The well-being of mice is assessed based on six endpoints every 12 hours (beginning at 12h post-CLP); tree severity grades (i.e. 0, 1 or 2 points) are assigned. Euthanasia is indicated when: score ≥8 and/or by inability to trigger the startle reflex a...
Article
Purpose: To develop an assay that can enable the quantification of intra- and extracellular nitric oxide (NO) levels in liver biopsies without application of potentially harmful exogenous NO traps. Theory: Electron paramagnetic resonance (EPR) spectroscopy is currently the most appropriate method of measuring NO in biological samples due to the...
Conference Paper
Introduction: Systemic inflammatory response syndrome (SIRS) is a highly complex cascade of pro- and anti-inflammatory mechanisms, which results in a generalized activation of the immune system. Reactive oxygen species (ROS) and mitochondria, as one of the major sources of them play a key role in this process. Considering the deleterious effects o...
Article
Introduction: Nitric oxide was suggested to regulate p53-dependent expression of heat shock proteins and changes in cellular metabolism. Methods: Here we examined the longitudinal changes of NO metabolites, NO2 and NO3, ATP, a marker of mitochondrial function, and the expression of heat shock proteins (HSP)-72 and -90α in patients, adults and ch...
Conference Paper
Introduction: Nitric oxide (NO) is a potent signaling molecule maintaining numerous physiological and pathophysiological processes. Because of its short lifespan, the detection of NO by electron paramagnetic resonance spectroscopy (EPR) in frozen tissues requires stabilization by specific exogenous NO-traps. Such NO-traps are unfeasible in clinica...
Conference Paper
Introduction: Altered mitochondrial function by excessive production of reactive oxygen species (ROS) has been considered an important factor in pathogenesis of organ failure in sepsis. Methods: We investigated effects of two specific mitochondria-targeted antioxidants (SkQ1: lipophilic; MitoTEMPO: hydrophilic) on outcome, inflammatory response...

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