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Corroyer, Sophie. "Agression oxydante et processus de lesion-reparation : role du systeme des cyclines et du systeme des insulin-like growth factors". Paris 5, 1998. http://www.theses.fr/1998PA05N130.
Pełny tekst źródłaVentura, Emilie. "Stress oxydant et vieillissement : modulation de la NADPH oxydase". Montpellier 2, 2008. http://www.theses.fr/2008MON20128.
Pełny tekst źródłaOxidative stress is the result of an imbalance between production of oxidants and antioxidant defense mechanisms. The NADPH oxidase is a key enzyme for excessive production of oxidants, strengthening the interest of its modulation. NADPH oxidase is involved in the initiation and progression of age-related diseases such as cardiovascular diseases and dementia. Through an epidemiological study consisted of 517 subjects (79. 5 ± 7. 1 years), we determined NADPH oxidase activation and its main determinants with age. Among the factors tested, homocysteine and inflammation were significantly associated with NADPH oxidase activity in a multivariate analysis. These data are confirmed in vitro because homocysteine thiolactone and lipopolysaccharide induce a dose-dependent activation and expression of NADPH oxidase in cell line THP-1. In an in vitro on THP-1 and animal studies, we studied the negative modulation of the NADPH oxidase by natural antioxidants (polyphenols) and enzymatic antioxidants (melon extract rich in SOD and catalase). These nutritional antioxidants negatively modulate the activity but also the expression of NADPH oxidase. In conclusion, NADPH oxidase activity is associated with age and is positively regulated by inflammation and homocysteine. The superoxide anion production is associated with cardiovascular and neurodegenerative diseases. NADPH oxidase may be modulated in vitro by natural antioxidants. Links with dementia, cardiovascular disease or mortality must be further study. The antioxidant supplements efficiency must be clarified in animal models and then on a clinical study
Rossary, Adrien. "Implication de la NADPH oxydase dans les phénomènes de stress oxydant". Lyon 1, 2007. http://www.theses.fr/2007LYO10271.
Pełny tekst źródłaFalvelly, Diane de. "Réponse immunitaire, sida et cancer: rôle du stress oxydant et des vitamines anti-oxydantes". Paris 5, 1997. http://www.theses.fr/1997PA05P131.
Pełny tekst źródłaPage, Audrey. "Etude de la modulation de la réponse cellulaire au stress oxydatif par les protéines VP24 des virus Marburg et Ebola". Phd thesis, Ecole normale supérieure de lyon - ENS LYON, 2012. http://tel.archives-ouvertes.fr/tel-00671994.
Pełny tekst źródłaAllanore, Yannick. "Implication du stress oxydant et propriètés anti-oxydantes des inhibiteurs calciques dihydropyridiniques au cours de la sclérodermie systémique". Paris 5, 2004. http://www.theses.fr/2004PA05N08S.
Pełny tekst źródłaFree radicals are suspected to play a key role in the successive vascular, dysmmune and fibrotic lesions which occur in sistemic sclerosis. Our results emphasize monocyte free radical superoxide anion production wich may account for the various oxidative stress circulating markers observed in the disease. We also demonstrate that calcium channel blockers of dihydropyridine type can inhibit monocyte activation and superoxyde anion production. These drugs seem to act in modulation of superoxyde anion production through inhibition of PMA-induced phosphorylations and protein kinase c activity inhibition. These results, together with previous data on their impact on microvasculature, highlith the major role of dihydropyridine type calcium channel blockers in the treatment of systemic sclerosis
Rangel, Manuel. "Analyse du rôle de la NADPH oxydase et du stress oxydant dans les cellules dendritiques". Phd thesis, Université de Grenoble, 2012. http://tel.archives-ouvertes.fr/tel-00767151.
Pełny tekst źródłaGoux, Aurélie. "NADPH Oxydase et Stress Oxydant au cours de l'Insuffisance Rénale Chronique : modulation par les HDL". Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20166/document.
Pełny tekst źródłaCardiovascular (CV) diseases are the first cause of mortality during chronic kidney disease (CKD) and cannot only be explained by traditional risk factors (age, gender, dyslipidemia, hypertension). Oxidative stress, which has been associated with CKD, appears as a non-traditional risk factor closely interconnected with inflammation and malnutrition.This study aimed at investigating oxidative stress in CV complications in uremic rats. Then, HDL proteomic profile and in vitro functionality of HDL were compared between hemodialyzed (HD) patients and control subjects.First, an animal model of CKD associated with malnutrition, the adenine-fed rats, was set up in order to study CV oxidative stress. NADPH oxidase activity was increased three-fold, but the maximal activity of mitochondrial respiratory chain complexes and SOD were not different between groups. Superoxide anion output was associated with accumulation of osteopontin and of pro-collagen type I. In a second part, HDL proteomic study from HD and control subjects was performed to characterize qualitative modifications associated with the decrease in HDL observed in CKD. HDL anti-oxidative activities from these subjects were studied in vitro in a model of copper-induced LDL oxidation and in a cellular model of NADPH oxidase activation. Compared to control, HDL from HD patients failed to protect LDL oxidation. By contrast, HDL modulation of NADPH activity is maintained in HD patients but could be impaired by elevated inflammation.These results suggest that oxidative stress is a key event in cardiac complications during CKD. Among protective endogenous mechanisms, HDL anti-oxidative properties could be impaired in HD patients
Duroc, Yann. "Etude des relations structure-fonction de la protéine ORF 138 responsable de la stérilité mâle cytosplasmique Ogura". Paris 11, 2004. http://www.theses.fr/2004PA112187.
Pełny tekst źródłaThe ORF138 protein (encoded by the mitochondrial genome) is a mitochondrial membrane protein responsible of Ogura cytoplasmic male sterility (CMS) in Brassicaceae. In sterile plants microspore abortion is apparently due to premature degeneration of the anther tapetum, by a still unknown mechanism. This is the only induced phenotype whereas ORF138 is present in all tissues. The objectives of this work were to develop molecular and biochemical tools for the study of this protein, and to obtain relevent information for setting up hypotheses about the mechanism of male sterility. We showed that the association of the hydrophobic and hydrophilic domains of the protein is essential for its effect. A domain of 15 amino acids, sharing predicted secondary structure with two other proteins of unrelated CMS's, was highlighted and showed to play a role in this effect. We showed that ORF138 was integrated in the mitochondrial inner membrane of rapeseed and formed homooligomers. A proteic complex of size ranging between 750 and 900 kDa implying ORF138 was also identified. We also proved that ORF138 can be copurified with mitochondrial nucleoproteic components of male sterile plants. An increased accumulation of mitochondrial alternative oxydase probably accompanied by an increased activity, was observed in the sterile plants compared to fertiles. The connection between oxidative stress and alternative oxydase activity is well-known, and a possible bond between an oxidizing stress and the premature death of the tapetum constitutes one of the most promising tracks for the elucidation of the sterility mechanism
Joffe, Ricardo. "The role of mesophyll conductance in the regulation of photosynthesis under ozone-induced oxidative stress in poplar : ecophysiological, anatomical and biochemical aspects". Electronic Thesis or Diss., Université de Lorraine, 2022. http://www.theses.fr/2022LORR0289.
Pełny tekst źródłaOzone (O₃) is one of the most harmful and widespread air pollutants considerably affecting photosynthesis and thus crop yields and plant health worldwide. The CO₂ diffusion conductance within leaf mesophyll (gm) is widely considered to be a major limiting factor of photosynthesis under stress and non-stress conditions. This work aimed to investigate the effects of O₃-induced oxidative stress on gm and to decipher underlying mechanisms driving its regulation at a physiological, anatomical and biochemical level. A selection of several genotypes of the tree model Populus × canadensis Moench was submitted to chronic O₃ exposure at 120 ppb for 21d under controlled conditions in phytotronic chambers in order to analyse gas exchange, antioxidants pool and leaf structural and ultrastructural traits. Chronic O₃ caused a substantial decrease of gm, which was thus a major limiting factor of the net assimilation rate (Anet), ahead of stomatal conductance to CO₂ (gsc) and of the maximum carboxylation capacity of the Rubisco enzyme (Vcmax). Total pools of the main antioxidations ascorbate and glutathione were not related to gm but the signalling molecule malondialdehyde (MDA) might have mitigated O₃-caused decrease of gm. On a structural level, this observed decrease was mainly driven by O₃-induced modifications of subcellular traits, notably cell wall and cytoplasm thickening, inter-chloroplast spacing as well as the ratio of exposed chloroplasts to mesophyll surface area (Sc/Sm). However, the observed relationship between gm and anatomy but also the gm response to O₃ were genotype-dependent. The dynamic response of gm to O₃ was also investigated testing a single genotype during alternating periods of short-term acute O₃ exposure at 200 ppb and recovery. The assumed contribution of biochemical determinants of gm was analysed by quantifying the expression levels of several potential CO₂-diffusion facilitating carbonic anhydrases (CA). Under acute O₃ stress, gm was highly responsive but exhibited also some degree of post-stress resilience. The response of the expression level of α-CA1 to the applied treatment may suggest the involvement of this CA isoform in the short-term regulation of gm. This work underlines the importance of gm as a major limitation of Anet but also the necessity of its consideration in a comprehensive assessment of photosynthesis response to environmental constrains. These results further suggest that gm might be a very promising target for plant engineering in order to enhance photosynthetic yield and stress resistance of field and biomass crops
Lévy, Elise. "Maladies neurodégénératives et stress oxydant". Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASB028.
Pełny tekst źródłaAlzheimer's disease and prion diseases are incurable neurodegenerative diseases associated with the transconformation of a polypeptide: the Aß peptide and the prion protein (PrP) respectively. These misfolded polypeptides then form different aggregates in the brain, leading to neuronal death. In a healthy individual, PrP has a neuroprotective function, but in patients suffering from Alzheimer or prion diseases, the toxicity of some pathological aggregates is mediated by this protein. Moreover, both pathologies are associated with an early chronic oxidative stress, that is toxic. It can promote and be promoted by protein aggregation, without the aggregates involved in this vicious circle being precisely identified.To study oxidative stress in these diseases, I developed innovative cellular models to monitor oxidation markers in real time, and bioinformatic tools to analyze the results. My work shows that the unique expression of the healthy form of Aß or PrP protects cells from an exogenous oxidant. However, the addition to the culture medium of the same cells of recombinant Aß and PrP promotes the appearance of oxidative stress, only for cells expressing normal PrP. This effect is visible for A in the form of amyloid fibrils, and for PrP in the form of monomer, oligomers and potentially amyloid fibrils. This work thus validates the central role of normal PrP in physiology and pathology. My results could suggest a role of glutathione peroxidases in mediating the protective effect of normal PrP, and an activation of NADPH oxidases via PrP in the presence of pathological aggregates
Starck, Marjorie. "Apolipoprotéine E, estrogènes et stress oxydant". Nancy 1, 2000. http://www.theses.fr/2000NAN12006.
Pełny tekst źródłaAn imbalance between oxidant and antioxydant defense systems plays a central role in the pathogenesis of a number of age-related human diseases, notably cardiovascular diseases. Hormonal or estrogen replacement therapies (HRT or ERT) in post-menopausal women are expected to play antioxydant functions. Estrogens have both direct pro-oxidant and anti-oxidant activities in vitro. This pro-oxidant activity is unlikely to occur in vivo, while the antioxidant activity is modest. We aimed at evaluating the impact of ERT or HRT on biological parameters related to oxidative stress. To do so, we measured the serum concentrations of an indicator of total antioxidant status (TAS) and related factors such as copper, zinc, iron and transferrin in a population of 229 randomly selected postmenopausal women with or without HRT or ERT, as well as in 100 premenopausal women. Usual biological parameters were also assessed. Menopause was characterized by higher serum concentrations of alkaline phosphatase, apolipoproteins AI and E, zinc and TAS. Among these parameters, ERT or HRT use influenced alkalie phosphatase and alipoprotein E, bringing them back to premenopausal levels. HRT also influenced the concentrations of TAS, which were higher in treated than in untreated postmenopausal women. Uric acid, total proteins and albumin were positively correlated to TAS independently on replacement therapies. In conclusion, at physiological concentration, ERT or HRT participate in the increase of the antioxidant capacity of serum in postmenopausal women
Noichri, Yosri. "Stress oxydant et infarctus du Myocarde". Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS479/document.
Pełny tekst źródłaMyocardial infarction is the leading cause of death in developed nations despite of recent advances in the management of this disease. Oxidative stress is involved in the physiopathology of Myocardial Infarction. Our study showed a decreased antioxidant activities in patients with Acute Myocardial Infarction. A part of the present study was designed to explore Peroxiredoxin Thioredoxin activity. It’s considered as a major antioxidant system and it control hydrogen peroxide levels which mediate the signal transduction, including apoptosis signal. Molecular mechanisms underlying the oxidative stress toxicity in cardiomyocytes have to be more elucidated and may help the evolving of therapeutic care strategies of coronary heart disease
Chaaya, Rana Youssef. "Rôle du stress oxydant induit par les monoamine oxydases dans la fibrose rénale : étude in vivo dans un modèle d'ischémie reperfusion chez le rat". Toulouse 3, 2010. http://thesesups.ups-tlse.fr/884/.
Pełny tekst źródłaThe deterioration of the kidney graft is characterized by progressive renal dysfunction accompanied by interstitial fibrosis and tubular atrophy (IFTA). Immunological and non-immunological stress are the main cause of progression towards IFTA. During my PhD, we focused on the non-immunological injuries induced by ischemia-reperfusion (IR) and cyclosporin toxicity (CsA) which remain two stress factors putting a damper on the outcome of the renal graft. In the kidney, a major endogenous source of reactive oxygen species (ROS) is the mitochondrial enzyme, monoamine oxidase (MAO). Our previous works in the laboratory showed that the blockage of the MAOs by the administration of the irreversible MAO-inhibitor pargyline (Pg) prevents H2O2 production in the early reperfusion stage following IR. However, the role of these enzymes on renal function and chronic diseases has still not been elucidated. The aim of my PhD work was to clarify the role of MAO-induced oxidative stress in renal fibrosis and to investigate the protective effect of early MAO inhibition on renal structure and function on the long-term. Therefore, we used a rat model of IFTA consisting in unilateral nephrectomy followed by IR and daily CsA administration (IR +CsA). Two groups of rats received a single injection of Pg before or after IR. Animals were sacrificed at 7, 14 and 28 days after IR and renal function, histological alterations, inflammatory and fibrotic genes were evaluated. Our results showed that the blockage of MAO by Pg either before or after IR improved renal function on the time-period studied and reduced significantly tubular necrosis and apoptosis observed at 7 days after IR+CsA. The prevention of the oxidative stress by Pg administered before IR leads to a net decrease in inflammation associated to lower IL-1( and TNF-( genes expression, in TGF-(1 expression and in necrosis and apoptosis at 28 days post IR+CsA. This protective effect was accompanied by a significant decrease in the accumulation of the ECM from 7 days as well as the normalization of antioxidant (SOD1, catalase) and inflammatory (COX2, LOX5) genes expression leading to inhibit the appearance of IFAT 28 days after IR+CsA. In conclusion, our data strongly suggest that the blockage of MAO by pargyline pre-treatment may constitute an important new therapeutic target against IFTA progression during kidney transplantation
Morel, Carole. "Etudes de la régulation de la sulfhydryl oxydase QSOX1 et de son implication dans l'apoptose induite par les stress oxydants". Phd thesis, Université de Franche-Comté, 2007. http://tel.archives-ouvertes.fr/tel-00311794.
Pełny tekst źródłaNous avons tenté d'établir un modèle de protection par E2 des cellules PC12/ERa soumises à un stress oxydant induit par H2O2 ou le complexe Fe(III)-HQ. Malgré différentes conditions testées, aucune protection par E2 n'a pu être obtenue.
Nous avons ensuite étudié la régulation de l'expression de QSOX1 dans le cerveau de Rates ovariectomisées traitées ou non par E2. Dans trois aires cérébrales exprimant fortement ERa et ERb, le niveau de messagers QSOX1 diminue en présence de E2.
Enfin, nous avons étudié l'implication de QSOX1 dans les stress oxydants. Dans les cellules PC12 soumises au stress oxydant, l'expression des messagers et de la protéine QSOX1 augmente. Suite au stress oxydant, la viabilité des cellules MCF-7 surexprimant QSOX1 diminue moins fortement que celle des cellules contrôles. La diminution de l'apoptose est associée à une moindre dépolarisation des mitochondries dans ces cellules.
Nos travaux ont ainsi permis de confirmer l'estrogéno-dépendance de QSOX1 in vivo et de montrer pour la première fois le rôle de QSOX1 dans la protection des cellules contre l'apoptose induite par les stress oxydants. Ces résultats ouvrent de nouvelles perspectives et renforcent l'intérêt de l'étude de QSOX1 dans la neuroprotection par E2.
Morel, Carole. "Etudes de la régulation de la sulfhydril oxydase QSOX1 et de son implication dans l'apoptose induite par les stress oxydants". Besançon, 2007. http://www.theses.fr/2007BESA2041.
Pełny tekst źródłaThe quiescin/sulthydryl oxidase protein QSOXI is an enzym that catalises disulfide bond formation. Ln vivo, its substrats are still unknown and its cellular roles remain to be determined. Oxidative stress are especially involved in neurodegenerative diseases. 17f3- estradiol (E2) hormone has neuroprotective effects. Our aims were to study the regulation of QSOXI expression by E2 and QSOXI involvement in oxidative stress and E2 neuroprotection. We attempted to establish a model of protection by E2 of PC12/ERa cells submited to oxidative stress induced by H2O2 or Fe(III)-HQ complex. Ln spite of different tested conditions, no protection by E2 was obtained. Then, we studied the regulation of QSOXl expression in brain of ovariectomized female rat treated or not by E2. Ln three cerebral areas that strongly expressed ERα et ERβ3, the level of QSOXl messengers decreased in the presence of E2. Finally, we studied the QSOXI involvement in oxidative stress. Ln PC12 cells submitted to oxidative stress, QSOXI messenger and protein expression increased. After oxidative stress, the viability of MCF-7 cells that over expressed QSOXI decreased less strong than viability of control cells. The decrease of apoptosis is associated to a lesser mitochondria depolarisation in QSOXI over expressing MCF- 7 cells. Our works enabled to confirm the estrogeno-dependance of QSOXl in vivo and to show for the first time the role of QSOXI in cell protection against oxidative stress-induced apoptosis. These results open new prospects and reinforce the interest of QSOXI study in the context of neuroprotection by E2
Donadieu, Emilie. "Stress oxydant et vieillissement de l'oreille interne". Aix-Marseille 2, 2007. http://www.theses.fr/2007AIX20701.
Pełny tekst źródłaWe have developed for the first time a cochlear cryosectioning method, which permit direct histological and immunohistochemical applications. This method allowed us to realise a complete and detailed analysis of the age-related hearing loss and hypoxia-induced hearing loss structural alterations and their molecular mechanisms. We thus determined the important role of oxidant stress in cochlea degeneration. Aside to the classical damages caused by ROS on DNA, RNA and lipids, the ROS induced apoptosis in selective cochlea regions such as the spiral ganglion and spiral ligament as well as cytoskeleton perturbations in neural cellules of spiral ganglion, all leading to hearing loss. In addition, adaptation mechanisms such as neoangiogenesis settled down in order to decrease against oxidant stress and slow down hearing loss
Amri, Fatma. "Contribution à l’étude des mécanismes de la glioprotection anti-oxydante et anti-inflammatoire sur des modèles in vitro et in vivo de neurodégénérescences et d'ischémie cérébrale : implication potentielle des globines endogènes du système nerveux central". Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4090.
Pełny tekst źródłaOxidative stress plays a major role in the death of neuronal cells under various neuropathological conditions. However, reactive astrocytes, by producing neuroprotective and antioxidant factors, are able to protect neurons against oxidative stress. Therefore, protecting glial cells from harmful factors is essential to prevent nerve cell damage. Brain globins, in particular, neuroglobin (Ngb) and hemoglobin (Hb), expressed in neurons and glial cells, play an important role in the metabolism of oxygen. Recently, it has been demonstrated that these proteins exert neuroprotective effects in experimental models of neurodegenerative diseases. However, no glioprotective effect has been reported. The objectives of this thesis work are to demonstrate the protective effects of Hb and Ngb in cultured astrocytes in the presence of oxidative stress and to elucidate the intracellular mechanisms involved. We have demonstrated That Hb and Ngb are able to promote the survival of astrocytes under oxidative stress conditions by significantly reducing over-production of ROS, overexpression of pro-inflammatory genes (IL-6, IL-33, iNOS) Mitochondrial dysfunction and stimulation of caspase-3/7 activity. We have also shown that anti-apoptotic effects involve the activation of ERK-MAPK signaling pathways. In addition, we verified the glioprotective effects on an animal model of chronic oxidative stress, KO mice TP53INP1, as well as on an animal model of hypoxia
Kermorvant-Duchemin, Elsa. "Stress nitro-oxydant et microcirculation : caractérisation des effets biologiques des acides trans-arachidoniques, nouveaux médiateurs du stress nitro-oxydant". Paris 5, 2008. http://www.theses.fr/2008PA05P648.
Pełny tekst źródłaTrans-arachidonic acids are major products of NO2·-mediated isomerization of arachidonic acid within the cell membrane, and have been proposed as new mediators of nitro-oxidative stress. However, their biological relevance is unknown. We characterized the influence of trans-arachidonic acids on neuro-retinal microvasculature and endothelial cell signaling. We showed that trans-arachidonic acids exert an acute endothelium-dependent vasorelaxant effect on rat brain pial microvasculature, through interactive activation of big conductance calcium-dependant potassium channels with heme-oxygenase-2, and in turn, soluble guanylyl cyclase. Long-term effects of trans-arachidonic acids on microvasculature include a selective time- and concentration-dependent apoptosis of microvascular endothelial cells in vitro, resulting in retinal microvascular degeneration ex and in vivo, in a model of ischemic retinopathy. These effects are mediated by an upregulation of the anti-angiogenic factor thrombospondin-1. Our findings provide new insight into the molecular mechanisms of nitro-oxidative stress on neurovascular tone and microvascular injury and suggest new therapeutic avenues in the management of disorders involving nitro-oxidative stress such as ischemic retinopathies and encephalopathies
Flamant, Cyril. "Mucoviscidose et système oxydant / anti-oxydant : étude de gènes modificateurs". Paris 6, 2005. http://www.theses.fr/2005PA066297.
Pełny tekst źródłaSmani, Moneïm. "Stress oxydant et nucléoside diphosphate kinases : étude moléculaire". Bordeaux 2, 2006. http://www.theses.fr/2006BOR21400.
Pełny tekst źródłaThe family of nm23 genes (non-metastatic clone 23) code for the nucleoside diphosphate kinases (NDPK). These proteins are involved in physiological and pathological processes being modulated by oxidative stress. We studied oxidative stress and NDPK-A and B interactions in a cellular model and an animal model : the mouse. In vitro, the overexpression of NDPK-A and B in the Baf3 cell line does not affect their mitotic capacity, but enhances their resistance to oxidative stress. In vivo, acute oxidative stress induces hepatocyte necrosis without apoptosis signs, followed by a regenerative process. In the nm23-M1-/-mouse, the response to oxidative stress in hepatocyte is modified. A molecular study shows a modification of cellular signaling pathways. We conclude that NDPKs promote cell protection against oxidative injury
Capul, Catherine. "Evaluation par relaxation protonique plasmatique de stress oxydants inflammatoires". Toulouse 3, 1995. http://www.theses.fr/1995TOU30210.
Pełny tekst źródłaGele, Patrick. "Stress oxydant et inflammation : cibles pharmacologiques de la neuroprotection". Lille 2, 2004. http://www.theses.fr/2004LIL2S016.
Pełny tekst źródłaOxidative stress and inflammation are two noxious mechanisms involved in several pathologies. In the current work, we focused on several cerebral physiopathological animal models. After a cerebral ischemia-reperfusion injury, these two mechanisms leads to neuronal and vascular injuries. We hypothesize that a chronic fenofibrate treatment could exert a neuroprotective effect, according to its anti-oxidative and anti-inflammatory properties. The effect was demonstrated in Apolipoprotein E deficient mice, before to be explored in wild-type animals. PPARα was required for the neuroprotective effect of fénofibrate. The increase of antio-oxydative defenses and the vascular anti-inflammatory effect under fénofibrate treatment were evaluated in a neurodegenerative disease, the Parkinson's disease. A chronic treatment by fenofibrate made the dopaminergic neurons more resistant to the pro-oxidative toxin MPTP. Demonstrated with a chronic treatment, we were interested in the acute neuroprotection by PPARα agonists administration, which could diminish the cerebral infracted volume. We also demonstrated a such effect for simvastatine, already kown for its chronic treatment induced-neuroprotection. At last, we focused on the hemorrhagic transformation during thrombolysis and we demonstrate the deleterious effect of the thrombolysis products. The experimental results, based on clinically used chemicals, should permit an expected application to Human in a middle dated term
Bianchi, Arnaud. "Proliférateurs de peroxysomes et stress oxydant : impact de l'acide arachidonique et de l'acide clofibrique sur l'expression de protéines anti-oxydantes (métallothionéines et superoxydes dismutases) dans les cellules humaines HepG2". Nancy 1, 2002. http://www.theses.fr/2002NAN10024.
Pełny tekst źródłaPeroxysome proliferators and oxidizing stress: impact of arachidonic acid and clofibric acid on the expression of anti-oxidizing proteins (metallothioneins and superoxidize dismutases) in the human cells HepG2. Peroxysome Proliferator (PP) constitutes a family of chemical substances of different nature, which have in common the property to lead an increase of the number and of the enzymatic activities of the peroxysomes at the rodents. These activities produce reactive sorts of oxygen (ROS) who lead to a situation of oxidizing stress being able to infer hepatocarcinoma. Among these PP, this work was interested to clofibric acid, belonging to the family of fibrates used in the treatment of hyperlipidémia, and to arachidonic acid ( AA), a polyinsatured fatty acid, which plays a role of second messenger in different way, as in apoptose or in the cellular proliferation. The molecular mechanisms involved in these biologic response being badly known, this work presents the results obtained on human hepatoblastoma cells (HepG2) subjected to treatments with AA or clofibric acid. Marker of oxidant stress as well as expression of anti-oxidizing proteins were studied. Expression of an anti-oxidizing protein, metallothionein IIA, is strongly decreased by clofibric acid, independently of the nuclear receptor activated by the PP (PPAR). When HepG2 cell is treated with AA, expression of MnSOD, as well as its activity is induced for 24 hours of treatment with AA. However, an accumulation of H2O2 and products of lipid peroxidation is observed after 24 hours of treatment, this effects were abolished in the presence of inhibitors of AA metabolism. The study on the way of transduction of the signal leading to the induction of the MnSOD gene shows the importance of the p38 Mitogen Activated Protein Kinase (MAPK) pathway, activated by the ROS produced during the metabolism of AA, as well as proteins kinase C. While NF-kB is activated in the form of an inactive dimer, induction of the MnSOD gene by AA is correlated with AP-1 activation, herself dependent on the p38 MAPK. Pathway. In conclusion, clofibric acid seems to have little effect on HepG2 cells, contrary to what is shown for the rodents. On the other hand, AA leads to an oxidative stress by the ROS produced by her metabolism, which play the role of second messenger by activating a way of transduction leading to an anti-oxidizing response, but accumulation of ROS induce oxidizing damages being able to modify the cellular life
Coatrieux, Christelle. "Monoamine oxydases et athérosclérose : signalisation mitogène et étude in vivo". Toulouse 3, 2007. http://thesesups.ups-tlse.fr/38/.
Pełny tekst źródłaReactive oxygen species (ROS) are involved in the activation of pathways, such as cell proliferation and involved in the development of many diseases including atherosclerosis. Monoamine oxidases (MAOs) catalyze the oxidative deamination of biogenic amines, such as serotonin and tyramine. The degradation of biogenic amines by MAOs generates large amounts of ROS that may play a role in the signaling of these agents like cell proliferation. ROS generated by MAO-A activate a mitogenic pathway, the MMP2/sphingolipids pathway, involved in smooth muscle cell proliferation. This signalling is mimicked by exogenous hydrogen peroxide. Furthermore, we report preliminary data on the mechanisms involved upstream the activation of MMP2 (which implicates furin and MT1-MMP). Lastly, the protective effect of MAO inhibitors was evaluated on an animal model for atherosclerosis, apoE-/- mice. This study indicated that hydrazinic MAO inhibitors were efficient in inhibiting the development of atherosclerotic lesions in apoE -/- mice, because of carbonyl scavenger properties and not due to their IMAO effect ; a non hydrazinic IMAO wasn't as protective. These data indicate that MAO-dependent oxidative stress is not involved in the formation of early atherosclerotic lesions, which doesn't exclude a role in advanced lesions. In conclusion, this work demonstrates a role of MAO-dependent oxidative stress in SMC proliferation, via a new stress-induced signalling mechanism, the MMP2/sphingolipid pathway
Bouayed, Jaouad. "Etude de la corrélation anxiété / statut oxydatif des granulocytes chez la souris et évaluation des effets antioxydants / neuroactifs des polyphénols extraits de Prunus domestica L". Thesis, Metz, 2007. http://www.theses.fr/2007METZ026S.
Pełny tekst źródłaIn this study, the linear and significant correlation between level of anxiety and peripheral oxidative status has been established. Indeed, the more the level of anxiety increases the more the intracellular level of reactive oxygen species of granulocytes is elevated. Our findings showed that the blood granulocytes of anxious mice may be more prone to oxidative damages altering their functions. These results highlighted the impact of anxiogen stress on the cellular oxidative status, and on the accumulation of intracellular ROS which is an essential etiologic factor. We have also found that chlorogenic acid protected granulocytes from oxidative stress, and possess anxiolytic properties. The antiradical power of seven varieties of French plums including the Mirabelle was comparatively evaluated in this study using ABTS test. Moreover, the protective effect of these plums on freshly isolated granulocytes from oxidative stress was also investigated in comparison with the vitamin C. Our results showed that polyphenols were the major contributor in the antioxidant activity exhibited by plums, and emphasize the preventive advantage of plum consummation from diseases linked to oxidative stress. The chemical profile permitted to reveal that neochlorogenic acid was the predominant polyphenolic in tested plums. The previsiouly protocol has been extended to some plants to quantify total phenolics, total flavonoids and total antioxidant activity. The protective effect of Momordica charantia L. fruit and of Desmodium adscendens L. leaves on granulocytes from oxidative stress has been highlighted, which gives to these plants an additional therapeutic value
Dzondo, Gadet Michel. "Traduction des ARNm du placenta humain dans le système acellulaire du germe de blé : optimisation par des molécules oxydantes, identification des protéines, régulation au cours du stress oxydant, rôle du bore". Nancy 1, 2000. http://www.theses.fr/2000NAN11324.
Pełny tekst źródłaCombès, Audrey. "Implication de la protoporphyrinogène oxydase dans l'homéostasie mitochondriale du fer et le statut redox des thiols chez la levure Saccharomyces cerevisiae". Paris 6, 2009. http://www.theses.fr/2009PA066391.
Pełny tekst źródłaChamproux, Alexandre. "Impact du stress oxydant sur l'intégrité de l'épigénome spermatique murin". Thesis, Université Clermont Auvergne (2017-2020), 2018. http://www.theses.fr/2018CLFAC004/document.
Pełny tekst źródłaIn Mammals, the success of fertilization and embryonic development, are associated to the quality of the reproductive cells: male gametes (spermatozoa) and female gametes (oocytes); each bringing half of the genetic heritage of the future individual. This genetic heritage may be compromised by various processes a very common one being radical attacks in cases of oxidative stress, it could diminish the quality of gametes and therefore the success of reproduction. It is well described that sperm DNA oxidative damage (SDOD) is one of the causes of male infertility frequently associated with reproductive failures in the context of natural or artificial conception in humans. To better understand the impact of oxidative damage on the quality of sperm, our team generated mouse models with SDOD. Characterization of these transgenic mice has shown that SDOD alone was associated with increased embryo defects, miscarriages and perinatal mortality. The team also brought forward that SDOD concerns preferentially specific regions of the sperm nucleus. In addition, the team suggested that sperm chromosomes were not identically susceptible to oxidative damage.In this thesis work, I developed and implemented fluorescence in situ hybridization (FISH) protocols to study chromosome positioning in the mouse sperm. I confirmed that susceptibility of chromosomes to oxidation is determined by their position in the murine sperm nucleus. In parallel, I addressed the question whether the sperm epigenome (particularly DNA methylation) was modified in a situation of post-testicular oxidative stress. Preliminary results seem to show that SDOD disturbs the sperm epigenetic profile.In parallel, in a pre-clinical approach, I contributed to show that an oral antioxidant supplementation can correct SDOD by modifying the antioxidant response of the epididymal tissue of the treated animals
Robin, Emmanuel. "Mitochondrie et réponse à l'hypoxie : de l'adaptation au stress oxydant". Lille 2, 2006. http://www.theses.fr/2006LIL2S034.
Pełny tekst źródłaOxygen (O2), as the last electrons acceptor of the mitochondrial electrons transfer chain (METC) is essential to multicellular organisms survival. During its reduction in H2O, intermediary reactive oxygen species (ROS) have been produced. On the one hand, ROS have been involved in several cellular signals pathways, and on the other hand their strong oxidative properties have been linked to cellular mortality. This duality is present during hypoxia or ischemia. The aim of this dissertation was to analysed the ROS production during hypoxia and ischemia before reperfusion. With this end, a new fluorescent FRET probe (HSP-FRET) has been used. A ROS production has been detected during the very first minutes of hypoxia or ischemia. The localization of ROS production detected by the HSP-FRET probe was probably the Q0 site of the mitochondrial complex III. The initial ROS species was probably superoxide anion quickly transform in hydrogen peroxide (H2O2) by superoxide dismutase (SOD1). In this context of hypoxia or ischemia, ROS have been, one more time, a dual property. We have observed that ROS production by METC was necessary to O2 sensing by inhibiting prolyl hydroxylases. This inhibition induced the hypoxic stabilization of the hypoxia inducible factor (HIF). But ROS production during ischemia has been involved in cellular mortality observed during reperfusion. Nitric oxide (NO)was able to decrease this mortality rate by decreasing oxidant stress and lipid peroxydation. A mitochondrial protection has been observed since recovery of mitochondrial membrane potential (m) during reperfusion was better after NO administration during ischemia
Plantivaux, Amandine. "Implication du stress oxydant en réponse à des perturbations environnementales". Nice, 2006. http://www.theses.fr/2006NICE4035.
Pełny tekst źródłaOxidative stress occurs when the physiological balance between pro-oxidants and antioxidants is disrupted and the oxidants favored, with possible cellular damages. This imbalance can be caused by environmental modifications. The marine invertebrate Anemonia viridis (sea anemone) is an appropriate model to study the oxidative stress. This animal harbors photosynthetic symbionts in its cells. By their photosynthetic activity, the symbionts create daily hyperoxia in the host tissues. In order to understand how the animal can deal with such an hyperoxia, their superoxide dismutases (SOD), key enzymes of detoxication, were characterized. The symbiotic association between the sea anemone and the zooxanthellae also faces environmental modifications. Many stresses (temperature, UV) can disrupt the symbiosis, leading to the bleaching of the animal host. The damages caused by a rise in temperature were studied, especially the protein carbonylation. Exposure to UV rays is another example of environmental alteration, which increases the production of oxidative molecules. Skin being the first protection of the organism against UV, it is submitted to oxidative stress. In collaboration with the cosmetic firm Vincience, assays to measure the antioxidant activity of a molecule were developed on cultured human skin cells
Mohammedi, Kamel. "Déterminants génétiques de la néphropathie diabétique : rôle du stress oxydant". Paris 7, 2012. http://www.theses.fr/2012PA077047.
Pełny tekst źródła: Oxidative stress is involved in the pathogeny of diabetic nephropathy. The antioxidant enzymes play a major role in the detoxification of reactive oxygen species and have a protective effect against diabetic nephropathy. We investigated associations of allelic variations in SOD1, SOD2, CAT and GPXI genes with diabetic nephropathy in patients with type 1 diabetes. Methods: Thirty SNPs in the SOD1, SOD2, CAT and GPXI regions were analyzed in 1285 Caucasian type 1 diabetic patients from the SURGENE prospective study (n=340; 10-year follow-up), GENESIS France-Belgium (n=501) and GENEDIAB (n=444) cross-sectional studies. Cox proportional hazards and logistic regression analyses were used to estimate hazard ratios or odds ratios for the incidence and the prevalence of diabetic nephropathy. Ail analyses were adjusted or stratified by retinopathy stages. Results: In the SURGENE cohort, we observed associations of variants of SOD1 (rs 1041740 and rs!7880135), SOD2 (rs4880, rs2758329 and rs8031), CAT (rs7947841) and GPXI (rs3448) with the prevalence and the incidence of diabetic nephropathy and with the estimated glomerular filtration rate. These variants were also associated with nephropathy in the participants of the GENESIS and GENEDIAB cohorts. Conclusion: SOD1, SOD2, CAT and GPXI genes were associated with the development and the progression of diabetic nephropathy in type 1 diabetic subjects. These results are consistent with a major role for the antioxidant enzymes in the renoprotection against oxidative stress in subjects with type 1 diabetes. Further studies are needed to identify the functional variants that modulate these genetic effects on diabetic nephropathy
Bulteau, Anne-Laure. "Le protéasome : implication dans le vieillissement et le stress oxydant". Paris 7, 2002. http://www.theses.fr/2002PA077036.
Pełny tekst źródłaZerrad-Saadi, Amal. "Stress oxydant et LDL : mécanismes de l'effet protecteur des HDL". Paris 5, 2008. http://www.theses.fr/2008PA05P640.
Pełny tekst źródłaThe capacité of HDL to protect LDL against oxidative stress is well established. However, mechanisms involved in such activity remain undetermined. Our firts aim was to assess the relationship between physicochemical properties of sub-fractions of LDL and their antiatherogenic in particular antioxidative (AOX) activities. We have demonstrated that HDL3 is depleted in spingomyelin and enriched in spingosine-1-phosphate as compared to HDL2. In addition, HDL3 displayed an elevated ratio of apolipoprotein AI (apoAI) to apoAII, and increased activities of HDL-associated enzymes with AOX properties. We have also studied mechanisms involved in the AOX activity of HDL Our data suggest a two-step mechanism involving transfer of phospholipids hydroperoxides (PLOOH) from oxidized LDL to HDL ; this step is influenced by the fluidity of the PL monolayer de HDL, and the reduction of PLOOH to redox-inactive PLOH largely through the action of two methionine residues of apoAI. This study emphasizes the importance of HDL in mitigating potential atherogenecity of LDL
Thomas, Audrey. "Effet sur le microenvironnement tumoral d’une modulation pharmacologique du stress oxydant". Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05T086/document.
Pełny tekst źródłaSeveral reports have demonstrated the involvement of reactive oxygen species (ROS) in carcinogenesis, through promotion of cancer cell proliferation and invasion. But ROS could also have consequences on non cancerous cells which are part of the tumor microenvironment, such as immune cells. Therefore, a pharmacological modulation of oxidative stress can induce a cytotoxic effect on tumor cells but its consequences on microenvironment are unknown. The aim of our studies was to evaluate the effects of a pharmacological modulation of oxidative stress on immune cells from the tumor microenvironment. At low dose, Arsenic trioxide (As203), an oxidative stress modulator, was shown to exert antitumor effects in colon tumor-bearing mice. We observed that this effect was related to As203-induced regulatory T cells (Tregs) -selective depletion in vitro and in vivo and was mediated by oxidative and nitrosative bursts. The differential effect of As203 on Tregs versus other CD4 cells was related to difference in the cells’redox status. We also observed that vinorelbine, an anticancer agent, could interfere with the antitumor immune response. We showed that vinorelbine could alter the function of immune cells surrounding tumor cells by a bystander toxic effect against tumor effector cells. In vivo experiment in A549 tumor bearing nude mice showed that adoptive transfer of A549 immune splenocytes was not able to delay tumor growth when vinorelbine-pretreated A549 cells were used for immunization. This effect was mediated by ROS and was inhibited by an oxidative stress modulator, mangafodipir, which restored antitumor immune function. Therefore, our work showed that oxidative stress modulators can influence tumor microenvironment and more specifically, immune cells. They could be used to restore antitumor immune response
Parmentier, Christine. "Métabolisme du glutathion et stress oxydant : implication de la gamma-glutamyltransférase". Nancy 1, 1998. http://www.theses.fr/1998NAN10359.
Pełny tekst źródłaDidier, Christine. "Thioredoxine et régulation redox : conséquences sur l'adaptation cellulaire au stress oxydant". Université Joseph Fourier (Grenoble), 2001. http://www.theses.fr/2001GRE10049.
Pełny tekst źródłaGueye, Fatou. "Drépanocytose et polymorphismes génétiques : épidémiologie, prédiction de gravité et stress-oxydant". Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1044/document.
Pełny tekst źródłaThe primary objective of this thesis was to determine the isolated and combined effects of alpha-thalassemia, inductors polymorphisms (QTLs) of HbF and genotype G6PD in a context of natural progression of sickle cell disease (Studies 1 and 2). Study 1 was undertaken to evaluate for the first time the allelic frequencies of these modifiers genes in 301 Senegalese SS children. Unlike other African populations, the G6PD Betica Variant was predominant over the A (-) variant. In addition, 12% of our cohort had G6PD deficiency combined with no alpha-thalassemia. These patients will be favoured for the realization of a transcranial doppler. The results obtained in Study 2 allowed us to conclude that alpha thalassemia and QTLs of HbF are interdependent and should not be studied separately for accurate clinical prediction. Indeed, a combination of alpha thalassemia with at least 2 QTLs of HbF is required to significantly delay the first complication of the disease. However, a homozygous alpha thalassemia, even associated with 3 to 6 QTLs of HbF, increases the frequency of CVOs during childhood. Therefore, a heterozygous alpha-thalassemia with at least two QTL HbFs would be the most favourable genotype for the occurrence of CVOs. The second objective of this thesis was to study the interrelationships between oxidative stress and the clinical severity of the disease (Studies 3 to 4). Sickle cell disease is characterized by high oxidative stress that may explain some of the clinical manifestations. Our results showed that homozygous alpha-thalassemia appears to reduce oxidative stress, which would contribute to its protective effect on certain complications of the hemolytic sub-phenotype. In addition, patients with the least hospitalization and CVO appear to have better antioxidant defense (catalase and GPx activities increased). In Study 4 we studied 4 SNPs of oxidative stress genes (rs4880 of the SOD2 gene, rs207454 of the XO gene, rs233322 of the MPO gene and rs35652124 of the NFE2L2 gene). The rs4880 SNP would have a favourable effect on the biological level (less reticulocytosis, increased GPx activity) but without associated clinical translation. The same is true for rs233322, which is associated with greater haemolysis and oxidative stress (AOPP). On the other hand, a tendency to a protective effect of rs207454 for some complications (hospitalizations, osteonecrosis, sepsis, STA) was observed. Our work contributes to the understanding of the impact of modifiers genes in sickle cell disease. It could therefore, through a positive selection of at-risk patients, improve the management of the disease in countries where the basic treatments (hydroxyurea, transcranial doppler, blood transfusion) cannot be offered to all
Alazzam, Bachar. "Stress oxydant chez Campylobacter jejuni : implication du système thiorédoxine - thiorédoxine réductase". Rennes 1, 2011. http://www.theses.fr/2011REN1S160.
Pełny tekst źródłaCampylobacter jejuni, a microaerophilic pathogen Gram-negative bacterium, is the causative agent of a large number of food-borne enteritis. This bacterium is able to survive in different environments and adapt to non-optimal growth conditions. Among these conditions, oxidative stress is a major stress for all living organisms that disturbs the cellular redox potential and inactivates numerous enzymes. Various systems can allow reversion but genome annotation of C. Jejuni suggests that it possesses the thioredoxin-thioredoxin reductase (TrxAB) system only. Therefore, importance of this system was analysed during C. Jejuni oxidative stress adaptation. Thus, we developed a synthetic medium having defined compound composition (MCLMAN medium) allowing the study of this bacterium oxidative stress response. Identification of proteins specifically reduced by TrxAB revealed its contribution to all main metabolic pathways; including reduction of unique enzymes considered as essential for other organisms. Furthermore, TrxAB encoding genes could not be inactivated in C. Jejuni thus TrxAB system appears of vital importance in this bacterium
Bancel, Brigitte. "Stress oxydatif et défenses anti-oxydantes dans la cancérogenèse gastrique et le cancer avéré". Lyon 1, 2005. http://www.theses.fr/2005LYO10297.
Pełny tekst źródłaLeclerc, Julia. "Etude d’un système respiratoire de Porphyromonas gingivalis, pathogène impliqué dans les infections parodontales". Thesis, Rennes 1, 2015. http://www.theses.fr/2015REN1B032/document.
Pełny tekst źródłaPeriodontal diseases are chronic inflammatory infections caused by bacteria in oral biofilm they are the first cause of loss of tooth in industrial countries with an important cost for the society. The biofilm comprises more than 500 bacterial species. Amongst them, Porphyromonas gingivalis, a Gram-negative bacterium, is well known as a major causative agent of periodontitis. Although considered as mainly anaerobe, P. gingivalis tolerates low oxygen concentration, therefore enhancing its ability to colonize the oral cavity. Our aim was to decipher the biological processes underpinning the resistance of P. gingivalis to oxygen and reactive oxygen species (ROS) and to characterise the transition from anaerobiosis to hypoxia. In silico studies of P. gingivalis genomes have revealed the presence of a putative oxygen-dependent respiratory system involving a cytochrome bd oxidase CydAB. We constructed a mutant deleted for cydAB genes in the P. gingivalis ATCC 33277 strain. Our study showed that cydAB mutation increased the sensibility of the mutant to reactive oxygen species such as the anion-superoxide generator paraquat and hydrogen peroxide. Moreover we demonstrated that CydAB is involved in the aerotolerance of P. gingivalis, and in oxygen consumption, as demonstrated by high resolution respirometry assay. Many regulations in response to ROS and oxygen are still unexplained in P. gingivalis, including the activation of cydAB expression by oxygen exposure. Two genes encoding FNR-like regulators were identified in the genome of P. gingivalis. One of them encodes the HcpR regulator which controls part of the nitrosative stress response. The second gene PGN_1569 was the focus of our study. By mutation and transcriptome analysis, we demonstrated that this FNR-like regulator repressed its own transcription and activated the expression of 4 gene clusters in anaerobiosis, but not including cydAB genes. The expression of these 4 gene clusters is also controlled by other redox regulators, OxyR and/or SigH and/or RprY. Therefore, this study pointed out the interplay between FNR and known oxidative stress response regulators of P. gingivalis. Further work will study the functions of the hypothetical proteins encoded by the FNR regulon. Interestingly, the fnr mutant displayed higher ability than the wild-type strain to form biofilm in anaerobiosis
Soares, Anísio Francisco. "Effets du stress oxydant sur le fonctionnement des adipocytes : adiponectine et prostaglandines". Lyon, INSA, 2005. http://theses.insa-lyon.fr/publication/2005ISAL0123/these.pdf.
Pełny tekst źródłaOxidative stress is suspected to play a major role in numerous pathophysiological states, such as : atherosclerosis, type 2 diabetes, neurodegenerative deseases. . . Prostaglandins are produced by cyclooxygenases (COX) from arachidonic acid. Prostaglandins are key players in adipose cell differentiation through 15dPGJ2, the most efficient endogenous ligand to PPARgamma, a nuclear receptor which is able to induce adipose cell differentiation. Our main goal was to measure the effects of oxidative stress on adipose cell differentiation and functions. We measured adiponectin production, the expression of mRNA coding adiponectin and 4 hydroxy-nonenal (4-HNE) a marker of lipid peroxidation, in 3T3-L1 adipocytes in response to oxidative stress induced by glucose oxidase. We show that oxidative stress induced by glucose oxidase, increased 4-HNE production and decreased adiponectin secretion, an adipokin mainly produced by adipocytes which improves insulin sensitivity. We also showed that 15dPGJ2 covalently binds PPARgamma. In conclusion, our results underline the importance of oxidative stress in the development of type 2 diabetes through the decreased production of adiponectin. The demonstration of a covalent binding between 15dPGJ2 and PPARgamma points out the important physiological role of that prostaglandin
Soares, Anísio Francisco Géloën Alain. "Effets du stress oxydant sur le fonctionnement des adipocytes adiponectine et prostaglandines /". Villeurbanne : Doc'INSA, 2006. http://docinsa.insa-lyon.fr/these/pont.php?id=soares.
Pełny tekst źródłaContient 2 articles en anglais co-rédigés par l'auteur. Titre provenant de l'écran-titre. Bibliogr. p. 114-129. Index.
Van, der Werf Remmelt. "Evaluation du pouvoir anti-oxydant des aliments : recherche de leurs effets modulateurs sur le stress oxydant dans le cas du diabète". Phd thesis, Université de Strasbourg, 2013. http://tel.archives-ouvertes.fr/tel-01037983.
Pełny tekst źródłaRezaïki, Lahcen. "Métabolisme respiratoire chez Lactococcus lactis dans un environnement oxydant et identification de composants de la chaîne respiratoire". Paris 11, 2004. http://www.theses.fr/2004PA112133.
Pełny tekst źródłaLactococcus lactis is mainly used in the food industry, and has been mainly studied for its capacities to ferment sugar sources. Recently our laboratory discovered that l. Lactis are capable of a respiration metabolism when exogenous heme and oxygen are present in the medium. Respiration growth results in improved biomass, higher ph and a striking increased long term survival compared to fermentation metabolism. My thesis project was focused on the respiratory metabolism of l. Lactis, and principally addressed two objectives : the identification of respiratory chain components, and clarification of the factors that associate improved survival with respiration growth. We showed by mutagenesis that menaquinones function to assure electron transfer to cytochrome oxidase. We also demonstrate a role of menaquinones in generating superoxyde species, and in extracellular iron reduction. Our results suggest that nadh dehydrogenase noxa and noxb may be acting as electron donors for the respiration chain. The role of cytochrome bd oxidase, already known for its function as the only terminal oxidase in l. Lactis, was confirmed by our mutants cyda and cydb obtained by a random mutagenesis approach. Our results indicate that greater l. Lactis survival after respiration metabolism (compared to aeration growth in the absence of hème) is associated with, and likely due to a decrease in cytoplasmic oxidative stress and an increase of ph. The environment created by respiratory chain activity also improve the long term survival of fermenting bacteria present in the same medium
Mougeolle, Alexis. "Effet du stress oxydant sur les cavéoles dans les cellules musculaires squelettiques". Thesis, Bordeaux, 2014. http://www.theses.fr/2014BORD0298/document.
Pełny tekst źródłaSarcopenia is an age-related degenerative disease which is characterized by a progressive and involuntary loss of muscle mass and strength. It is accompanied by an impairment of muscle regeneration and accumulation of reactive oxygen species. Caveolae are invaginations of the plasma membrane. In muscle, they play a role in the differentiation of satellite cells and in maintaining the contractile unit of the differentiated skeletal muscle. Some myopathies are resulting from the absence of caveolae in muscle. Caveolae are also involved in mediating signals related to the regulation of oxidative stress. To better understand the mechanisms involved in the development of sarcopenia, we investigated here the relationship between oxidative stress and caveolae. Mouse muscle cells were treated with H2O2 and decreased levels of caveolin-1 and -3 were demonstrated in myoblasts and myotubes, respectively. It therefore appears that caveolae constituent proteins are actually sensitive to oxidative stress in muscle cells. In the presence of H2O2, caveolae functions (endocytosis and resistance to mechanical stress) were also significantly degraded in myoblasts. Altogether, these data suggest that oxidative stress would affect caveolae, which could have consequences on regeneration and maintenance of muscle integrity during aging
Lefevre, Sophie. "Modèle levure de l'ataxie de Friedreich : stress oxydant, apoptose et dynamique mitochondriale". Paris 6, 2010. http://www.theses.fr/2010PA066204.
Pełny tekst źródłaBroin, Mélanie. "Implication de CDSP32, une thiorédoxine chloroplastique, dans la réponse au stress oxydant". Montpellier, ENSA, 2001. http://www.theses.fr/2001ENSA0022.
Pełny tekst źródłaRichier, Sophie. "Adaptation au stress oxydant de l'association cnidaires-dinoflagellés : rôle de la symbiose". Nice, 2004. http://www.theses.fr/2004NICE4107.
Pełny tekst źródłaIn a symbiotic association, organisms must adapt, at physiological and molecular level, to essential conditions for their mutual partner. In the symbiosis between the temperate sea anemone Anemonia viridis and a photosynthetic Dinoflagellate Symbiodinium sp. , animal tissues are daily submitted to endogenous hyperoxia/anoxia transitions, with O2 concentration reaching three times the normoxia. In order to understand mechanisms implied in protection against oxygen toxicity, one of the enzymes involved in antioxidant defence, the superoxide dismutase (SOD) has been studied. Biochemical and molecular analyses showed a large diversity of SOD isoformes, associated to unusual characteristics and the involvement of such isoformes in the resistance to either endogenous or exogenous (100 % O2) hyperoxia but also to prooxidant period such as thermal increase. Even resistant, this association can be disrupted. One of the mechanisms suggested would be an apoptotic process of the animal cell or symbiont under environmental stress. Several stresses were tested to demonstrate the implication of prooxidant period in the apoptotic phenomenon. Data suggest the induction of programmed cell death and caspase-like proteasic activity during oxidative stress. The later would be a key parameter in the disruption parameter of the symbiotic Cnidarians, commonly called “bleaching”
Payet, Olivier. "Modulation des transporteurs rétiniens du glutamate par l'ischémie et le stress oxydant". Montpellier 2, 2003. http://www.theses.fr/2003MON20129.
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