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28512. Oxid dusnatý v hypotalamo-hypofyzární regulaci - II. Stres, zánět a apoptóza
- Creator:
- Maruna, Pavel
- Type:
- model:article, article, Text, and TEXT
- Subject:
- oxid dusnatý--imunologie--metabolismus, apoptóza--genetika--účinky léků, stres fyziologický--imunologie--metabolismus--patofyziologie, systém hypotalamus-hypofýza--imunologie--metabolismus--patofyziologie, zánět--imunologie--metabolismus, hypofýza--imunologie--metabolismus--patofyziologie, and lidé
- Language:
- Czech and English
- Description:
- Cíl studie: Charakterizovat úlohu oxidu dusnatého za fyziologických a patologických podmínek hypotalamo-hypofyzární osy, zejména při stresové odpovědi, zánětu a apoptóze. Typ studie: Souhrnný článek. Pracoviště: Ústav patologické fyziologie 1. LF Univerzity Karlovy v Praze. Závěr: Vedle role, kterou oxid dusnatý zaujímá ve fyziologické regulaci hypotalamických a hypofyzárních hormonů v klidovém období, přibývá rovněž poznatků o jeho úloze jako modulátoru stresové hypothalamo-pituitární osy. NO ovlivňuje syntézu, centrální i periferní účinky kortikoliberinu a ACTH. Zmínit je třeba i předpokládaný význam NO v procesu zánětu a apoptózy v hypofýze. Novější poznatky, získané výzkumem na geneticky modifikovaných zvířatech s vyřazenou tvorbou NO, poskytují nový pohled na skutečnou roli NO v hypotalamo-pituitární regulaci., Objective: To characterize an influence of nitric oxide in both physiological and pathological states involving hypothalamus and pituitary gland – stress response, inflammation and apoptosis. Design: Review. Setting: Department of Pathological Physiology, 1st Faculty of Medicine, Charles University in Prague. Conclusion: Except its physiological role in a hypothalamic-pituitary regulation in a rest phase, NO acts as a new neuromediator of a hypothalamic-pituitary stress axis. NO modulates corticoliberine and ACTH synthesis and effects. We discuss a potential role of NO in both inflammatory and apoptotic changes in pituitary gland, too. The recent research on genetically modified animals with knockout NO synthesis gives a new insight into a role of NO in hypothalamic-pituitary regulation., Pavel Maruna, and Lit. 23
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
28513. Oxidační stres u Alzheimerovy choroby a jeho důsledky
- Creator:
- Chmátalová, Zuzana and Skoumalová, Alice
- Format:
- braille, text, and regular print
- Type:
- model:article, article, Text, práce podpořená grantem, and TEXT
- Subject:
- Alzheimerova nemoc--patofyziologie, oxidační stres, reaktivní formy kyslíku, imunitní systém - jevy--fyziologie, poškození DNA, RNA štěpení, proteiny--chemie, lipidy--chemie, sacharidy--chemie, přechodné prvky--chemie, neurodegenerativní nemoci--patofyziologie, biochemické jevy, patologie, and lidé
- Language:
- Czech and English
- Description:
- Oxidační stres je do určité míry fyziologickým důsledkem řady biochemických a bioenergetických pochodů a doprovází aerobní organizmy po celý jejich život. Podílí se na přirozeném stárnutí organizmu a významnou úlohu zastává v imunologické odpovědi. Každý organizmus má vyvinutý komplexní antioxidační systém, který ho chrání před radikálovým poškozením. Selhání tohoto vysoce specializovaného systému může vést k nevratnému poškození biomolekul a závažně tím poškodit jejich fyziologické funkce. Radikálové poškození a ztráta funkcí mozkových buněk je charakteristická pro neurodegenerativní onemocnění jako Alzheimerova choroba (ACH). To je důvod, proč se zvýšený oxidační stres považuje za iniciální impulz vzniku tohoto závažného progredientního onemocnění. Článek podává přehled patobiochemických mechanizmů oxidačního stresu v mozkové tkáni doprovázejících rozvoj Alzheimerovy choroby., Oxidative stress is to some extent a physiological consequence of biochemical and bioenergetic processes and accompanies aerobic organisms throughout their lives. Oxidative stress contributes to the natural aging and plays an important role in the immune response. Each organism has developed a complex system of antioxidant defense which protects it against the free radical damage. The failure of this highly specialized system can lead to irreversible damage to biomolecules and thereby seriously damage their physiological functions. Radical damage and loss of functions of brain cells is characteristic of neurodegenerative diseases such as Alzheimer’s disease. This is the reason why the increased oxidative stress is thought to be the initial impetus for developing this progressive disease. This article brings an overview of pathobiochemical mechanisms of oxidative stress in the brain tissue that accompany progression of Alzheimer´s disease., Chmátalová Z., Skoumalová A., and Literatura
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
28514. Oxidační stres u nádorových onemocnění
- Creator:
- Holeček, Václav
- Type:
- model:article, article, Text, and TEXT
- Subject:
- oxidační stres, nádory--etiologie--metabolismus--terapie, volné radikály--analýza--farmakologie--škodlivé účinky, antioxidancia--aplikace a dávkování--farmakologie--terapeutické užití, látky modulující angiogenezi--farmakologie, volné radikály, antioxidanty, nádory, and angiogeneze
- Language:
- Czech and English
- Description:
- Holeček V. and Lit.: 32
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
28515. Oxidační stres v průběhu akutní pankreatitidy
- Creator:
- Vávrová, Lucie, Kodydková, Jana, Macášek, Jaroslav, Ulrych, Jan, and Žák, Aleš
- Format:
- braille, text, and regular print
- Type:
- model:article, article, Text, and TEXT
- Subject:
- pankreatitida, akutní nemoc, oxidační stres, antioxidancia, studie případů a kontrol, výběr pacientů, lidé, and financování organizované
- Language:
- Czech and English
- Description:
- Cíl studie: stanovení parametrů oxidačního stresu a statutu antioxidačního systému v průběhu akutní pankreatitidy Typ studie: observační, strukturálně vyvážená studie případů a kontrol Materiál a metody: Do studie bylo zařazeno 13 pacientů s akutní pankreatitidou (AP) a dále na základě věku a pohlaví spárované dvě kontrolní skupiny, a to skupina zdravých osob (KON) a osob, které prodělaly v minulých 2-3 letech akutní pankreatitidu (PAP). Pacientům s AP byly odebírány vzorky celkem 4, nejprve během prvních 24 hodin od objevení příznaků, poté po 72 hodinách, třetí odběr byl prováděn 5. den a poslední odběr 10. den onemocnění. U všech pacientů byly stanovovány kromě základních klinických a biochemických parametrů aktivity antioxidačních enzymů, koncentrace některých antioxidantů (redukovaný glutation (GSH), vitamin A a E) a parametry oxidačního stresu (konjugované dieny v precipitovaných LDL (CD/LDL) a oxidované LDL(ox-LDL)). Ke statistickému zpracování výsledků byl použit program STATISTICA (Stat Soft, CZ). Výsledky: Výsledky naší studie potvrzují zvýšený oxidační stres u pacientů s AP, a to zvýšenými hladinami CD/LDL u všech odběrů AP ve srovnání s CON (p < 0,05) a vzrůstajícími hladinami ox-LDL v průběhu AP s maximem 5. den AP. Pozorovali jsme rovněž změny v antioxidačním systému u AP pacientů; u těchto pacientů jsme zjistili snížené aktivity glutationperoxidázy a arylesterázové i laktonázové paraoxonázy během všech odběrů a dále pak snížené hladiny sérových antioxidantů – albuminu, vitaminu A a vitaminu E při porovnání s kontrolní skupinou. Závěr: Ve studii byl pozorován zvýšený oxidační stres a porušený antioxidační systém v časné fázi AP s gradací mezi třetím a pátým dnem AP., Objective: to assess oxidative stress and antioxidant status in acute pancreatitis and their natural course over the 10-day period. Design: observation, matched case-control study Material and methods: Into our study 13 patients with acute pancreatitis (AP) were included together with 13 sex- and agehealthy controls (CON) and 13 sex- and age- matched controls enrolled from persons that suffered from AP 2 – 3 years ago (PAP). We observed the antioxidant status of AP patients during the disease and the samplings were taken four times – on the first 24 hours of disease (AP1), after 72 hours from disease onset (AP3), on the 5th (AP5) and on the 10th day (AP10). In all studied groups markers of oxidative stress (level of conjugated dienes in precipitated LDL, oxidized LDL) and levels of antioxidants were assessed. We measured activities of superoxide dismutase (CuZnSOD), catalase (CAT), glutathione peroxidase 1 (GPX1) and glutathione reductase (GR) in erythrocytes and arylesterase (PON1-A) and lactonase (PON1-L) activities of paraoxonase in serum and concentrations of reduced glutathione (GSH) in erythrocytes and concentrations of vitamins E and A in serum. Results: In our study we confirmed increased oxidative stress in AP, with higher levels of CD/LDL in all AP samplings compared to CON (p < 0.05) and with increasing levels of ox-LDL during the AP with the maximum on the 5th day. We have shown altered status of antioxidant system; the activities of both PON1 activities as well as activity of GPX1 were depressed in all AP samplings in comparison to CON. We have also observed decreased levels of serum antioxidants – albumin, vitamin A and vitamin E in AP Conclusion: High oxidative stress and impaired antioxidant status was observed during early phase of AP with the gradation between 3rd and 5th day of AP., Vávrová L., Kodydková J., Macášek J., Ulrych J., Žák A., and Literatura 24
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
28516. Oxidation resistance of LDL in hypertriglyceridaemic patients treated with ciprofibrate
- Creator:
- Nagyová, A., Rašlová, K., and Ginter, E.
- Type:
- article, model:article, and TEXT
- Subject:
- atherosclerosis, ciprofibrate, LDL, and oxidative modification
- Language:
- English
- Description:
- The oxidative modification of low density lipoprotein (LDL) plays an important role in the pathogenesis of atherosclerosis. LDL of subjects with atherogenic lipoprotein phenotype (ALP) is known to be more susceptible to oxidation. We studied the effect of the hypolipidaemic drug ciprofibrate on the susceptibility of LDL to in vitro oxidation. Nine patients with primary hypertriglyceridaemia and hypoalphalipoproteinaemia (mean plasma triglycerides 3.76 mmol.L1 and HDL-cholesterol 0.74 mmol.l-1) were treated with ciprofibrate for 12 weeks. The susceptibility of LDL to in vitro Cu2 +-mediated oxidation was assessed by measuring conjugated diene formation at 234 nm. Ciprofibrate therapy significantly prolonged the lag time (93±7 min vs. 102±11 min, P = 0.02). The maximal rate of diene production was 11 % lower, but the decrease was not significant. A significant positive correlation was observed between maximal rate and maximal amount of dienes formed. Thiobarbituric acid reacting substances (TBARS) and lipid hydroperoxides (LPO) in oxidatively-modified LDL, isolated from the plasma of patients before and after drug treatment, were unchanged. The results suggest that ciprofibrate therapy has a favourable effect by increasing the in vitro resistance of LDL against oxidation.
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
28517. Oxidative activity of human polymorphonuclear leukocytes stimulated by the long-chain phosphatidic acids
- Creator:
- Petković, M., Vocks, A., Schiller, J., and Arnhold, J.
- Type:
- article, model:article, and TEXT
- Subject:
- Elastase release, Human PMNs, Luminol-amplified chemiluminescence, Phosphatidic acid, and Signal transduction
- Language:
- English
- Description:
- It has already been suggested that phosphatidic acids (PAs) play an important role in the regulation of signaling pathways involved in the production of reactive oxygen species (ROS) by human polymorphonuclear leukocytes (PMNs). The present study was performed to elucidate the effects of extracellularly added PAs – 1,2-distearoyl- (DSPA) and 1-stearoyl-2-arachidonoyl-sn-glycero-phosphate (SAPA) – on the ROS production and on the elastase release by human PMNs. ROS production was monitored by luminol-amplified chemiluminescence and the elastase activity was measured in the supernatant of the PA-stimulated human PMNs by colorimetric assay. Obtained effects were compared with those of cells stimulated by either a chemotactic tripeptide, phorbol ester or calcium ionophore. Our results show that long-chain PAs at concentrations higher than 3 × 10-5 mol/l stimulate the ROS production by human PMNs, whereas they were ineffective in promoting the elastase release. The chemiluminescence pattern of the SAPA-stimulated cells exhibited a biphasic curve, whereas cell stimulation with DSPA resulted in a monophasic chemiluminescence curve. Stimulation of the ROS production by PAs in dependence of the fatty acid composition required the activity of protein kinases.
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
28518. Oxidative and immune response in experimental exposure to electromagnetic fields :
- Creator:
- Surcel, D.
- Type:
- model:article and TEXT
- Language:
- English
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
28519. Oxidative stress and down syndrome. Do antioxidants play a role in therapy?
- Creator:
- Jana Muchová, Žitňanová, I., and Zdeňka Ďuračková
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, Downův syndrom, oxidační stres, antioxidanty, polyfenoly, Down syndrome, oxidative stress, antioxidants, polyphenols, cognitive functions, physical activities, 14, and 612
- Language:
- English
- Description:
- Oxidative stress is a phenomenon associated with imbalance between production of free radicals and reactive metabolites (e.g. superoxide and hydrogen peroxide) and the antioxidant defences. Oxidative stress in individuals with Down syndrome (DS) has been associated with trisomy of the 21st chromosome resulting in DS phenotype as well as with various morphological abnormalities, immune disorders, intellectual disability, premature aging and other biochemical abnormalities. Trisomy 21 in patients with DS results in increased activity of an important antioxidant enzyme Cu/Zn superoxide dismutase (SOD) which gene is located on the 21st chromosome along with other proteins such as transcription factor Ets-2, stress inducing factors (DSCR1) and precursor of beta-amyloid protein responsible for the formation of amyloid plaques in Alzheimer disease. Mentioned proteins are involved in the management of mitochondrial function, thereby promoting mitochondrial theory of aging also in people with DS. In defence against toxic effects of free radicals and their metabolites organism has built antioxidant defence systems. Their lack and reduced function increases oxidative stress resulting in disruption of the structure of important biomolecules, such as proteins, lipids and nucleic acids. This leads to their dysfunctions affecting pathophysiology of organs and the whole organism. This paper examines the impact of antioxidant interventions as well as positive effect of physical exercise on cognitive and learning disabilities of individuals with DS. Potential terapeutic targets on the molecular level (oxidative stress markers, gene for DYRK1A, neutrophic factor BDNF) after intervention of natural polyphenols are also discussed., J. Muchová, I Žitňanová, Z. Ďuračková., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
28520. Oxidative stress and neuronal NOS activity: Putative determinants of rapid blood pressure increase after renal denervation in anesthetized rats
- Creator:
- Walkowska, A., Sadowski, J., and Kompanowska-Jezierska, E.
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, nitric oxide, renal denervation, free radicals, 14, and 612
- Language:
- English
- Description:
- Long-term effects of renal denervation (DNX) commonly include a decrease in blood pressure (BP), observed in both normotensive animals and various models of hypertension. On the other hand, short term BP re sponses vary. We examined how post-DNX increase in BP observed in this study depends on baseline metabolic and functional status of an imals, with a special interest for the role of oxidative stress. Anesthetized Wistar rats on standard (STD), low-sodium (LS) or high-sodium (HS) diet were used, untreated or pre-treated with tempol, a superoxide scavenger, or N(omeg a)-propyl-L-arginine (L-NPA), an inhibitor of neuronal NOS (nNOS). Early BP and renal hemodynamic responses were examined to right- and then left- side DNX performed using an own relatively non-invasive technique. Left kidney cortical, outer- and inner-medullary blood flows (CBF, OMBF, IMBF) were co ntinuously recorded as laser- Doppler fluxes. Sequential denervat ions significantly increased BP to final 19 %, 12 %, and 6 % above control level in HS, LS, and STD groups, respectively. CBF, a measure of total renal perfusion, increased in LS and STD but not in HS rats. Tempol pretreatment prevented the post-denervation BP increase on each diet. Selective inhibition of nNOS prevented BP increase in STD and HS groups, a modest incr ease persisted in LS rats. We propose that enhanced afferent impulsation from intrarenal chemoreceptors related to oxidative stress in the kidney was the background for acute BP increase after DNX. The response was triggered by a release of brain sympatho-excitatory centers from inhibition by renal afferents, this was followed by widespread sympathetic cardiovascular stimulation., A. Walkowska, J. Sadowski, E. Kompanowska-Jezierska., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public