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EN
Introduction: Oxidative stress is largely responsible for numerous skin complications that occur in the course of various diseases as well as accelerated skin aging. A high amino acid diet, supplemented with whey protein concentrate (WPC), is well-balanced and has well-absorbing proteins, which are an ideal source of essential amino acids. Purpose: To assess what changes will occur in the antioxidant barrier of unharmed skin of rats on a high amino acid diet. Materials and methods: The study was conducted on sexually mature male Wistar rats (160-180g): 1. control (standard feed), 2. high amino acid diet (WPC-80 80% whey protein) administered for 7 days at a dose of 0.3g/kg of body weight, 3. WPC-80 for 7 days at a dose of 0.5g/kg of body weight, 4. WPC-80 for 14 days at a dose of 0.3g/kg of body weight, 5. WPC-80 for 14 days at a dose of 0.5g/kg of body weight. Total antioxidant capacity, total oxidative status and oxidative stress index were determined. Results: Enrichment of a standard diet with WPC-80 did not affect the total oxidative status of undamaged healthy rat skin. This study shows that a diet rich in amino acids in rats caused an increase in total antioxidant capacity, but statistically significant values were obtained after 14 days of administering WPC at a dose of 0.5mg/kg of body weight. Conclusions: Enrichment of a standard diet with WPC-80 strengthens the antioxidant barrier in unwounded healthy rat skin.
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The current study was undertaken to elucidate a possible neuroprotective role of dehydroepiandrosterone (DHEA) against the development of Alzheimer's disease in experimental rat model. Alzheimer's disease was produced in young female ovariectomized rats by intraperitoneal administration of AlCl3 (4.2 mg/kg body weight) daily for 12 weeks. Half of these animals also received orally DHEA (250 mg/kg body weight, three times weekly) for 18 weeks. Control groups of animals received either DHAE alone, or no DHEA, or were not ovariectomized. After such treatment the animals were analyzed for oxidative stress biomarkers such as hydrogen peroxide, nitric oxide and malondialdehyde, total antioxidant capacity, reduced glutathione, glutathione peroxidase, glutathione reductase, superoxide dismutase and catalase activities, antiapoptotic marker Bcl-2 and brain derived neurotrophic factor. Also brain cholinergic markers (acetylcholinesterase and acetylcholine) were determined. The results revealed significant increase in oxidative stress parameters associated with significant decrease in the antioxidant enzyme activities in Al-intoxicated ovariectomized rats. Significant depletion in brain Bcl-2 and brain-derived neurotrophic factor levels were also detected. Moreover, significant elevations in brain acetylcholinesterase activity accompanied with significant reduction in acetylcholine level were recorded. Significant amelioration in all investigated parameters was detected as a result of treatment of Al-intoxicated ovariectomized rats with DHEA. These results were confirmed by histological examination of brain sections. These results clearly indicate a neuroprotective effect of DHEA against Alzheimer's disease.
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Carboxylated osteocalcin (Gla-OC) contributes to the bone formation, whereas its undercarboxylated form (Glu-OC) takes part in the energy metabolism. In vitro studies had shown that treatment of osteoblast-like cells with advanced glycation end product-modified bovine serum resulted in reduced synthesis of collagen 1 and osteocalcin. The aim of this study was to find association between Gla-OC and markers of protein glycation, oxidation and nitration, as well as pro-inflammatory and antioxidant defense markers in obese subjects. Non-obese [(body mass index (BMI)<30 kg/m; n=34)] and obese subjects (30
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Purpose. The study presents a comparative analysis of the threshold power and exercise-induced changes in the blood antioxidative stress parameters in a standard rowing test between two measurements (terms of the study). Basic procedures. The study comprised 15 subjects aged between 20 and 23 years, members of the Polish National Youth Rowing Team at the end of preparatory phase of the annual training cycle in 2003 (Term I) and in 2004 (Term II). At both terms selected indices of antioxidative stress and the threshold power (AT4) induced by physical exercise with graded intensity were analyzed. Main findings. At the second term of the study, as compared with the first term, a higher activity of superoxide dismutase in blood samples at rest was found. At the same time a decreased activity of glutathione peroxidase in blood samples after exercise was observed. The level of lipid peroxidation products in red cells (TBARS) regarded as the marker of free radical-induced damage was also significantly lower. The results indicated that at the second term of the study the rate of anaerobic metabolism measured with the blood lactate level was lower than at the first term despite the fact that the threshold power values between both terms of the study did not reveal any significant differences. Conclusions. The annual training cycle in young rowers, although not contributing significantly to the increase of the threshold power, induced positive changes in their antioxidant defense systems; namely, the lower level of TBARS after exercise and the higher SOD activity at rest.
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Despite numerous theories, the etiology and pathogenesis of primary varicose veins remain unclear. The etiology of chronic venous diseases (CVDs) known as chronic venous insufficiency (CVI) is related to leukocyte trapping. Leukocyte trapping involves trapping of white cells in vessel walls followed by their activation and translocation outside the vessel. Release of reactive oxygen species (ROS) from trapped white cells has been documented. Superoxide dismutase (SOD) directly inhibits the generation of free radicals and compounds that are produced during oxidation by ROS, such as malonyldialdehyde (MDA). The aim of this study was to determine the involvement of free radicals in the etiology of venous changes. The following material was used for the study: fragments of sufficient or insufficient venous system and varices from 31 patients diagnosed with chronic venous disease in the 2nd or 3rd degree, according to clinical state, etiology, anatomy and pathophysiology (CEAP), which were qualified for surgical procedure. The levels of oxidative stress markers strongly correlated with lesions observed by USG in insufficient and varicose veins. In both a higher concentration of MDA was observed, which is a sign of lipid peroxidation. Antioxidative mechanisms, SOD activity and total antioxidative power expressed as FRAP were inversely proportional to MDA concentration. In insufficient and varicose veins both FRAP and SOD activities were significantly lower than in normal veins. The severity of clinical changes was inversely dependent on the efficiency of scavenging of ROS, which additionally proves the participation of free radicals in pathogenesis of CVDs.
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Paraoxonase 1 (PON1), contained in plasma high-density lipoproteins, plays an important role in the protection of plasma lipoproteins and cell membranes from oxidative damage. Previous studies indicate that human PON1 is stimulated by high NaCl concentrations. The aim of this study was to characterize in more detail the effect of salts on serum PON1. Paraoxon-hydrolyzing activity of human serum was stimulated by 81.6% following the addition of 1 M NaCl. The effect of NaCl was dose-dependent between 0.5 and 2 M. PON1 activity toward phenyl acetate was reduced by 1 M NaCl by 55.2%. Both the paraoxon- and phenyl acetate-hydrolysing activity was slightly lower in heparinized plasma than in serum, but NaCl had similar stimulatory and inhibitory effects on these activities, respectively. In rat, rabbit, and mouse, NaCl reduced PON1 activity. KCl had a similar effect on human PON1 as NaCl. Sodium nitrite also stimulated human PON1 but much less effectively than chloride salts. In contrast, sucrose, sodium acetate and sodium lactate had no significant effect. NaBr was a less effective PON1 activator than NaCl, whereas the effect of NaJ was non-significant. The activity of human PON1 toward homogentisic acid lactone and γ-decanolactone was unaltered by NaCl. These data indicate that: 1) high concentrations of chlorides stimulate human PON1 activity toward paraoxon but not other substrates, 2) PON1 is inhibited by Cl- in other mammalian species, 3) the potency of human PON1 activation by halogene salts increases with decreasing atomic mass of the halide anion.
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This study investigated the effects of supplementation with Krill oil on levels of pro-oxidant/antioxidant balance markers and levels of pro-inflammatory cytokines in professional rowers submitted to exhaustive exercise.This double-blind study included 17 members of the Polish National Rowing Team. Subjects were randomly assigned a supplemented group (n=9) which received two capsules (500 mg) of Krill oil daily for 6 weeks, or a placebo group (n=8). At the beginning and at the end of preparatory camp, subjects performed a 2000 m maximum effort test on a rowing ergometer. Blood samples were taken from the antecubital vein prior to each exercise test, 1 minute after completing the test, and after 24-hours of rest. The following redox parameters were assessed in erythrocytes: superoxide dismutase (SOD), glutathione peroxidase (GPx), and thiobarbituric acid reactive substances (TBARS) concentration. Additionally, creatine kinase (CK) activity was measured in plasma samples, while tumor necrosis factor (TNF-α) concentrations were measured in the serum.Exercise significantly increased values of SOD, TNF-α and TBARS in both groups, but recovery levels of TBARS were significantly lower in athletes receiving Krill oil compared with the control group.Based on these results we conclude that supplementation with Krill oil (1 g per day) in trained rowers diminished post exercise oxidative damage to erythrocytes during recovery, but had no effect on antioxidant enzymes, TNF-α and serum lipid profiles.
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Wolne rodniki (WR) to atomy lub cząsteczki, posiadające wolne niesparowane elektrony. Ich nadmiar prowadzi do rozwoju stresu oksydacyjnego - przyczyny wielu chorób nowotworowych, neurodegeneracyjnych, zapalnych oraz starzenia się organizmu. Głównymi egzogennymi źródłami wolnych rodników są m.in.: zanieczyszczenia przemysłowe, dym tytoniowy, promieniowanie jonizujące oraz pola magnetyczne. Cel. Celem pracy jest ocena działania pola magnetycznego niskiej częstotliwości na proces peroksydacji lipidów w tkance mięśniowej zwierząt doświadczalnych. Materiał i metody. Materiał badawczy stanowiły dorosłe szczury, samce rasy Sprague-Dawley w wieku 3-4 miesięcy. Zwierzęta podzielono na 3 grupy badawcze: I - grupa kontrolna; II grupa poddana działaniu pola magnetycznego o następujących parametrach: 7 mT, 40 Hz, 30 min/dzień, 2 tyg.; III grupa - poddana działaniu pola magnetycznego o parametrach: 7 mT, 40 Hz, 60 min/dzień, 2 tyg. U badanych zwierząt wykonano pomiar stężenia produktów peroksydacji lipidów (TBARS[h1]) w homogenatach tkanki mięśniowej po zakończeniu ekspozycji na działanie pola magnetycznego. Wyniki. Po działaniu zmiennego pola magnetycznego o częstotliwości 40 Hz, indukcji 7 mT, w czasie 30, 60 min/dzień przez 2 tygodnie zaobserwowano wzrost stężenia TBARS w tkance mięśniowej szczura. Wnioski. Pole magnetyczne niskiej częstotliwości (Low Frequency Magnetic Field - LFMF) o parametrach stosowanych w magnetoterapii wywołuje istotne zmiany w procesie generacji reaktywnych form tlenu.
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Free radicals (FR) are atoms or molecules with unpaired electrons. They may lead to the development of the oxidative stress, which is a cause of many neoplastic, neurodegenerative, inflammatory diseases and aging of the organism. The main exogenous sources of free radicals are among others: industrial pollution, tobacco smoke, ionizing radiation, and magnetic field. Goal: The aim of this study was to evaluate the influence of the low magnetic field on the parameters of the oxidative stress (TBARS[h2]) in rat's muscles. Materials and methods. Thirty male rats, weight of 280-300 g were randomly divided into three experimental groups: control I and treatment II i III (Low Frequency Magnetic Field LFMF). Animals in the group II were exposed to the LFMF of the following parameters: frequency 40 Hz, induction 7 mT for 0.5 h/day for 14 days (this kind of the ELFMF is mostly used in magnetotherapy), while the group III was subjected to the field: 40 Hz, 7 mT for 1h/day for 14 days. Control rats were kept in the separate room and were not exposed to the to ELFMF. Immediately, after the last exposure, the part of muscles was taken under pentobarbital anaesthesia. The effects of the exposure to the LFMF on the oxidative states were assessed by the measurements of concentration of TBARS in muscles homogenates. Results. Exposure to the LFMF with the following parameters: 40 Hz, 7 mT, 30 and 60min/day for 2 weeks caused significant increase in TBARS concentration in the muscles homogenates. Conclusion. Low magnetic field used in magnetotherapy causes the significant changes of the process of generation of the reactive forms of oxygen in the muscles.
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Molecular oxygen (O2), constituting the basis of life on Earth, is classified as a substance with oxidizing properties. Reacting with organic compounds, it leads to their oxidation and at the same time participates in reduction processes. In aerobic organisms, over 90% of oxygen undergoes a total four-electron reduction to produce water molecules (O2 + 4 H+ + 4e- → 2 H2O). The remaining 10% of oxygen, however, is not fully reduced, which results in the production of molecules referred to as reactive oxygen species (ROS). In high concentrations ROS can interact with cellular components (DNA, proteins and lipids), leading to the oxidation of these macromolecules. The resulting oxidation products interfere with the proper functioning of the body by influencing gene expression, intercellular signaling and apoptosis. These changes have been observed in numerous pathological conditions, such as neurodegenerative, cardiovascular, metabolic, autoimmune diseases, and cancer. However, in the context of evolution, living organisms developed specialized repair mechanisms to prevent cellular accumulation of the products of DNA, protein and lipid oxidation, including enzymatic mechanisms (e.g. nucleases, proteases, phospholipases) or removal of damaged DNA, proteins and lipids by apoptosis or autophagy. This article briefly discusses the mechanisms of oxidative modification of cell components and the main repair systems responsible for the removal of lesions in cells by oxidative damage.
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Content available remote Association between intestinal and antioxidant barriers in children with cancer
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Objective: Reactive oxygen species (ROS) play a role in cancerogenesis processing and damage tissues. Furthermore, oncological treatment may impair proper function of the gut barrier. The aim of this study was to measure intestinal permeability in children in clinical remission for solid tumours and to search for a possible relationship between free radicals and the intestinal barrier. No such investigation in children has been reported so far. Research Methods and Procedures: The prospective study consisted of 19 paediatric patients with cancer after completion of chemotherapy. 32 healthy children from the outpatients clinics were recruited for measurement of intestinal permeability and antioxidant barrier as a control group. Intestinal permeability was assessed by measurement of urinary lactulose and mannitol after oral challenge. Antioxidant enzymes: superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in erythrocytes were assessed. Ischemia modified albumin (IMA) concentration was measured in serum. Results: Cancer patients excreted less mannitol and more lactulose versus controls. The ratio of lactulose to mannitol was significantly higher in oncological children vs control (mean 0.188 and 0.0453, respectively, p=0.0006,). Significantly higher IMA level in the oncological group vs control was noted (mean 123.8 and 87.3 U/ml, respectively, p=0.0037). No correlation between intestinal permeability and oxidative stress barrier was found. Conclusions: Our data shows that intestinal barrier is damaged in paediatric cancer patients after chemotherapy. IMA is believed to play a protective role in the defence against tissue damage. No correlation was found between these two barriers.
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Flavonoids exhibit prooxidant cytotoxicity in mammalian cells due to the formation of free radicals and oxidation products possessing quinone or quinomethide structure. However, it is unclear how the cytotoxicity of flavonoids depends on the ease of their single-electron oxidation in aqueous medium, i.e., the redox potential of the phenoxyl radical/phenol couple. We verified the previously calculated redox potentials for several flavonoids according to their rates of reduction of cytochrome c and ferricyanide, and proposed experimentally-based values of redox potentials for myricetin, fisetin, morin, kaempferol, galangin, and naringenin. We found that the cytotoxicity of flavonoids (n=10) in bovine leukemia virus-transformed lamb kidney fibroblasts (line FLK) and murine hepatoma (line MH-22a) increases with a decrease in their redox potential of the phenoxyl radical/phenol couple and an increase in their lipophilicity. Their cytotoxicity was decreased by antioxidants and inhibitors of cytochromes P-450, α-naphthoflavone and isoniazide, and increased by an inhibitor of catechol-O-methyltransferase, 3,5-dinitrocatechol. It shows that although the prooxidant action of flavonoids may be the main factor in their cytotoxicity, the hydroxylation and oxidative demethylation by cytochromes P-450 and O-methylation by catechol-O-methyltransferase can significantly modulate the cytotoxicity of the parent compounds.
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Serine proteases HtrA1 and HtrA2 are involved in cellular stress response and development of several diseases, including cancer. Our aim was to examine the involvement of the HtrA proteins in acute oxidative stress response induced in hamster kidney by estrogen treatment, and in nephrocarcinogenesis caused by prolonged estrogenization of male Syrian hamster. We used semi-quantitative RT-PCR to estimate the HtrA1 and HtrA2 mRNA levels in kidney tissues, and Western blotting to monitor the amount of the HtrA proteins. Within the first five hours following estrogen administration both HtrA1 mRNA and the protein levels were increased significantly. No changes in the expression of HtrA2 were observed. This indicates that HtrA1 may be involved in the response against oxidative stress induced by estrogen treatment in hamster kidney. During prolonged estrogenization, a significant reduction of the HtrA1 mRNA and protein levels was observed after 6 months of estradiol treatment, while the expression of HtrA2 was significantly elevated starting from the third month. This suggests an involvement of the HtrA proteins in estrogen-induced nephrocarcinogenesis in hamster. Using fluorescence in situ hybridization we localized the HtrA1 gene at the qb3-4 region of Syrian hamster chromosome 2, the region known to undergo a nonrandom deletion upon prolonged estrogenization. It is possible that the reduced level of HtrA1 expression is due to this chromosomal aberration. A full-length cDNA sequence of the hamster HtrA1 gene was obtained. It codes for a 50 kDa protein which has 98 and 96% identity with mouse and human counterparts, respectively.
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Content available remote Immunoinflammatory responses in gastrointestinal tract injury and recovery
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Inflammation is a non-specific immune response to infection, irritation or other injury, the key features being redness, warmth, swelling and pain. A number of mediators are released which alter the resistance of mucosa to injury induced by noxious substances. Oxidative stress is a unifying mechanism of injury in many types of disease processes, including gastrointestinal diseases. It has been defined as an imbalance in the activity of pro and antioxidants. Pro-oxidants favour free radical formation while antioxidants inhibit or retard the same. A number of markers of oxidative stress have been identified. This review provides an overview of various mediators of inflammation and oxidative stress, and diverse approaches for prevention and treatment of gastrointestinal inflammation.
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The anticancer activity of aziridinyl-quinones is mainly attributed to their NAD(P)H:quinone oxidoreductase 1 (NQO1)-catalyzed two-electron reduction into DNA-alkylating products. However, little is known about their cytotoxicity in primary cells, which may be important in understanding their side effects. We found that the cytotoxicity of aziridinyl-unsubstituted quinones (n = 12) in mice splenocytes with a low amount of NQO1, 4 nmol × mg-1 × min-1, was caused mainly by the oxidative stress. Aziridinyl-benzoquinones (n = 6) including a novel anticancer agent RH1 were more cytotoxic than aziridinyl-unsubstituted ones with the similar redox properties, and their cytotoxicity was not decreased by an inhibitor of NQO1, dicumarol. The possible reasons for their enhanced cytotoxicity are discussed.
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The lifespan of budding yeast cells is divided into two stages: reproductive and post-reproductive. The post-reproductive stage of the yeast's lifespan has never been characterized before. We have analyzed the influence of various mutations on the post-reproductive (PRLS) and replicative (RLS) lifespans. The results indicate that PRLS demonstrates an inverse relationship with RLS. The observed lack of differences in the total lifespan (TLS) (expressed in units of time) of strains differing up to five times in RLS (expressed in the number of daughters formed) suggests the necessity of revision of opinions concerning the use of yeast as a model organism of gerontology.
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In order to characterize the possible mechanism(s) of cytotoxicity of a neuroleptic agent 6,7-dinitrodihydroquinoxaline-2,3-dione (DNQX) we examined the redox properties of DNQX, and its mononitro- (NQX) and denitro- (QX) derivatives. The irreversible electrochemical reduction of the nitro groups of DNQX was characterized by the reduction peak potentials (Ep,7) of -0.43 V and -0.72 V vs. Ag/AgCl at pH 7.0, whereas NQX was reduced at Ep,7 = -0.67 V. The reactivities of DNQX and NQX towards the single-electron transferring enzymes NADPH:cytochrome P-450 reductase and NADPH:adrenodoxin reductase/adrenodoxin complex were similar to those of model nitrobenzenes with the single-electron reduction potential (E17) values of -0.29 V - -0.42 V. DNQX and NQX also acted as substrates for two-electron transferring mammalian NAD(P)H:quinone oxidoreductase (DT-diaphorase). The cytotoxicity of DNQX in bovine leukemia virus-transformed lamb kidney fibroblasts (line FLK) was prevented by antioxidants and an inhibitor of NQO1, dicoumarol, and was enhanced by the prooxidant alkylating agent 1,3-bis(2-chloromethyl)-1-nitrosourea. A comparison with model nitrobenzene compounds shows that the cytotoxicity of DNQX and NQX reasonably agrees with the ease of their electrochemical reduction, and/or their reactivities towards the used enzymatic single-electron reducing systems. Thus, our data imply that the cytotoxicity of DNQX in FLK cells is exerted mainly through oxidative stress.
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Background: Primary hyperparathyroidism (PHPT) is one of the most common endocrine disorders and defined as excessive secretion of parathormone. PHPT is a risk factor of several cardiovascular diseases, which could be caused by alterations in oxidant-antioxidant balance. Materials and methods: Blood serum collected from 52 consecutive patients with PHPT treated surgically constituted our study material, whereas 36 healthy volunteers were our control group. Oxidative stress was evaluated in both patients and control subjects by assessment of malondialdehyde (MDA) and lipid hydroperoxides (LHP). Antioxidants were evaluated by the measurement of superoxide dismutase (SOD), ceruloplasmin (CER), catalase (CAT), sulfhydryl (SH) groups, glutathione (GSH), glutathione peroxidase (GSH-Px), glutathione transferase activity (GST) and glutathione reductase (GR). Moreover, total antioxidant capacity (TAC) and total oxidative status (TOS) were measured and oxidative stress index (OSI) was calculated. Results: OSI was increased in patients with PHPT when compared to normal controls, whereas TAC was lower in PHPT. The levels of CER, MnSOD, GR, SH groups and MDA were significantly decreased in PHPT. The levels of serum LHP, catalase and SOD were significantly higher in patients with PHPT than in healthy patients. The erythrocyte CAT activity and GST were significantly increased in patients after parathyroidectomy. The erythrocyte GR and GPx were up-regulated postoperatively, whereas SOD activity decreased. Conclusions: In PHPT there are several alterations in the balance between the production of reactive oxygen species and antioxidant defense system.
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Specificity of targeting of the oxidative stress towards lipid and protein fractions in a model of estrogen-induced Syrian hamster nephrocarcinogenesis was evaluated. The amount of proteins modified by oxidative stress was significantly elevated as early as one month after the initial implantation of estradiol to the experimental versus the control group, while the stress did not affect lipids. Subcellular localization of the oxidative stress target was determined by the analysis of protein oxidation in subcellular fractions of kidney cells. The endoplasmic reticulum membranes were the fraction most affected by the oxidative stress.
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Content available Health benefits of black tea
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Tea is the most common beverage in the world. It is consumed mostly as green tea, oolong, or black tea. Depending on the manufacturing process, different varieties of tea can be produced. As tea is one of the most popular beverages, it could be a tremendously important source of polyphenolic constituents. Tea leaves are a source of polyphenols, especially catechins, which are known for their antioxidative activity. Various studies suggest that polyphenolic compounds present in black tea are associated with beneficial effects in prevention of cardiovascular diseases. In addition, anti-aging, antidiabetic and many other health beneficial effects associated with tea consumption have been reported. The review highlights the potential of black tea, its health benefits in terms of antioxidative, antimutagenic and anticarcinogenic properties as well as protective agents against cardiovascular diseases.
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Content available Związek stresu oksydacyjnego z jaskrą
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Glaucoma has long been considered exclusively a disease of the eye. Today it is known that glaucoma is an occular manifestation of systemic diseases. The pathomechanisms of glaucoma seem to be similar to those observed in other neurodegenerative disorders such as Alzheimer’s disease where nerve cell death, oxidative damage and inflammatory response are observed. The one known and proved glaucoma risk factor – elevated intraocular pressure (IOP), is neither necessary nor sufficient for the development and progression of glaucoma. What is more, IOP normalization does not always prevent disease progression. The data on oxidative stress in glaucomatous disturbances seem not only to conflict other observations but rather complement the mechanical, vascular, genetic and immunologic theories of glaucoma pathogenesis. The aim of the work is a summary of the latest research on the role of oxidative stress in glaucoma.
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Do niedawna jaskra była uważana za schorzenie wyłącznie okulistyczne. Dzisiaj wiadomo, że jest ona oczną manifestacją ogólnoustrojowych zaburzeń. Patomechanizmy występujące w jaskrze wydają się podobne do obserwowanych w pozostałych chorobach neurodegeneracyjnych, takich jak np. choroba Alzheimera, gdzie obserwuje się śmierć komórek nerwowych, uszkodzenia związane z szokiem tlenowym, azotowym i odpowiedzią zapalną. Jedyny znany i potwierdzony czynnik ryzyka jaskry – podwyższone ciśnienie wewnątrzgałkowe (CWG) nie jest ani wystarczający, ani konieczny do rozwoju i progresji jaskry. Normalizacja CWG często nie zapobiega postępowi choroby. Obserwacje związku stresu oksydacyjnego z jaskra zdają się nie tylko nie zaprzeczać innym teoriom rozwoju jaskry (mechanicznym, naczyniopochodnym, genetycznym i immunologicznym), ale je uzupełniać. Celem pracy jest zestawienie najnowszych wyników badań nad rolą stresu oksydacyjnego w patogenezie jaskry.
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