Amount Of Lipid Peroxidation Products Research Articles

Post-Translational Modifications Evoked by Reactive Carbonyl Species in Ultraviolet-A-Exposed Skin: Implication in Fibroblast Senescence and Skin Photoaging.

Photoaging is an accelerated form of aging resulting from skin exposure to ultraviolet (UV) radiation. UV-A radiation deeply penetrates the dermis and triggers the generation of reactive oxygen species (ROS) which promotes damage to DNA, lipids and proteins. Lipid peroxidation results from the oxidative attack of polyunsaturated fatty acids which generate a huge amount of lipid peroxidation products, among them reactive carbonyl species (RCS) such as α, β-unsaturated hydroxyalkenals (e.g., 4-hydroxynonenal), acrolein or malondialdehyde. These highly reactive agents form adducts on free NH2 groups and thiol residues on amino acids in proteins and can also modify DNA and phospholipids. The accumulation of RCS-adducts leads to carbonyl stress characterized by progressive cellular and tissular dysfunction, inflammation and toxicity. RCS-adducts are formed in the dermis of skin exposed to UV-A radiation. Several RCS targets have been identified in the dermis, such as collagen and elastin in the extracellular matrix, whose modification could contribute to actinic elastosis lesions. RCS-adducts may play a role in fibroblast senescence via the modification of histones, and the sirtuin SIRT1, leading to an accumulation of acetylated proteins. The cytoskeleton protein vimentin is modified by RCS, which could impair fibroblast motility. A better identification of protein modification and carbonyl stress in the dermis may help to develop new treatment approaches for preventing photoaging.

Особливості системних патобіохімічних реакцій на ішемію-реперфузію головного мозку у щурів із цукровим діабетом

The objective of the research was to study the signs of oxidative stress, the state of proteolysis, and the proteinase-inhibiting system of the blood plasma in rats with streptozotocin-induced diabetes mellitus (60 mg/kg intra-abdominally), complicated by cerebral ischemia-reperfusion. Levels of products of lipid peroxide oxidation, protein oxidative modification, nitrogen oxide metabolites, and activity of the antioxidant protection enzymes were determined by means of biochemical methods one hour after completion of the reperfusion period and on the 12th day. Increased intensity of lipid peroxidation was found to occur in the blood plasma of rats without diabetes mellitus in both terms of observation. This was accompanied by an increase in the activity of all the antioxidant enzymes, while in animals with diabetes the amount of lipid peroxidation products decreased in the ground of prevailing depression of all the antioxidant protection enzymes. Irrespective of a tendency of changes in the amount of POM products with cerebral ischemia-reperfusion, their content is reliably higher in animals with diabetes mellitus in both terms of observation than those in animals without diabetes, which is indicative of a higher intensity of their oxidation. Without diabetes, the proteolytic activity of the blood plasma reacts by increasing the values of the studied parameters against the background of suppression of the proteinase inhibitory system during the entire observation period, in rats, with diabetes the parameters of plasma proteolysis and the state of the proteinase-inhibiting system remain without changes in both terms of the observation. The data obtained allowed us to state that diabetes mellitus considerably modifies the response of the systemic pathobiochemical indices to cerebral ischemia-reperfusion.

Effect of extracts from eggs of Helix aspersa maxima and Helix aspersa aspersa snails on Caco-2 colon cancer cells.

BackgroundColorectal cancer is the third most commonly diagnosed cancer. Natural compounds, administered together with conventional chemotherapeutic agent(s) and/or radiotherapy, may be a novel element in the combination therapy of this cancer. Considering the anticancer properties of compounds derived from different tissues of various snail species confirmed earlier, the purpose of the present research was to evaluate the effect of extracts from eggs of Helix aspera maxima and Helix aspersa aspersa snails, and fractions of extracts containing particles of different molecular weights on Caco-2 human epithelial colorectal adenocarcinoma cells.MethodsThe extracts and fractions were analyzed for antioxidant activity, phenols and total carbohydrates using colorimetric methods. Lipid peroxidation products and glutathione in eggs were also examined using these methods. Crude protein and fat in eggs were determined. Molecular weights of egg proteins and glycoproteins were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Astaxanthin, selected vitamins and amino acids in eggs were measured using liquid chromatography methods, and minerals by emission spectroscopy, mass spectrometry or X-ray fluorescence. The action of extracts on the cell viability was determined by the MTT (methylthiazolyldiphenyl-tetrazolium bromide) test, based on the mitochondrial oxidative activity, after 24 and 72 h of treatment. The influence of fractions on the cell viability was assayed after 24 h. The effect of extracts on the percentage of live and dead cells was evaluated by the trypan blue assay, in which live cells exclude trypan blue, while dead cells take up this dye, after 12, 24, 48 and 72 h of treatment. Their influence on the integrity of cell membranes was determined based on the activity of LDH (lactate dehydrogenase), released from damaged cells, after 24 and 72 h of treatment. Then, the effect of extracts on the content of lipid peroxidation products in cells was examined using colorimetric method, after 24 h of treatment. Their influence on types of cell death was determined by flow cytometry, after this time.ResultsThe extracts and their fractions containing molecules <3 kDa decreased the cell viability, after 24 h of treatment. The extracts reduced the percentage of live cells (also after 48 h), increased the degree of cell membrane damage and the amount of lipid peroxidation products, induced apoptosis and reduced necrosis.ConclusionsAntioxidants, phenols, lipid peroxidation products, anticancer peptides, restriction of methionine, appropriate ratio of essential amino acids to non-essential amino acids, vitamin D3, Ca, Mg, S, Cu, Mn, Zn, Se and other bioactive compounds comprised in the extracts and their additive and synergistic effects may have influenced Caco-2 cells. Natural extracts or the chemical compounds contained in them might be used in the combination therapy of colorectal cancer, which requires further research.

Melittin Ameliorates Endotoxin-Induced Acute Kidney Injury by Inhibiting Inflammation, Oxidative Stress, and Cell Death in Mice.

Sepsis-related acute kidney injury (AKI) is a worldwide health problem, and its pathogenesis involves multiple pathways. Lipopolysaccharide (LPS) is an endotoxin that induces systemic inflammatory responses. Melittin, a main constituent of bee venom, exerts several biological activities such as antioxidant, anti-inflammatory, and antiapoptotic actions. However, whether melittin protects against endotoxin-induced AKI remains undetermined. Here, we aimed to examine the potential action of melittin on LPS-induced renal injury and explore the mechanisms. We showed that acute renal failure and structural damage after injection of LPS were markedly attenuated by administration of melittin. The peptide also suppressed expression of markers of direct tubular damage in kidneys of the LPS-treated mice. Mechanistically, melittin reduced systemic and renal levels of cytokines and inhibited renal accumulation of immune cells with concomitant suppression of nuclear factor kappa-B pathway. Increased amounts of lipid peroxidation products after LPS treatment were largely decreased by melittin. Additionally, the peptide decreased expression of nicotinamide adenine dinucleotide phosphate oxidase 4 and enhanced nuclear factor erythroid-2-related factor 2-mediated antioxidant defenses. Moreover, melittin inhibited apoptotic and necroptotic cell death after LPS treatment. Lastly, we showed that melittin improved the survival rate of LPS-injected mice. These results suggest that melittin ameliorates endotoxin-induced AKI and mortality through inhibiting inflammation, oxidative injury, and apoptotic and necroptotic death of tubular epithelial cells.

Neuroprotective effect of morin against unpredictable chronic mild stress induced oxidative stress and behavioural deficits in Wistar rats

Morin is a bioflavonoid widely found in fruits and vegetables, which possesses the protective activity to various neurological diseases. An earlier report showed that the administration of morin had antidepressant-like effect against acute stress conditions. Acute stress induces only transient changes in the brain while the prolonged stress increases vulnerability to mental disorders. To better understand its anti depressive activity, we explored the neuroprotective role of morin against unpredictable chronic mild stress (UCMS) induced rats. Male Wistar rats were randomized and grouped into control, UCMS exposed (different stressors) UCMS and morin (30 &amp; 60 mg/kg) co-treated and morin alone treated (60 mg/kg). Morris water maze test (MWMT) and sucrose preference test (SPT) were employed to study the effect of morin on learning, memory and anhedonia of rats. In addition, the levels of thiobarbituric acid (TBARS) and reduced glutathione (GSH) and the activities of super oxide dismutase (SOD), catalase and glutathione peroxidase (GPx) were estimated. Behavior studies indicated that morin treatment significantly increased the memory and sucrose intake as shown by MWMT and SPT respectively. Moreover, it exhibited the antioxidant activity by reducing the amount of lipid peroxidation products (TBARS) and GSH and activities of enzymatic antioxidants in UCMS rats. Our experiment suggested that the antidepressant-like actions of morin could be due to its potent antioxidant property.

Aspects of free radical oxidation in the large bowel in ulcerative colitis and Crohn’s disease

Research into the accumulation patterns of protein oxidative modification (POM) products and lipids in Crohn’s disease (CD) and ulcerative colitis (UC) could have important implications for understanding the pathogenesis and improving the diagnosis and therapy for these diseases. The aim of this study was to investigate the aspects of free radical oxidation (FRO) in the large bowel and their possible correlations with clinical symptoms of UC and CD. In the Wistar rat model used in the experiment, CD was induced with 2,4,6-trinitrobenzenesulfonic acid, and UC was induced with oxazolone. Clinical status was assessed using the Disease activity index (DAI). Lipid peroxidation (LPO) products were measured in the heptane and isopropanol phases of the intestinal mucosa extract. POM products were measured following spontaneous and stimulated oxidation. The DAI ( Me (Q25–Q75)) was increased in both CD and UC on days 3 and 7 of the experiment: for CD, it was equally increased on days 3 and 7 (7 (3-7)) and was 11 (11–11) and 11 (9–11) for UC on days 3 and 7, respectively. The amount of primary, secondary and end LPO products in the heptane and isopropanol phases, as well as the total amount of POM products, was increased in the homogenized mucosa of the large bowel. In the CD group, the relative content of secondary basic POM products was increased on day 7 of the experiment. The following patterns of FRO were revealed: accumulation of LPO products in the UC group and accumulation of POM products in the CD group; UC is characterized by the accumulation of mostly LPO products in the heptane phase and secondary LPO products in the isopropanol phase; CD is characterized by the accumulation of secondary basic POM products. DAI scores were correlated with the amount of LPO products in the isopropanol phase and the amount of POM products in the spontaneous oxidation mode. The highest number of strong correlations was observed in the UC group. Our findings suggest a very serious contribution of FRO changes to the pathogenesis of UC and CD, meaning that LPO and POM products could be regarded as diagnostic markers and indicators of treatment efficacy.

Антиоксидантная активность производного коричной кислоты в условиях истощающих физических нагрузок в эксперименте

Изучена антиоксидантная активность производного коричной кислоты — соединения ATACL — на фоне истощающих физических нагрузок. Физические нагрузки воспроизводили у крыс в тесте «Принудительное плавание». Соединение ATCL вводили в дозе 100 мг/кг в течение 10 дней плавания. У группы крыс отрицательного контроля через 10 дней принудительного плавания, по сравнению с интактными животными, было отмечено повышение количества продуктов перекисного окисления липидов в мышечной ткани: малонового диальдегида и диеновых конъюгатов на 189 % (p &lt; 0,05) и 40,4 % (p &lt; 0,05). В свою очередь наблюдалось снижение активности ферментов антиоксидантной защиты (АОЗ): супероксиддисмутазы на 40,6 % (p &lt; 0,05), каталазы на 33,8 % (p &lt; 0,05), глутатионпероксидазы на 30,1 % (p &lt; 0,05) относительно показателей интактной группы крыс. Применение исследуемого производного коричной кислоты позволило скорректировать данные нарушения — наблюдали повышение содержания СОД, каталазы и ГП в мышечной ткани на 59,3 % (p &lt; 0,05), 127,3 % (p &lt; 0,05) и 106,2 % (p &lt; 0,05), соответственно, и снижение уровня ТБК-активных продуктов и диеновых конъюгатов в мышечной ткани на 75,11 % (p &lt; 0,05) и 33,6 % (p &lt; 0,05) относительно группы отрицательного контроля. Таким образом, производное коричной кислоты (ATACL) на фоне физической нагрузки способно проявлять антиоксидантную активность.

Influence of football activities on the amount of lipid peroxidation products and enzyme activity in adolescent saliva

Influence of football activities on the amount of lipid peroxidation products and enzyme activity in adolescent salivaI.S. Aliyev, S.A. AliyevAzerbaijan State Academy of Physical Education and Sport, 98 Fatali Khan Khoyski Str., AZ1072 Baku, Azerbaijan;*For correspondence:

The contribution of lipid peroxidation to membrane permeability in electropermeabilization: A molecular dynamics study

Electroporation or electropermeabilization is a technique that enables transient increase in the cell membrane permeability by exposing cells to pulsed electric field. However, the molecular mechanisms of the long-lived cell membrane permeability, which persists on the minutes time scale after the pulse treatment, remain elusive. Experimental studies have suggested that lipid peroxidation could present a mechanism of this prolonged membrane permeabilization. In this study we make the first important step in quantifying the possible contribution of lipid peroxidation to electropermeabilization. We use free energy calculations to quantify the permeability and conductance of bilayers, containing an increasing percentage of hydroperoxide lipid derivatives, to sodium and chloride ions. We then compare our calculations to experimental measurements on electropermeabilized cells. Our results show that the permeability and conductance increase dramatically by several orders of magnitude in peroxidized bilayers. Yet this increase is not sufficient to reasonably account for the entire range of experimental measurements. Nevertheless, lipid peroxidation might be considered an important mechanism of prolonged membrane permeabilization, if exposure of cells to high voltage electric pulses leads to secondary lipid peroxidation products. Our analysis calls for experimental studies, which will determine the type and amount of lipid peroxidation products in electropermeabilized cell membranes.

Leaf fatty acid remodeling in the salt-excreting halophytic grass Spartina patens along a salinity gradient

Spartina patens is a highly dispersed halophytic grass invader in Mediterranean marshes. It is also characterized by having a high degree of resistance to salinity, one of the main drivers of plant zonation in salt marshes. Nevertheless, the physiological basis behind the extreme resistance of S. patens requires more detailed studies. In the present work, we aimed to study how membrane fatty acid remodeling could contribute to the resistance of this plant to salt. Spartina patens individuals exposed to increasing levels of salinity and its leaf fatty acid profile under lipid peroxidation products evaluated under all tested concentrations. A significant increase in the relative amounts of the saturated fatty acids (SFA) was observed, namely palmitic acid (C16:0), essential for PS II functioning, and stearic (C18:0) acid. The chloroplastidial trans-hexadecenoic acid (C16:1t) as well as the polyunsaturated linoleic (C18:2) and linolenic (C18:3) acids showed significant decreases in all the salt treatments. These changes led to a reduction in the double bond index in salt-treated plants which reflects reduction of the fluidity of the chloroplast membranes, which could contribute to maintain the membrane impermeable to the toxic exogenous Na. Despite the decrease observed in the total fatty acid contents in plants exposed to high salt concentrations the amounts of lipid peroxidation products decreased highlighting the resistance of this species towards toxic exogenous salt concentrations. Membrane fatty acid remodeling could represent an efficient mechanism to maintain the photosynthetic machinery of S. patens highly efficient under salt stress.

Induction of anthocyanin accumulation and status of protective system in winter rape plants treated with 5-aminolevulinic acid

Effects of exogenous 5-aminolevulinic acid (ALA) on development and certain biochemical parameters of winter rape plants (Brassica napus L.) were studied. Plant growing on 50–200 mg/L ALA solutions for 7 days resulted in an accumulation of anthocyanins in cotyledonous leaves and changed in leaf color from green to violet. An application of 200 mg/L ALA under a stronger illumination (66.2 instead of 40.5 μmol photons/(m2 s)) elevated the anthocyanin content 1.8 times in cotyledons (up to 3.15 ± 0.37 mmol/g dry wt) and 1.3 times in hypocotyls (up to 2.71 ± 0.36 mmol/g dry wt). In the plants enriched with anthocyanins, the hypocotyl linear growth was significantly suppressed (63% of control) and the far stronger suppression of the root growth (46% of control) took place. In the treated plants, chlorophylls a and b accumulated much slower than in the control during vegetation. For both pigments, the corresponding values were 44 and 38% by the fourth day of development, 37 and 27% by the fifth day, 31 and 27% by the sixth day, and 24 and 21% by the seventh day. Thus, the difference between the treated and untreated plants progressively diminished. Levels of carotenoids obeyed a similar pattern. In 7-day-old seedlings treated with 200 mg/L ALA, the activity of the key enzyme of anthocyanin biosynthesis—dihydroflavonol-4-reductase (DFR)—was 1.8 times as high as the control. Simultaneously, the content of proline was 2.2-fold higher; the level of heme noncovalently bound to protein, as well as levels of hydrogen peroxide and reactive oxygen species, exceeded the control level 60, 30, and 25%, respectively. Meanwhile, amounts of lipid peroxidation products and those of superoxide radical were as low as 29 and 62% of the control. In anthocyanin-enriched cotyledons, antiradical and total antioxidant activities were, respectively, 38 and 42% higher than in the control. Therefore, the set of metabolic rearrangements was revealed in the protective and energy systems of winter rape plants in response to exogenous ALA. The reduction in uptake of exogenous ALA by the system synthesizing tetrapyrroles of chlorophyllic nature and decrease in their production were found. Induction of accumulation of anthocyanin antioxidants as a consequence of almost twofold activation of DFR was shown. Simultaneously, the increased contents of heme and proline, together with the rise in antioxidant and antiradical activities, were found. Overall, this reduced the superoxide-generating capacity and lipid peroxidation in intracellular membranes but slightly elevated ROS and H2O2 levels above the control.

Microelemental homeostasis correction of and oxidative stress in patients with acute intestinal obstruction

To improve the results of treatment of patients with acute small bowel obstruction. The research is based on the results of a comprehensive survey 202 people with acute small bowel obstruction. Reamberin was used in 102 patients treatment. It was established that metalloenzymes take an active part in the formation of endotoxemia in people with acute small bowel obstruction. Also, in patients as a result of an imbalance between oxidant and antioxidant systems, accumulated a significant amount of lipid peroxidation products, along with it a decrease activity of enzymes of antioxidant system. reamberin application in complex treatment of acute small bowel obstruction provided the reduction in the time correction of oxidative stress by preventing the growth and activity of lipid peroxidation products with simultaneous stimulation of the antioxidant system and contributed to the normalization of microelement homeostasis.

Deep fried edible oils disturb hepatic redox equilibrium and heightens lipotoxicity and hepatosteatosis in male Wistar rats.

Hepatosteatosis is a complex disorder, in which insulin resistance and associated dyslipidemic and inflammatory conditions are fundamental. Dietary habit, especially regular consumption of fat and sugar-rich diet, is an important risk factor. Coconut and mustard oils (CO and MO) are medium-chain saturated and monounsaturated fats that are common dietary ingredients among the Indian populations. Present study analyzed the effect of prolonged consumption of the fresh and thermally oxidized forms of these oils on glucose tolerance and hepatosteatosis in male Wistar rats. Thermally oxidized CO (TCO) and MO (TMO) possessed higher amount of lipid peroxidation products and elevated p-anisidine values than their fresh forms. Dietary administration of TCO and TMO along with fructose altered glucose tolerance and increased hyperglycemia in rats. Dyslipidemia was evident by elevated levels of triglycerides and reduced high density lipoprotein cholesterol (HDLc) levels in fructose and edible oil-fed group ( p < 0.05). Additionally, hepatic antioxidant status was diminished and oxidative stress markers were elevated in TCO- and TMO-fed rats. Substantiating these, hike in liver function marker enzyme activities were also observed in these animals. Supporting this, histological analysis revealed higher incidence of microvesicles and hepatocellular ballooning. Results thus suggest that consumption of thermally oxidized fats may cause hepatic damage.

Constitutive and cold-induced resistance of rye and wheat seedlings to oxidative stress

The influence of cold hardening of rye (Secale cereale L.) and wheat (Triticum aestivum L.) seedlings on their resistance to the oxidative stress (OS) agents, namely, 50 mM hydrogen peroxide or 5 mM iron (II) sulfate was studied. Unhardened rye seedlings were more resistant to hydrogen peroxide than those of wheat, since their growth was less inhibited, and they accumulated lesser amounts of lipid peroxidation products after a treatment with H2O2. The interspecific differences in responses to FeSO4 were less significant. The unhardened seedlings of rye, in comparison with those of wheat, possessed more active guaiacol peroxidase (GPO) and more levels of anthocyanins and proline. In response to the OS agents, the unhardened rye seedlings enhanced activities of superoxide dismutase and catalase, whereas the wheat seedlings enhanced GPO activity and proline content. The cold hardening (6 days at 2°C) increased activities of antioxidant (AO) enzymes, contents of proline, sugars, and anthocyanins in seedlings of both species, and made the seedlings more resistant to the OS agents. After the cold hardening, rye seedlings were more resistant to OS than wheat seedlings. The hardened seedlings of both species activated the AO enzymes in response to H2O2 or FeSO4 greater than the unhardened ones. However, the hardened wheat seedlings, in contrast to the unhardened ones, did not augment the proline content in contact with the OS agents. The conclusion was drawn on different contributions of AO enzymes and low-molecular weight compounds to the basal and induced by the cold—hardening resistances of rye and wheat seedlings to OS.

PP45 - Microwave versus electrical oven heating influence on oxidative stress parameters, flavonoids and polyphenols content of five different commercial cooking oils

Consumers are increasingly concerned about the health aspects of food preparation. There is data to support that foods treated with microwaves (MW) develop harmful substances. Vegetable oils are susceptible to lipid peroxidation due to the chemical structure, but also contain antioxidant compounds. Peroxidation products can have harmful effects for human health. The aim of the study was to evaluate the variation of total antioxidant capacity and antioxidant degradation in relation to lipid peroxides formation during conventional and microwave oils heating. Sunflower, corn, soybean, palm and a mixed oil (sunflower, grape, flaxseed and rice oil) were purchased from the local market. To simulate home cooking, different exposure times were tested 5, 10 and 15 min. For all samples, and for each exposure time, Trolox Equivalent Antioxidant Capacity (TEAC), lipid peroxides as thiobarbituric reactive substances (TBARS), conjugated dienes, vitamin E as α-tocopherol, flavonoids and total polyphenols were determined. After 15 minutes heating the best retention for vitamin E was observed for the palm oil (MW 12 mM/l), and corn oil (convection 17 mM/l). The highest total antioxidant capacity after heating belonged to mixed & palm oil (MW 4.6 eq. TROLOX/l) and soybean oil (convection 7.5 mM eq. TROLOX/l). Highest levels of TBARS belonged to the mixed oil (convection 54 uM/l) and soybean oils (MW 83 uM/l). Highest conjugated dienes levels were observed for soybean oil (MW 17 mM/l) and sunflower oil (convection 22 mM/l). The best retention for polyphenols was found in the mixed and sunflower oils (MW and convection 0.80.9 mg/ml. The retention of flavonoid was very small in all oils and the highest amount was found in corn and soybean oil (0.04 mg/ml). During the heating of edible vegetable oils commonly used, total antioxidant capacity along with the amount of vitamin E, flavonoids and polyphenols decreases, while the amount of lipid peroxidation products increases and these processes are more intense when using microwave heating than when using convection heating.

Antioxidant defense of rat organism at long-term per oral injection of taurine

Aim of this work was to study the activity of antioxidant defense enzymatic link, glucose-6-phosphate dehydrogenase activity and content of TBA-active products at long term per oral injection of taurine. Male Wistar rats (4.5 months old and with body weight 190–220 g) were used in the experiments. Animals were randomly divided into three groups: one control group and two experimental groups. During 28 days period, animals were daily injected in esophagus: control group – drinking water, experimental group I and II – solution of taurine (40 and 100 mg/kg of body weight, respectively). On the 29 th day, the animals were decapitated under light chloroform anesthesia, and liver, brain, testes and thigh muscle were extirpated. The tissues were homogenized and then centrifuged for 15 min at 1,000 g. In supernatant, the activities of superoxide dismutase, glutathione peroxidase, catalase and glucose-6-phosphate dehydrogenase, and content of TBA-active products were measured. Ratio of antioxidant enzymes activity to TBA-active products content (AOD/TBA) was calculated. It was determined, that in rat liver of I st experimental group, the activity of all antioxidant defense enzymes, glucose-6-phosphate dehydrogenase and content of TBA-active products increased. Under these conditions, the resistance of this tissue to oxygen free radicals, and AOD/TBA ratio also increases. In the II nd experimental group, the superoxide dismutase acti­vity was similar to control values, but other indices remained higher than in control group. Similar trend was observed in the thigh muscle of both experimental groups, where it was found that, activity of antioxidant enzymes and glucose-6-phosphate dehydrogenase increased, and the amount of lipid peroxidation products also elevated. At the same time, the AOD/TBA ratio was the highest in animals of the II nd experimental group. In testes of animals of the І ts experimental group, an increase in the glutathione peroxidase activity was established, and the content of TBA-active products was the highest among three groups. A rise in content of TBA-active products caused a decrease in AOD/TBA ratio in more than 4 times. In the II nd experimental group, it was found that the increase of antioxidant enzymatic activity and decrease of content of TBA-active pro­ducts, compared to the I st experimental group, caused an increase in AOD/TBA ratio. In brain tissue, glutathione peroxidase and catalase activity increased at a constant content of peroxidation products. This caused an increase in AOD/TBA ratio, that indicates growth of resistance to oxygen free radicals. Thus, the effect of long term per oral injection of taurine on the enzymatic link of antioxidant defense is tissue- and dose-dependent.

Impact of Traffic Emissions on Local Air Quality and the Potential Toxicity of Traffic-related Particulates in Beijing, China

ObjectiveAir-borne particulates from different sources could have different physicochemical properties and inflammatory potentials. This study aims to characterize the chemical compositions and the toxicity of ambient particulate matter (PM) associated with traffic emissions. MethodsThe concentrations of trace elements, organic carbon (OC), elemental carbon (EC) and polycyclic aromatic hydrocarbons (PAHs) in PM2.5 and PM10 were measured in samples collected at sites in Beijing, China. Their toxic effects on the pulmonary system of rats were investigated. Biochemical parameters (LDH, T-AOC, TP) and inflammatory cytokine(IL-6, IL-1, TNF-a) levels were measured in the lungs of rats exposed to traffic-related PM. Oxidative damage was observed. PM samples were taken from a near road site and an off road site in summer time in 2006. ResultsThe concentrations of the USEPA priority pollutant PAHs in both PM10 and PM2.5 were higher (299.658 and 348.412) at the near road site than those (237.728 and 268.472) at the off road site. The similar trend was observed for the concentrations of trace elements in PM. Compared to coarse particles (PM10), fine particles (PM2.5) have a greater adsorption capacity to enrich toxic elements than inhalable particles. Decrease in antioxidant capacity and an increase in the amount of lipid peroxidation products in rat lung tissues was observed. ConclusionThe findings of the present study suggest that the differing inflammatory responses of PM collected from the two road sites might have been mediated by the differing physicochemical characteristics.

Impact of co administration of selenium and quinolinic acid in the rat's brain

The effect of two different doses (1 μg and 50 μg Se/100 g body wt) of selenium on quinolinic acid toxicity was investigated in rat's brain. Male albino rats were maintained for 60 days as follows: (1) control group (normal diet), (2) Quinolinic acid group (55 μg/100 g body wt)/day, (3) high dose selenium (50 μg/100 g body wt)/day, (4) high dose selenium ((50 μg/100 g body wt) + Quinolinic acid (55 μg/100 g body wt)/day (5) low dose selenium (1 μg/100 g body wt)/day and (6) low dose selenium (1 μg/100 g body wt) + Quinolinic acid (55 μg/100 g body wt)/day. Results revealed that quinolinic acid intake lead to an increase in the oxidative stress as evidenced by decreased activity of antioxidant enzymes (SOD, catalase and GR), increased amount of lipid peroxidation products (MDA,HP and CD) and free fatty acids compared to control group. Co administration of selenium at a dose of 1 μg/100 g body wt along with quinolinic acid had reduced the oxidative stress induced by quinolinic acid and it also led to a change in the brain architecture as evidenced by the decreased activity of acetyl cholinesterase and decreased concentration of neurotransmitters. Histopathological studies revealed that selenium at a dose of 1 μg was more effective in reducing the oxidative stress and higher dose of selenium was toxic.

Protective effect of quercetin in the regression of ethanol-induced hepatotoxicity

This study examined the protective effects of quercetin on chronic ethanol-induced liver injury. Rats were treated with ethanol at a dose of 4 g/100 g/day for 90 days. After ethanol intoxication, levels of serum amino transferases were significantly elevated. Decreased activity of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase was also observed on ethanol administration. Increased amounts of lipid peroxidation products viz. hydroperoxides, conjugated dienes and malodialdehyde were observed on ethanol intoxication. Ethanol administration resulted in significant decrease in liver glutathione content. After 90 days, the control animals were divided into two groups, the control group and the control+quercetin group. Ethanol-treated group was divided into two groups, abstention group and quercetin-supplemented group. After 30 days, the animals were sacrificed and various biochemical parameters were analyzed. The changes in enzyme activities as well as levels of lipid peroxidation products were reversed to a certain extent by quercetin. Quercetin supplementation resulted in increase of glutathione content to a significant level compared to normal abstention group. Quercetin supplemented group showed a faster recovery than abstention group. This shows the protective effect of quercetin against chronic ethanol induced hepatotoxicity. Histopathological study is also in line with these results.

Influence of therapy on the antioxidant status in patients with melanoma

Some anticancer drugs can result in increased production of reactive oxygen species (ROS). Alkylating agents are the most frequently used drugs in chemotherapeutic regimens for the treatment of malignant melanoma. It is known that triazenes exhibit in vivo activity by alkylation of nucleic acids and proteins, but there is no data about ROS formation during oxidative metabolism. Single agents of most interest for treatment of malignant melanomas include 5-(3,3-dimethyltriazene-1-yl)-imidazole-4-carboxamide (DTIC) and nitrosoureas such as 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU), but complete response to these drugs is rare. The present study aimed to determine whether an oxidative stress occurs during the clinical course of melanoma and the influence of therapy on the antioxidant status of patients with melanoma. For this purpose, we investigated plasma concentrations of MDA as indices of the levels of lipid peroxidation products. In addition, we studied the activities of the antioxidant enzymes superoxide dismutases (SOD) and catalase (CAT) in patients with melanoma before any treatment, after surgical removal of melanoma, and after chemotherapy with DTIC or in combination with CCNU of the operated patients. Twenty one patients with melanoma were studied. Patients were operated prior to chemotherapy. After recovery for 10-20 days postoperatively, they were studied again for MDA, SOD and CAT activity. The patients were divided into two groups according to the chemotherapy (3-7 treatment cycles): with DTIC-given orally daily for 5 days, every 3 weeks as a single 2200 mg/kg dose and with the combination-DTIC (the same dose) + CCNU-administered orally at a dosage of 120 mg/m(2) once every 40 days in accordance with protocols, approved by the Bulgarian Ministry of Health. The total amount of lipid peroxidation products in plasma was assayed. Plasma levels of MDA and CAT activity were significantly higher, and erythrocyte SOD activity significantly lower, in patients with melanoma, than in control healthy volunteers (P < 0.0001). Ten to twenty days after surgery, oxidative stress decreased but levels of MDA increased as a result of therapy. Important sources of increased ROS production may be the monocytes, phagocytosis of tumour cells and the cancer tissues. Plasma MDA in patients treated with DTIC + CCNU were significantly higher (P < 0.001), but erythrocyte SOD statistically lower (P < 0.00001), compared with patients treated with DTIC only. However, a combination of DTIC + CCNU did not attenuate oxidative stress, or reduced antioxidant status. Patients treated with this combination are at bigger risk of oxidative injury. Therefore, this disturbance might be due to augmented generation of toxic ROS, possibly from the metabolism of CCNU. Increased oxidative stress follows an imbalance in antioxidant defence in non-treated patients with melanoma. The impaired antioxidant system favours accumulation of ROS, which may promote the cancer process. After complete removal of melanoma tissues, oxidative stress decreased. The antioxidant status of melanoma patients operated on was influenced by the different chemotherapeutic regimens used and may play an important role in the response. Patients on DTIC + CCNU are at higher risk of oxidative injury. This drug combination probably exerts its toxic activity by ROS, which could be products of the metabolism of CCNU.