Antioxidant Protective Mechanisms Research Articles

Physiological responses of wheat (Triticum aestivum L.) germination to elevated ammonium concentrations: reserve mobilization, sugar utilization, and antioxidant metabolism

To elucidate the physiological mechanisms of wheat (Triticum aestivum L.) germination in response to elevated ammonium (NH4 +) concentrations (EAC), Yumai49 (NH4 +-tolerant) and Lumai15 (NH4 +-sensitive) cultivars were supplied with a 5.0 mM NH4 +-N (EAC) treatment or a 5.0 mM NO3 −-N (CON) treatment as the control. There was a reduction in the seed germination index, plant biomass, radicle length, and other deleterious effects following the EAC treatment in both cultivars, but Yumai49 was more tolerant to EAC than Lumai15. When compared to CON, α-amylase activity and ATP content in seeds were significantly lower after the 3rd and 5th day of the EAC treatment in Lumai15 and Yumai49, respectively. Moreover, the ratio of abscisic acid to gibberellins in seeds was higher under EAC treatment as compared to CON, with a smaller ratio increase in Yumai49 than in Lumai15, indicating that the differences in hormone ratio caused by the EAC treatment was associated with lower seed reserve mobilization. The soluble sugar content in radicles increased while it was reduced in coleoptiles for both cultivars under the EAC treatment. However, Yumai49 exhibited a slight increase in seedling soluble sugar content, while Lumai15 exhibited a significant reduction in sugar content, as compared to CON. Moreover, Yumai49 exhibited a lower ratio reduction in coleoptile to radicle soluble sugar content as compared with Lumai15, indicating that Yumai49 was undergoing greater reserve mobilization and transportation to the radicle to support growth. The activities of pyruvate kinase and phosphoenolpyruvate carboxylase were increased under the EAC treatment in the radicles, with a greater increase seen in Yumai49 than in Lumai15, indicating that Yumai49 had a greater capacity to assimilate NH4 +. In addition, the EAC treatment enhanced the content of malonaldehyde and superoxide anions, and the activities of superoxide dismutase and peroxidase in the coleoptiles and radicles of both cultivars, with the magnitude of these increases greater in Yumai49 than in Lumai15. It is concluded that the NH4 +-tolerant cultivar, as compared to the sensitive cultivar, has a greater capacity to undertake reserve mobilization and ATP production in its seeds, a greater sugar utilization in its radicles, and a stronger antioxidant protection mechanism.

Antioxidant and Hepatoprotective Efficiency of Selenium Nanoparticles Against Acetaminophen-Induced Hepatic Damage.

Overdoses of acetaminophen (APAP), a famous and widely used drug, may have hepatotoxic effects. Nanoscience is a novel scientific discipline that provides specific tools for medical science problems including using nano trace elements in hepatic diseases. Our study aimed to assess the hepatoprotective role of selenium nanoparticles (Nano-Se) against APAP-induced hepatic injury. Twenty-four male rats were classified into three equal groups: a control group that received 0.9% NaCl, an APAP-treated group (oral administration), and a group treated with Nano-Se (10-20nm, intraperitoneal (i.p.) injection) and APAP (oral administration). APAP overdose induced significant elevations in liver function biomarkers, hepatic lipid peroxidation, hepatic catalase, and superoxide dismutase (SOD), decreased the reduced glutathione (GSH) content and glutathione reductase (GR) activity, and stimulated significant DNA damage in hepatocytes, compared to control rats. Nano-Se administration improved the hepatic antioxidant protection mechanism and decreased cellular sensitivity to DNA fragmentation. Nano-Se exhibits a protective effect against APAP-induced hepatotoxicity through improved liver function and oxidative stress mediated by catalase, SOD, and GSH and decreases hepatic DNA fragmentation, a hepatic biomarker of cell death. Nano-Se could be a novel hepatoprotective strategy to inhibit oxidative stress.

Interactions of lauryl gallate with phospholipid components of biological membranes

The effect of different amounts of lauryl gallate (LG) on properties of the model membranes of phosphatidylcholines (PC), differing in the presence of double bonds in the hydrocarbon chains, and phosphatidylglycerol (PG) was described in terms of phase behaviour of mixtures, interactions between both components, monolayers stability and their organization. The Langmuir monolayer technique was used to monitor the surface thermodynamics (i.e. the excess area and excess Gibbs energy of mixing) on the basis of surface pressure–area per molecule (π–A) isotherms. Simultaneously, morphology of the studied monolayers was visualized by the Brewster angle microscopy (BAM). This allowed evaluating the kind and magnitude of interactions which influence on the phase behaviour and structural properties of the monolayers. The obtained results can be helpful to reveal the mechanism of phospholipid antioxidant protection and important pharmacological (antimicrobial) role of lauryl gallate for production of effective therapeutic substances.

Influence of preparations containing phytoecdysteroids and plant steroid glycosides on the life span and stress resistance of Drosophila melanogaster

The clarification of the molecular mechanisms of the effect of a plant adaptogen’s active substance is a topical study direction. In the present work, we studied the effect of phytopreparations containing the Serratula coronata L. phytoecdysteroids (20-hydroxyecdysone and inocosterone) or the Trigonella foenumgraecum L. steroid glycosides (dioscin and protodioscin) on the expression of stress-response genes, stress resistance, and the life span of the Drosophila melanogaster. It was demonstrated that phytopreparations activate the mechanisms of antioxidant protection (Sod1), but reduce the level of induction of DNA repair (XPF and Rad51) and the apoptosis (Hid) genes. At the same time, the studied phytopreparations have a moderate adaptogenic and geroprotective effects associated with activation of the hormesis mechanisms.

Sisymbrium Officinale (L.) Scop. and its Polyphenolic Fractions Inhibit the Mutagenicity of Tert-Butylhydroperoxide in Escherichia Coli WP2uvrAR Strain.

One Sisymbrium officinale (L.) Scop. aqueous dry extract (SOE) and its polyphenolic fractions (Fb, Fc, Fd and Fe) were evaluated for their ability to inhibit the oxidative mutagenicity of tert-butylhydroperoxide in the Ames test. The possible involvement of desmutagenic and/or bioantimutagenic mechanisms was evaluated by applying a three-time based protocol (pre-treatment, co-treatment and post-treatment). Furthermore, some protective antioxidant mechanisms were investigated. The total polyphenol and flavonol amount was also determined, and the fingerprint was outlined by high-performance thin-layer chromatography and densitometry. SOE, Fb and Fe exhibited strong antimutagenicity against tert-butylhydroperoxide in all treatment protocols, this suggesting the involvement of both desmutagenic and bioantimutagenic mechanisms. These samples also showed antioxidant properties, including neutralization of the superoxide anion, lipid peroxidation inhibition and chelation and reduction of iron. Fb and Fe were rich in polyphenols and flavonols, so suggesting a possible role of these compounds in the antimutagenicity. Taking into account that oxidative stress is responsible for the damage of various environmental toxicants, particularly tobacco smoke, present results can support the traditional use of hedge mustard by smokers to restore the vocal cord function affected by the oxidative damage and suggest a possible application of SOE and its fractions as food supplements. Copyright © 2016 John Wiley & Sons, Ltd.

Inhibition of neuroinflammation in BV2 microglia by the biflavonoid kolaviron is dependent on the Nrf2/ARE antioxidant protective mechanism

Kolaviron is a mixture of biflavonoids found in the nut of the West African edible seed Garcinia kola, and it has been reported to exhibit a wide range of pharmacological activities. In this study, we investigated the effects of kolaviron in neuroinflammation. The effects of kolaviron on the expression of nitric oxide/inducible nitric oxide synthase (iNOS), prostaglandin E2 (PGE2)/cyclooxygenase-2, cellular reactive oxygen species (ROS) and the pro-inflammatory cytokines were examined in lipopolysaccharide (LPS)-stimulated BV2 microglial cells. Molecular mechanisms of the effects of kolaviron on NF-κB and Nrf2/ARE signalling pathways were analysed by immunoblotting, binding assays and reporter assays. RNA interference was used to investigate the role of Nrf2 in the anti-inflammatory effect of kolaviron. Neuroprotective effect of kolaviron was assessed in a BV2 microglia/HT22 hippocampal neuron co-culture. Kolaviron inhibited the protein levels of NO/iNOS, PGE2/COX-2, cellular ROS and the pro-inflammatory cytokines (TNFα and IL-6) in LPS-stimulated microglia. Further mechanistic studies showed that kolaviron inhibited neuroinflammation by inhibiting IκB/NF-κB signalling pathway in LPS-activated BV2 microglia. Kolaviron produced antioxidant effect in BV2 microglia by increasing HO-1 via the Nrf2/antioxidant response element pathway. RNAi experiments revealed that Nrf2 is needed for the anti-inflammatory effects of kolaviron. Kolaviron protected HT22 neurons from neuroinflammation-induced toxicity. Kolaviron inhibits neuroinflammation through Nrf2-dependent mechanisms. This compound may therefore be beneficial in neuroinflammation-related neurodegenerative disorders.

Pigments content in Сhlorella vulgaris under the influence of the sodium selenite and the ions of metals

We investigated the content of pigments in Chlorella vulgaris Beij. (Chlorophyta) under the influence of sodium selenite in concentrations based on Se4+ 0.5, 5.0, 10.0 and 20.0 mg/dm3 during one, three and seven days and under the influence of the simultaneous action of selenite in concentrations 10 mg Se4+/dm3 and ions of Zn2+, Mn2+, Co2+,Cu2+, Fe3+ in concentrations 5.00, 0.25, 0.05, 0.008 and 0.002 mg/dm3over seven days. This research was carried out to establish the conditions for obtaining algal lipidis substance enriched with selenium and biogenic metals in the aquaculture. The content of pigments was determined spectrophotometrically, the cellular walls were separatedby centrifuge in the percoll gradient and investigated microscopically. The pigments content in the Ch. vulgaris increased by 1.5–2.5 times in comparison with the control sample under the influence of 10 mg Se4+/dm3 with and without metal ions, in all variants of experimental influence due to binding of SeО32– with proteins and lipids. We found that selenium was included in all lipid fractions (triacylglycerols, dyacylglycerols, phospholipids, nonetherified fatty acids); the maximum amount of selenium-containing lipids wasrecorded in chloroplasts. The increase in the contents of carotenoids caused by the actions of experimental factors played an exceptional role in the mechanism of antioxidant protection that prevents destruction of chlorophyll and, accordingly, increases its amount in cells. Changes in the functioning of the photosynthetic apparatus of Ch. vulgaris affect the whole complex of metabolic transformation. Thus, the successful cultivation of chlorella, enriched with selenium and biogenic metals, is possible within seven days under the influence of 10 mg Se4+/dm3 and the above-mentioned concentration of metal ions.

The Favorable Effect of Mesenchymal Stem Cell Treatment on the Antioxidant Protective Mechanism in the Corneal Epithelium and Renewal of Corneal Optical Properties Changed after Alkali Burns.

The aim of this study was to examine whether mesenchymal stem cells (MSCs) and/or corneal limbal epithelial stem cells (LSCs) influence restoration of an antioxidant protective mechanism in the corneal epithelium and renewal of corneal optical properties changed after alkali burns. The injured rabbit corneas (with 0.25 N NaOH) were untreated or treated with nanofiber scaffolds free of stem cells, with nanofiber scaffolds seeded with bone marrow MSCs (BM-MSCs), with adipose tissue MSCs (Ad-MSCs), or with LSCs. On day 15 following the injury, after BM-MSCs or LSCs nanofiber treatment (less after Ad-MSCs treatment) the expression of antioxidant enzymes was restored in the regenerated corneal epithelium and the expressions of matrix metalloproteinase 9 (MMP9), inducible nitric oxide synthase (iNOS), α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1), and vascular endothelial factor (VEGF) were low. The central corneal thickness (taken as an index of corneal hydration) increased after the injury and returned to levels before the injury. In injured untreated corneas the epithelium was absent and numerous cells revealed the expressions of iNOS, MMP9, α-SMA, TGF-β1, and VEGF. In conclusion, stem cell treatment accelerated regeneration of the corneal epithelium, restored the antioxidant protective mechanism, and renewed corneal optical properties.

Oxidative stress in Microcystis aeruginosa as a consequence of global climate change

Cyanobacteria are phototrophic organisms with great ecological and economical importance. Species of the genus Microcystis are known for their potential ability to synthesize toxins, notably microcystins. There is a growing interest in the evaluation of oxidative stress in relation to the impact of global climate change on natural ecosystems in different trophic levels. Several studies have focused on the analysis of organismal responses to mitigate the damage by controlling the generation of reactive oxygen species. Variations in environmental factors caused by climate change generate a situation of oxidative damage in Microcystis aeruginosa as a direct or indirect consequence. In this study we evaluate the effects of ultraviolet radiation and temperature on physiological and biochemical responses of a native M. aeruginosa (strain CAAT 2005-3). The results from the exposure to ultraviolet radiation doses and temperature changes suggest a high ability of M. aeruginosa to detect a potential stress situation as a consequence of reactive species production and to rapidly initiate antioxidant defenses. Increased catalase activity is an antioxidant protection mechanism in M. aeruginosa for short and long term exposure to different changes in environmental conditions. However, we found a ultraviolet-B radiation threshold dose above which oxidative stress exceeds the antioxidant protection and damage occurs. In addition our results are in agreement with recent findings suggesting that microcystins may act as protein-modulating metabolites and protection against reactive oxygen species. It is concluded that cyanobacteria have adaptative mechanisms that could lead to the replacement of species highly susceptible to oxidative stress by others with a higher system of antioxidant protection.

Astrocyte-Dependent Vulnerability to Excitotoxicity in Spermine Oxidase-Overexpressing Mouse.

Transgenic mice overexpressing spermine oxidase (SMO) in the cerebral cortex (Dach-SMO mice) showed increased vulnerability to excitotoxic brain injury and kainate-induced epileptic seizures. To investigate the mechanisms by which SMO overexpression leads to increased susceptibility to kainate excitotoxicity and seizure, in the cerebral cortex of Dach-SMO and control mice we assessed markers for astrocyte proliferation and neuron loss, and the ability of kainate to evoke glutamate release from nerve terminals and astrocyte processes. Moreover, we assessed a possible role of astrocytes in an in vitro model of epileptic-like activity in combined cortico-hippocampal slices recorded with a multi-electrode array device. In parallel, as the brain is a major metabolizer of oxygen and yet has relatively feeble protective antioxidant mechanisms, we analyzed the oxidative status of the cerebral cortex of both SMO-overexpressing and control mice by evaluating enzymatic and non-enzymatic scavengers such as metallothioneins. The main findings in the cerebral cortex of Dach-SMO mice as compared to controls are the following: astrocyte activation and neuron loss; increased oxidative stress and activation of defense mechanisms involving both neurons and astrocytes; increased susceptibility to kainate-evoked cortical epileptogenic activity, dependent on astrocyte function; appearance of a glutamate-releasing response to kainate from astrocyte processes due to activation of Ca(2+)-permeable AMPA receptors in Dach-SMO mice. We conclude that reactive astrocytosis and activation of glutamate release from astrocyte processes might contribute, together with increased reactive oxygen species production, to the vulnerability to kainate excitotoxicity in Dach-SMO mice. This mouse model with a deregulated polyamine metabolism would shed light on roles for astrocytes in increasing vulnerability to excitotoxic neuron injury.

In Vitro Protective Effect and Antioxidant Mechanism of Resveratrol Induced by Dapsone Hydroxylamine in Human Cells.

Dapsone (DDS) hydroxylamine metabolites cause oxidative stress- linked adverse effects in patients, such as methemoglobin formation and DNA damage. This study evaluated the ameliorating effect of the antioxidant resveratrol (RSV) on DDS hydroxylamine (DDS-NHOH) mediated toxicity in vitro using human erythrocytes and lymphocytes. The antioxidant mechanism was also studied using in-silico methods. In addition, RSV provided intracellular protection by inhibiting DNA damage in human lymphocytes induced by DDS-NHOH. However, whilst pretreatment with RSV (10–1000 μM significantly attenuated DDS-NHOH-induced methemoglobinemia, but it was not only significantly less effective than methylene blue (MET), but also post-treatment with RSV did not reverse methemoglobin formation, contrarily to that observed with MET. DDS-NHOH inhibited catalase (CAT) activity and reactive oxygen species (ROS) generation, but did not alter superoxide dismutase (SOD) activity in erythrocytes. Pretreatment with RSV did not alter these antioxidant enzymes activities in erythrocytes treated with DDS-NHOH. Theoretical calculations using density functional theory methods showed that DDS-NHOH has a pro-oxidant effect, whereas RSV and MET have antioxidant effect on ROS. The effect on methemoglobinemia reversion for MET was significantly higher than that of RSV. These data suggest that the pretreatment with resveratrol may decrease heme-iron oxidation and DNA damage through reduction of ROS generated in cells during DDS therapy.

Leaf Age-Dependent Photoprotective and Antioxidative Response Mechanisms to Paraquat-Induced Oxidative Stress in Arabidopsis thaliana.

Exposure of Arabidopsis thaliana young and mature leaves to the herbicide paraquat (Pq) resulted in a localized increase of hydrogen peroxide (H2O2) in the leaf veins and the neighboring mesophyll cells, but this increase was not similar in the two leaf types. Increased H2O2 production was concomitant with closed reaction centers (qP). Thirty min after Pq exposure despite the induction of the photoprotective mechanism of non-photochemical quenching (NPQ) in mature leaves, H2O2 production was lower in young leaves mainly due to the higher increase activity of ascorbate peroxidase (APX). Later, 60 min after Pq exposure, the total antioxidant capacity of young leaves was not sufficient to scavenge the excess reactive oxygen species (ROS) that were formed, and thus, a higher H2O2 accumulation in young leaves occurred. The energy allocation of absorbed light in photosystem II (PSII) suggests the existence of a differential photoprotective regulatory mechanism in the two leaf types to the time-course Pq exposure accompanied by differential antioxidant protection mechanisms. It is concluded that tolerance to Pq-induced oxidative stress is related to the redox state of quinone A (QA).

Oxidative damage and antioxidant defense in thymus of malnourished lactating rats

ObjectiveMalnutrition has been associated with oxidative damage by altered antioxidant protection mechanisms. Specifically, the aim of this study was to evaluate oxidative damage (DNA and lipid) and antioxidant status (superoxide dismutase [SOD], glutathione peroxidase [GPx], and catalase [CAT] mRNA, and protein expression) in thymus from malnourished rat pups. MethodsMalnutrition was induced during the lactation period by the food competition method. Oxidative DNA damage was determined quantifying 8-oxo-7, 8-dihydro-2'-deoxyguanosine adduct by high-performance liquid chromatography. Lipid peroxidation was assessed by the formation of thiobarbituric acid-reactive substances. Levels of gene and protein expression of SOD, GPx, and CAT were evaluated by real-time polymerase chain reaction and Western blot, respectively. Antioxidant enzyme activities were measured spectrophotometrically. ResultsOxidative DNA damage and lipid peroxidation significantly increased in second-degree (MN-2) and third-degree malnourished (MN-3) rats compared with well-nourished rats. Higher amounts of oxidative damage, lower mRNA expression, and lower relative concentrations of protein, as well as decreased antioxidant activity of SOD, GPx, and CAT were associated with the MN-2 and MN-3 groups. ConclusionsThe results of this study demonstrated that higher body-weight deficits were related to alterations in antioxidant protection, which contribute to increased levels of damage in the thymus. To our knowledge, this study demonstrated for the first time that early in life, malnutrition leads to increased DNA and lipid oxidative damage, attributable to damaged antioxidant mechanisms including transcriptional and enzymatic activity alterations. These findings may contribute to the elucidation of the causes of previously reported thymus dysfunction, and might explain partially why children and adults who have overcome child undernourishment experience immunologic deficiencies.

Relation between glutathione S-transferase genes (GSTM1, GSTT1, and GSTP1) polymorphisms and clinical manifestations of sickle cell disease in Egyptian patients

ObjectivesClinical manifestations of sickle cell disease (SCD) result from sickling of Hb S due to oxidation, which is augmented by accumulation of oxygen-free radicals. Deficiencies in normal antioxidant protective mechanism might lead to clinical manifestations of SCD like vaso-occlusive crisis (VOC) and acute chest syndrome (ACS). The glutathione system plays an important role in the removal of endogenous products of peroxidation of lipids, thus protecting cells and tissue against damage from oxidative stress. Impairment of the glutathione system due to genetic polymorphisms of glutathione S-transferase (GST) genes is expected to increase the severity of SCD manifestations. This report describes a case control study aimed at studying the ethnic-dependent variation in the frequency of GST gene polymorphisms among participants selected from the Egyptian population and to find out the association between GST gene polymorphisms and the severity of SCD manifestations.MethodsWe measured the frequency distribution of the three GSTs gene polymorphisms in 100 Egyptian adult SCD patients and 80 corresponding controls. GSTM1 and GSTT1 genotypes were determined by multiplex polymerase chain reaction (PCR). GSTP1 genotyping was conducted with a PCR-restriction fragment length polymorphism assay.ResultsThe GSTM1 null genotype was significantly associated with ACS and VOC (P = 0.03 and 0.01, respectively). The GSTT1 null genotype was associated with significantly increased requirement of blood transfusion (P = 0.01). Absence of both GSTM1 and GSTT1 genes was significantly associated with pulmonary hypertension (P = 0.04). The non-wild-type GSTP1 polymorphism was not associated with clinical manifestations of SCD.DiscussionSome GST gene polymorphisms were significantly associated with the worsening of the clinical manifestations of SCD.

Linking phosphorus availability with photo-oxidative stress in plants.

Plants have evolved a plethora of mechanisms to circumvent the potential damaging effects of living under low phosphorus availability in the soil. These mechanisms include different levels of organization, from root-shoot signalling at the whole-plant level to specific biochemical responses at the subcellular level, such as reductions in photosynthesis and the consequent activation of photo- and antioxidant mechanisms in chloroplasts. Some recent studies clearly indicate that severe phosphorus deficiency can lead to alterations in the photosynthetic apparatus, including reductions in CO2 assimilation rates, a down-regulation of photosynthesis-related genes and photoinhibition at the photosystem II level, thus causing potential photo-oxidative stress. Photo-oxidative stress is characterized by an increased production of reactive oxygen species in chloroplasts, which at low concentrations can serve a signalling, protective role, but when present at high concentrations can cause damage to lipids, proteins and nucleic acids, thus leading to irreversible injuries. We discuss here the mechanisms that phosphate-starved plants have evolved to withstand photo-oxidative stress, including changes at the subcellular level (e.g. activation of photo- and antioxidant protection mechanisms in chloroplasts), cellular and tissular levels (e.g. activation of photorespiration and anthocyanin accumulation) and whole-plant level (alterations in source-sink relationships modulated by hormones). Of particular importance is the current evidence demonstrating that phosphate-starved plants activate simultaneous responses at multiple levels, from transcriptional changes to root-shoot signalling, to prevent oxidative damage. In this review, we summarize current knowledge about the occurrence of photo-oxidative stress in phosphate-starved plants and highlight the mechanisms these plants have evolved to prevent oxidative damage under phosphorus limitation at the subcellular, cellular and whole-plant levels.

Genome-based proteomic analysis of Lignosus rhinocerotis (Cooke) Ryvarden sclerotium.

Lignosus rhinocerotis (Cooke) Ryvarden (Polyporales, Basidiomycota), also known as the tiger milk mushroom, has received much interest in recent years owing to its wide-range ethnobotanical uses and the recent success in its domestication. The sclerotium is the part with medicinal value. Using two-dimensional gel electrophoresis coupled with mass spectrometry analysis, a total of 16 non-redundant, major proteins were identified with high confidence level in L. rhinocerotis sclerotium based on its genome as custom mapping database. Some of these proteins, such as the putative lectins, immunomodulatory proteins, superoxide dismutase, and aegerolysin may have pharmaceutical potential; while others are involved in nutrient mobilization and the protective antioxidant mechanism in the sclerotium. The findings from this study provide a molecular basis for future research on potential pharmacologically active proteins of L. rhinocerotis.

Placental Oxidative Status throughout Normal Gestation in Women with Uncomplicated Pregnancies.

The effects of gestational age on placental oxidative balance throughout gestation were investigated in women with uncomplicated pregnancies. Placental tissues were obtained from normal pregnant women who delivered at term or underwent elective pregnancy termination at 6 to 23 + 6 weeks of pregnancy. Placental tissues were analyzed for total antioxidant capacity (TAC) and lipid peroxide (malondialdehyde, MDA) levels using commercially available kits. Two hundred and one placental tissues were analyzed and the mean ± SD MDA (pmol/mg tissue) and TAC (µmol Trolox equivalent/mg tissue) levels for first, second, and third trimester groups were 277.01 ± 204.66, 202.66 ± 185.05, and 176.97 ± 141.61, P < 0.004 and 498.62 ± 400.74, 454.90 ± 374.44, and 912.19 ± 586.21, P < 0.0001 by ANOVA, respectively. Our data reflects an increased oxidative stress in the placenta in the early phase of normal pregnancy. As pregnancy progressed, placental antioxidant protective mechanisms increased and lipid peroxidation markers decreased resulting in diminution in oxidative stress. Our findings provide a biochemical support to the concept of a hypoxic environment in early pregnancy. A decrease in placental oxidative stress in the second and third trimesters appears to be a physiological phenomenon of normal pregnancy. Deviations from this physiological phenomenon may result in placental-mediated disorders.

Activation of antioxidant defenses in whole saliva by psychosocial stress is more manifested in young women than in young men.

Psychosocial stress has been long known to have deleterious effects on health. Nevertheless, an exposure to moderate stressors enhances resilience and promotes health benefits. Male and female organisms differ in many aspects of health and disease. The aim of this study was to investigate antioxidant activity and oxidative damage in saliva in a psychosocial stress paradigm in men and women. Here, we show that an acute stressor of moderate strength augments antioxidant activity and decreases oxidative damage in whole saliva of young people. An examination stress caused a significant increase of catalase activity, accompanied by a decrease of levels of oxidized proteins. Levels of thiobarbituric acid-reacting substances did not increase at stress, indicating that lipid peroxidation was not activated. The stress-induced alterations were more manifested in young women compared to young men. Thus, antioxidant protective mechanisms are more activated by a moderate stressor in young women than in young men.

Studies of the blood antioxidant system and oxygen-transporting properties of human erythrocytes during 105-day isolation

Effects of strict 105-day isolation on the blood antioxidant status, processes in erythrocyte membranes, and oxygen-binding properties of hemoglobin were studied in six male volunteers (25 to 40 years old) in ground-based simulation of a mission to Mars (Mars-105 experiment). The study was performed with venous blood samples and red blood cells isolated from them, which were collected during the baseline data collection period, on days 35, 70, and 105 of the experiment, and on days 7 and 14–15 after its completion. Biochemical (determination of enzyme activity and thin-layer chromatography) and biophysical (laser interference microscopy and Raman spectroscopy) methods showed changes in the relative content of lipid and phospholipid fractions, suggesting an increase in the membrane microviscosity and the content of TBA-RP (active lipid peroxidation products interacting with thiobarbituric acid). A significant increase in the activity of glucose-6-phosphate dehydrogenase and superoxide dismutase and a reduction in the catalase activity was found, which indicates both reparative processes in red blood cells and imbalance between the amount of generated reactive oxygen species and antioxidant protection mechanisms in cells. The hemoglobin affinity for oxygen and the blood level of oxyhemoglobin also increased. It is assumed that the adaptation of the body to stresses experienced during and after the experiment can disturb the balance between the antioxidant defense systems. The latter, in turn, leads to peroxidation of membrane phospholipids, alteration in their content, increase in membrane microviscosity, and eventual disturbance of the gas-exchange function of red blood cells.

Impact of hyperpigmentation on superoxide flux and melanoma cell metabolism at mitochondrial complex II.

Melanogenesis is a highly conserved process of cytophotoprotection from UV radiation present in many species. Although both mitochondrial function and UV radiation insults are well-documented promoters of increased cellular stress, their individual molecular relationships with skin pigmentation have not been clearly resolved. This study provides evidence for a direct relationship between cellular melanin content, superoxide flux, and mitochondrial function at complex II. Direct and significant correlation between increased pigmentation and complex II turnover was observed in genetically different melanoma cell lines of varied basal pigmentation states (P < 0.01). The same trend was also observed when comparing genetically identical cell cultures with increasing levels of induced pigmentation (P < 0.005). The observation of increased steady-state levels of the catalytic complex II succinate dehydrogenase subunit A alongside hyperpigmentation suggested coregulation of activity and pigment production (P < 0.01). The study also presents novel evidence for a relationship between hyperpigmentation and increased superoxide-generating capacity at complex II. By amperometrically monitoring superoxide flux from differently pigmented FM55 melanocytes and their isolated mitochondria, a dynamic and responsive relationship between pigmentation, complex II function, and intracellular superoxide generation was observed (P < 0.005). The data support hyperpigmentation as a protective antioxidant mechanism in response to complex II-mediated reactive oxygen species generation.