Induction of growth and antioxidant defense mechanisms in Matricaria chamomilla L. callus by vibration

In Vitro Cellular & Developmental Biology - Plant - Effect of sinusoidal vibration on the activity of some antioxidative enzymes, pigments, membrane stability, and total phenolic was...     

Selenium protects sorghum leaves from oxidative damage under high temperature stress by enhancing antioxidant defense system

Oxidative stress is commonly induced when plants are grown under high temperature (HT) stress conditions. Selenium often acts as an antioxidant in plants; however, its role under HT-induced oxidative stress is not definite. We hypothesize that selenium application can partly alleviate HT-induced oxidative stress and negative impacts of HT on physiology, growth and yield of grain sorghum [Sorghum bicolor (L.) Moench]. Objectives of this study were to investigate the effects of selenium on (a) leaf photosynthesis, membrane stability and antioxidant enzymes activity and (b) grain yield and yield components of grain sorghum plants grown under HT stress in controlled environments. Plants were grown under optimal temperature (OT; 32/22 °C daytime maximum/nighttime minimum) from sowing to 63 days after sowing (DAS). All plants were foliar sprayed with sodium selenate (75 mg L^?1) at 63 DAS, and HT stress (40/30 °C) was imposed from 65 DAS through maturity. Data on physiological, biochemical and yield traits were measured. High temperature stress decreased chlorophyll content, chlorophyll a fluorescence, photosynthetic rate and antioxidant enzyme activities and increased oxidant production and membrane damage. Decreased antioxidant defense under HT stress resulted in lower grain yield compared with OT. Application of selenium decreased membrane damage by enhancing antioxidant defense resulting in higher grain yield. The increase in antioxidant enzyme activities and decrease in reactive oxygen species (ROS) content by selenium was greater in HT than in OT. The present study suggests that selenium can play a protective role during HT stress by enhancing the antioxidant defense system.     

Crucial role of peroxiredoxin III in placental antioxidant defense of mice

We observed frequent stillbirth in peroxiredoxin III (PrxIII) knockout maternal mice. Quantitative real time PCR (qRT-PCR) and Western-blot analysis revealed increased oxidative stress in placentas that were deficient in PrxIII. We did not find significant difference between PrxIII knockout maternal mice and wild-type littermates in hematological parameters, fetal number, and embryonic development. Nevertheless, we noticed enhanced expression of PrxI in erythrocytes of pregnant knockout mice. Our results provided in vivo evidence that PrxIII played a crucial role in placental antioxidant defense. Up-regulation of PrxI might provide a compensation that protected erythrocytes against oxidative damage.     

Constitutive differences in antioxidant defense status distinguish alloxan-resistant and alloxan-susceptible mice.

Alloxan (AL), a potent generator of superoxide and hydroxyl radicals, selectively destroys rodent pancreatic beta-cells. Alloxan-susceptible (ALS/Lt) and AL-resistant (ALR/Lt) are inbred mouse strains derived in Japan by inbreeding CD-1 (ICR) mice with concomitant selection for high or low sensitivity to a relatively low AL dose. The present study was undertaken to examine whether resistance was mediated by differences in either systemic or beta-cell antioxidant defense status. Superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), and glutathione peroxidase (GPX) activities were determined in tissues of AL-untreated ALR/Lt and ALS/Lt male mice at 7 weeks of age. Specific activities of pancreatic SOD1, GR, and GPX were significantly increased in ALR/Lt mice compared with ALS/Lt mice. ALR/Lt mice further exhibited higher levels of glutathione in plasma, blood, pancreas, and liver combined with lower constitutive lipid peroxides in serum, liver, and pancreas. These results support the hypothesis that the selection process leading to the development of an AL-resistant mouse strain entailed accumulation of a gene or genes contributing to upregulated antioxidant status.     

Glutathione peroxidase-1 gene knockout on body antioxidant defense in mice

To determine the in vivo role of cellular glutathione peroxidase (E.C.1.11.1.9, GPX1), we challenged the GPX1 knockout [GPX1(-/-)], the GPX1 overexpressing [GPX1(+)], and their respective wild-type (WT) mice of different Se and vitamin E status with acute oxidative stress. After these mice were injected with pro-oxidants paraquat or diquat at 12 to 125 mg/kg of body weight, their survival rate and time were a function of their GPX1 activity levels. The GPX1 protection was associated with attenuation of NADPH and NADH oxidation, protein carbonyl and F(2)-isoprostanes formation, and alanine transaminase release in various tissues, and was irreplaceable by high levels of dietary vitamin E or other selenoproteins. The GPX1 expression was also protective against moderate oxidative stress induced by low levels of paraquat or diquat, particularly in the Se-deficient mice. Alteration of GPX1 expression showed no impact on the expression of other selenoproteins and antioxidant enzymes in unstressed mice. Total Se content in liver of the Se-adequate GPX1(-/-) mice was reduced by 60% the WT controls. In conclusion, normal expression of GPX1 is essential and overexpression of GPX1 is beneficial to protect mice against acute oxidative stress.     

Foliar application of melatonin delay leaf senescence in maize by improving the antioxidant defense system and enhancing photosynthetic capacity under semi-arid regions

Melatonin is an important plant growth regulator which plays a key role in plant growth and development. The objective of the current research was to evaluate the effect of foliar application of melatonin (MF) on photosynthetic efficiency, antioxidant defense mechanism, and its relation with leaf senescence in maize crop grown in a semi-arid region. A field experiment was conducted during 2017 and 2018 growth season, where melatonin was applied to the foliage at concentrations of 0 (MF₀), 25 (MF₁), 50 (MF₂), and 75 (MF₃) μM at the ninth leaf stage. Foliar application of melatonin significantly improved chlorophyll content, net photosynthetic rate, soluble sugar content, and soluble protein content during the process of leaf senescence. The application of melatonin also enhanced antioxidant enzyme activities including superoxide dismutase, catalase, and peroxidase, while reduced malondialdehyde and reactive oxygen species accumulation. Melatonin foliar application also increased total leaf area per plant, grains per ear, thousand grain weight and grain yield of maize crop in a semi-arid region. The application of melatonin significantly improved photosynthetic activity, antioxidant defense mechanism, and yield of maize crop in a semi-arid region, where the most effective treatment was MF2.

     

Participation of cholinergic mechanisms in realizing the effects of bicuculline]

Screening and electrophysiological methods were applied to the verification of the hypothesis on a possibility of participation of cholinergic structures in the realization of bicucullin effects. M- and N-cholinolytics (benactizine, atropine, aprophen, and pediphen) failed to arrest the convulsions induced in mice by bicucullin adminstration. At the same time substances inducing accumulation of gamma-aminobutyric acid (GABA) in the brain, i.e. aminooxycetic acid and depakin produced a manifest protective action in convulsions caused by bicucullin administration. In electrophysiological experiments there was also revealed an incapacity of M-cholinolytic benaltizine to arrest the bicucullin effects. Bicucullin proved to diminish depression of the test response in the restoration cycle of the primary response of the rat sensory motor cortex at the intervals of 40--125ms between the stimuli, whereas benactizine decreased the late facilitation of the test response at the intervals of 150--300ms between the stimuli. There was also noted no interaction between benactizine and bicucullin by this test. On the basis of these data a conclusion was drawn that bicucullin effects were caused by the block of postsynaptic GABA receptors, and were not connected with the cholinergic structures activity.     

Taurine protects the antioxidant defense system in the erythrocytes of cadmium treated mice

The present study was undertaken to investigate the protective role of taurine (2-aminoethanesulfonic acid) against cadmium (Cd) induced oxidative stress in murine erythrocytes. Cadmium chloride (CdCl(2)) was chosen as the source of Cd. Experimental animals were treated with either CdCl(2) alone or taurine, followed by Cd exposure. Cd intoxication reduced hemoglobin content and the intracellular Ferric Reducing/Antioxidant Power of erythrocytes, along with the activities of antioxidant enzymes, glutathione content, and total thiols. Conversely, intracellular Cd content, lipid peroxidation, protein carbonylation, and glutathione disulphides were significantly enhanced in these cells. Treatment with taurine before Cd intoxication prevented the toxin-induced oxidative impairments in the erythrocytes of the experimental animals. Overall, the results suggest that Cd could cause oxidative damage in murine erythrocytes and that taurine may play a protective role in reducing the toxic effects of this particular metal.     

Megakaryocytopoiesis in culture: modulation by cholinergic mechanisms

Treatment of murine bone marrow cultures with the cholinergic agonist carbamylcholine enhanced megakaryocytic colony growth by as much as 65%. In contrast, adrenergic agonists had no such effect. Addition to cultures of dibutyryl cyclic GMP (db-cGMP) also enhanced megakaryocytic colonies up to 50%, whereas dibutyryl cyclic AMP (db-cAMP) had no effect. Sodium nitroprusside and sodium nitrite, putative guanyl cyclase activators, also enhanced colony numbers, as did imidazole, a postulated cGMP phosphodiesterase inhibitor. Preincubation of marrow for two hours with carbamylcholine resulted both an increase in colony numbers (58%) and percent of progenitors in DNA synthesis (48%, compared to 14% for controls) as determined by tritiated thymidine suicide studies. Treatment of mice with the acetylcholinesterase inhibitor neostigmine resulted in an increase in CFU-M/humerus (62%) and percent in DNA synthesis (45%). These data indicate that 1) cholinergic, but not adrenergic, agonists modulate megakaryocytopoiesis in culture; 2) this effect may be mediated by cyclic GMP; and 3) only a brief period of exposure of marrow cells to agonist results in enhancement of megakaryocytic colonies.     

Peroxiredoxins in antioxidant defense and redox regulation

Peroxiredoxins constitute a family of peroxidases that lack prosthetic groups or catalytically active heteroatoms. Instead, their peroxidatic activity is due to a strictly conserved cysteine that is activated within a novel catalytic triad in which the cysteine thiol is coordinated to an arginine and a threonine or serine residue. Donor substrates are thiol compounds which differ between subtypes of peroxiredoxins and species. In pathogenic trypanosomatids that lack heme- or seleno-peroxidases peroxiredoxins have been shown to represent the major devices to detoxify hydroperoxides and an equivalent role may be assumed for other protozoal parasites and many bacterial pathogens. In mammals equipped with more efficient peroxidases the peroxiredoxins appear to be responsible for the redox regulation of diverse metabolic processes. The substantial differences in the cosubstrate requirements of the peroxiredoxins of pathogenic microorganisms and their mammalian host may be exploited to selectively inhibit the antioxidant defense of pathogens. Thereby, the pathogen would be more readily eliminated by the innate immune response of the host's phagocytes.     

Complementary antioxidant defense by cytoplasmic and mitochondrial peroxiredoxins in Leishmania infantum

In Kinetoplastida 2-Cys peroxiredoxins are the ultimate members of unique enzymatic cascades for detoxification of peroxides, which are dependent on trypanothione, a small thiol specific to these organisms. Here we report on two distinct Leishmania infantum peroxiredoxins, LicTXNPx and LimTXNPx, that may be involved in such a pathway. LicTXNPx, found in the cytoplasm, is a typical 2-Cys peroxiredoxin encoded by LicTXNPx, a member of a multicopy gene family. LimTXNPx, encoded by a single copy gene, LimTXNPx, is confined to the mitochondrion and is unusual in possessing an Ile-Pro-Cys motif in the distal redox center, replacing the common peroxiredoxin Val-Cys-Pro sequence, apart from an N-terminal mitochondrial leader sequence. Based on sequence and subcellular localization, the peroxiredoxins of Kinetoplastida can be separated in two distinct subfamilies. As an approach to investigate the function of both peroxiredoxins in the cell, L. infantum promastigotes overexpressing LicTXNPx and LimTXNPx were assayed for their resistance to H(2)O(2) and tert-butyl hydroperoxide. The results show evidence that both enzymes are active as peroxidases in vivo and that they have complementary roles in parasite protection against oxidative stress.     

The effects of alpha 1-adrenergic and muscarinic cholinergic stimulation on prostaglandin release by rabbit iris

We have investigated the effects of norepinephrine (NE) and acetylcholine (ACh) on prostaglandin (PGE2 and 6 keto-PGF1 alpha) production by rabbit iris, measured by radioimmunoassay (RIA), and the type of phospholipase activated by NE in irides in which phosphatidylinositol (PI) was doubly prelabeled with [3H] myo-inositol and [1-14C] arachidonic acid (14C-AA), quantitated by radiometric and chromatographic methods. PGE2 output in 60 min (3.6 micrograms/g tissue) was 2.6 times greater than 6 keto-PGF1 alpha. PG production is time-dependent and it is stimulated by NE and ACh in a dose-dependent manner. The NE- and ACh-induced release of PGE2, measured by RIA, is mediated through alpha 1-adrenergic and muscarinic cholinergic receptors, respectively, and it requires Ca2+ for maximal stimulation. Studies on the mechanism of AA release from PI in irides doubly prelabeled with 14C-AA and [3H] myo-inositol revealed the following: (a) Both NE and ACh increased the breakdown of PI, and this was accompanied by a significant increase in the release of AA and consequently PGE2. The stimulatory effects of NE and ACh are mediated through alpha 1-adrenergic and muscarinic cholinergic receptors respectively. (b) The NE-induced formation of 3H-lyso PI and the NE-induced metabolism of 14C-1,2-diacyl-glycerol (DG) are time-dependent. Two pathways for AA release from PI are probably operative in the iris: (a) An indirect release by PI-specific phospholipase C which produces DG, followed by the actions of DG- and monoacylglycerol lipases on DG to release AA. (b) A direct release by phospholipase A2. Whether lyso PI is a product of the polyphosphoinositide response remains to be established. Other phospholipids such as phosphatidylcholine and phosphatidylethanolamine could also serve as a source for AA in PG synthesis. In conclusion, the data presented provide evidence that in the iris the neuro-transmitter-stimulated release of PG and AA, from phosphoinositides, for PG synthesis is coupled to the activation of alpha 1-adrenergic and muscarinic cholinergic receptors.     

Restoration of host defense mechanisms in man by levamisole

Levamisole, a broad-spectrum anthelmintic, increased the delayed hypersensitivity skin reaction to tuberculin and to DNCB in about one third of the patients. Levamisole and the racemate tetramisole temporarily increased serum antibody titres in response to vaccination against influenza.     

Neuroprotective effects of zinc on antioxidant defense system in lithium treated rat brain

With a view to find out whether zinc affords protection against lithium toxicity the activities of antioxidant enzymes and lipid peroxidation profile were determined in the cerebrum and cerebellum of lithium treated female Sprague Dawley rats. Lipid peroxidation was significantly increased in both the cerebrum and the cerebellum of animals administered with lithium for a total duration of 4 months as compared to the normal control group. On the contrary, the activities of catalase and glutathione-s-transferase (GST) were significantly reduced after 4 months of lithium treatment. The activity of superoxide dismutase (SOD) was significantly increased in the cerebrum after 4 months lithium administration, whereas in the cerebellum the enzyme activity was unaffected. No significant change in the levels of reduced glutathione (GSH) was found in either cerebrum or cerebellum after 2 months of lithium treatment. However, 4 months lithium treatment did produce significant changes in GSH levels in the cerebrum and in the cerebellum. Zinc supplementation for 4 months in lithium-treated rats significantly increased the activities of catalase and GST in the cerebellum, showing that the treatment with zinc reversed the lithium induced depression in these enzyme activities. Though, zinc treatment tended to normalize the SOD activity in the cerebrum yet it was still significantly higher in comparison to normal levels. From the present study, it can be concluded that the antiperoxidative property of zinc is effective in reversing the oxidative stress induced by lithium toxicity in the rat brain.     

Effect of drugs influencing central serotonergic mechanisms on pentazocine-induced catalepsy in mice

Cataleptic effect of pentazocine in mice was affected by pretreatment with dexfenfluramine, fluoxetine, buspirone, p-chlorophenylalanine, cyproheptadine, mianserin, cisapride, ondansetron, pindolol and propranolol. The results suggest that drugs which influence the activity of central serotonergic systems do modulate pentazocine-induced catalepsy in mice.     

Cooperative action of antioxidant defense systems in Drosophila

Molecular oxygen is key to aerobic life but is also converted into cytotoxic byproducts referred to as reactive oxygen species (ROS). Intracellular defense systems that protect cells from ROS-induced damage include glutathione reductase (GR), thioredoxin reductase (TrxR), superoxide dismutase (Sod), and catalase (Cat). Sod and Cat constitute an evolutionary conserved ROS defense system against superoxide; Sod converts superoxide anions to H(2)O(2), and Cat prevents free hydroxyl radical formation by breaking down H(2)O(2) into oxygen and water. As a consequence, they are important effectors in the life span determination of the fly Drosophila. ROS defense by TrxR and GR is more indirect. They transfer reducing equivalents from NADPH to thioredoxin (Trx) and glutathione disulfide (GSSG), respectively, resulting in Trx(SH)(2) and glutathione (GSH), which act as effective intracellular antioxidants. TrxR and GR were found to be molecularly conserved. However, the single GR homolog of Drosophila specifies TrxR activity, which compensates for the absence of a true GR system for recycling GSH. We show that TrxR null mutations reduce the capacity to adequately protect cells from cytotoxic damage, resulting in larval death, whereas mutations causing reduced TrxR activity affect pupal eclosion and cause a severe reduction of the adult life span. We also provide genetic evidence for a functional interaction between TrxR, Sod1, and Cat, indicating that the burden of ROS metabolism in Drosophila is shared by the two defense systems.     

Green tea extract attenuates hepatic steatosis by decreasing adipose lipogenesis and enhancing hepatic antioxidant defenses in ob/ob mice

Excess hepatic lipid accumulation and oxidative stress contribute to nonalcoholic fatty liver disease (NAFLD). Thus, we hypothesized that the hypolipidemic and antioxidant activities of green tea extract (GTE) would attenuate events leading to NAFLD. Obese mice (ob/ob; 5 weeks old, n=38) and their lean littermates (n=12) were fed 0%, 0.5% or 1% GTE for 6 weeks. Then, hepatic steatosis, oxidative stress and inflammatory markers were measured. Obese mice, compared to lean controls, had greater hepatic lipids and serum alanine aminotransferase (ALT). GTE at 1% lowered (P<.05) hepatic lipids and ALT in obese mice. The GTE-mediated attenuation in hepatic steatosis was accompanied by decreased mRNA expression of adipose sterol regulatory element-binding protein-1c, fatty acid synthase, stearoyl CoA desaturase-1, and hormone-sensitive lipase and decreased serum nonesterified fatty acid concentrations. Immunohistochemical data indicated that steatotic livers from obese mice had extensive accumulation of tumor necrosis factor-α (TNF-α), whereas GTE at 1% decreased hepatic TNF-α protein and inhibited adipose TNF-α mRNA expression. Hepatic total glutathione, malondialdehyde and Mn- and Cu/Zn-superoxide dismutase activities in obese mice fed GTE were normalized to the levels of lean littermates. Also, GTE increased hepatic catalase and glutathione peroxidase activities, and these activities were inversely correlated with ALT and liver lipids. Collectively, GTE mitigated NAFLD and hepatic injury in ob/ob mice by decreasing the release of fatty acids from adipose and inhibiting hepatic lipid peroxidation as well as restoring antioxidant defenses and decreasing inflammatory responses. These findings suggest that GTE may be used as an effective dietary strategy to mitigate obesity-triggered NAFLD.     

Neuroprotective effects of scutellarin against hypoxic-ischemic-induced cerebral injury via augmentation of antioxidant defense capacity

An increasing number of studies has indicated that hypoxic-ischemic-induced cerebral injury is partly mediated via oxidative stress. Recent researches have focused on searching for drug and herbal manipulations to protect against hypoxic-ischemic-induced oxidative cell damage. Scutellarin is a flavonoid derived from the Erigeron breviscapus (vant.) and has been reported to exhibit neuroprotective properties. However, its precise mechanism, particularly its antioxidation mechanism, remains elusive. In the present study, we investigated the neuroprotective effects of scutellarin on middle cerebral artery occlusion (MCAO)-induced brain damage in rats, and oxygen-glucose deprivation (OGD)-induced toxicity in primary culture of rat cortical neurons. In vivo, intraperitoneal injections of scutellarin (20 and 60 mg/kg) improved the neurological score and diminished the percentage of brain infarct volume. At the same time, scutellarin significantly increased superoxide dismutase (SOD), catalase (CAT) activities and glutathione (GSH) level in ischemic brain tissues, enhancing endogenous antioxidant activity. Moreover, pretreatment of scutellarin (25, 50 and 100 μM) protected neurons against lethal stimuli, decreased the percentage of apoptotic cells and inhibited reactive oxygen species (ROS) generation in OGD-induced primary cortical neurons in vitro. These results suggest that the preventive and therapeutic potential of scutellarin in cerebral injury patients is, at least in part, ascribed to augmentation of cellular antioxidant defense capacity.     

The mechanisms of defense and dreaming.

This study examined the degree to which the phenomenological experience of dream intensity and its components are correlated with repression, splitting, and other defense mechanisms. The Dream Intensity Scale, Marlowe-Crowne Social Desirability Scale, Splitting Scale, Defense Style Questionnaire-40, and other related measures were administered to 583 subjects. It is demonstrated that repression as a personality trait is inversely and moderately related to the quantitative aspect of dream intensity (i.e., frequencies of dream awareness, nightmares, and multiple dreams in a single night) but does not influence qualitative sensory experiences in dreams (e.g., hearing sounds in dreams). Moreover, the present findings indicate that the more repressed people are, the less likely they are to report splitting and immature defenses, and the less frequently they experience dreams, with the effect of repression on defenses being greater than that on dream intensity. Accordingly, if both dreams and defense mechanisms are the critical materials to work through in a treatment, then starting with the former may be conducive to the therapeutic progress by provoking less resistance from the client. (PsycINFO Database Record (c) 2011 APA, all rights reserved)