Extent Of Oxidative Damage Research Articles

Linking MDA Levels and Blood Glucose in Streptozotocin-Induced Rat Diabetes: Implications for Diabetic Complications and Therapeutic Strategies

Diabetes mellitus is a chronic metabolic disorder characterized by elevated blood glucose levels resulting from insulin deficiency or resistance. Streptozotocin, a potent diabetogenic agent, is commonly employed to induce experimental diabetes by selectively damaging pancreatic beta cells, resulting in insulin deficiency and hyperglycemia. Elevated Malondialdehyde (MDA) levels, indicative of oxidative stress and lipid peroxidation, are closely linked to diabetic complications. This study aimed to investigate the association between MDA levels and blood glucose in Streptozotocin-induced rat diabetes, shedding light on potential therapeutic strategies. Spectrophotometric analysis was utilized to quantify MDA levels in rat tissues, providing insights into the extent of oxidative damage. The results revealed a significant correlation between MDA levels and blood glucose, highlighting the role of oxidative stress in diabetic pathogenesis. These findings underscore the importance of targeting oxidative stress in diabetes management to prevent complications. In conclusion, the study emphasizes the relevance of monitoring MDA levels as a biomarker for assessing oxidative stress in diabetic conditions and guiding therapeutic interventions.

The Occurrence of Oxidative Stress Induced by Silver Nanoparticles in Chlorella vulgaris Depends on the Surface-Stabilizing Agent.

Silver nanoparticles (AgNPs) are of great interest due to their antimicrobial properties, but their reactivity and toxicity pose a significant risk to aquatic ecosystems. In biological systems, AgNPs tend to aggregate and dissolve, so they are often stabilized by agents that affect their physicochemical properties. In this study, microalga Chlorella vulgaris was used as a model organism to evaluate the effects of AgNPs in aquatic habitats. Algae were exposed to AgNPs stabilized with citrate and cetyltrimethylammonium bromide (CTAB) agents and to AgNO3 at concentrations that allowed 75% cell survival after 72 h. To investigate algal response, silver accumulation, ROS content, damage to biomolecules (lipids, proteins, and DNA), activity of antioxidant enzymes (APX, PPX, CAT, SOD), content of non-enzymatic antioxidants (proline and GSH), and changes in ultrastructure were analyzed. The results showed that all treatments induced oxidative stress and adversely affected algal cells. AgNO3 resulted in the fastest death of algae compared to both AgNPs, but the extent of oxidative damage and antioxidant enzymatic defense was similar to AgNP-citrate. Furthermore, AgNP-CTAB showed the least toxic effect and caused the least oxidative damage. These results highlight the importance of surface-stabilizing agents in determining the phytotoxicity of AgNPs and the underlying mechanisms affecting aquatic organisms.

Early time course of oxidative stress in hippocampal synaptosomes and cognitive loss following impaired insulin signaling in rats: Development of sporadic Alzheimer’s disease

Oxidative stress, caused by impaired insulin signaling, plays a pivotal role in the pathogenesis of sporadic Alzheimer’s disease (sAD). We investigated the oxidative stress parameters in the synaptosomes prepared from the hippocampus tissue in order to identify their potential role in sAD development in intraperitoneal (IP) and intracerebroventricular (ICV) streptozotocin (STZ) injections models of insulin signaling impairment. Rats were harvested 1, 3, or 6 weeks post treatment. Spatial learning and memory, several antioxidants and oxidative stress markers were analyzed. Results showed a significant deficit in learning and memory in rats injected with STZ through IP and ICV routes. Glutathione, glutathione/oxidized glutathione, glutathione S-transferase, glutathione peroxidase, glutathione reductase, catalase, superoxide dismutase(SOD)-total, Zn/Cu(SOD), Mn/Fe(SOD) are significantly decreased in IP-STZ and ICV-STZ groups at 1, 3, and 6 weeks after STZ injection. Oxidized glutathione, thiobarbituric acid reactive species, glucose 6-Phosphate dehydrogenase, protein carbonyls, 4-Hydroxynonenal, and 3-Nitrotyrosine are significantly increased in IP-STZ and ICV-STZ groups at 1,3, and 6 weeks after STZ injection. Changes in oxidative stress parameters in ICV-STZ groups are greater than IP-STZ groups. STZ treatment induced cognitive impairments by 3-W and 6-W, and it was significantly correlated with the extent of oxidative damage. In conclusion, STZ administration through ICV route is deleterious in causing early synaptosomal oxidative damage that exacerbated with time and correlated with cognitive impairments. Our data implicate the involvement of oxidative stress as an early feature of sAD and provide insights into the behavioral and biochemical changes over the course of disease development.

Thiol-Disulfide Homeostasis in Skin Diseases.

Oxidative stress represents the imbalance between oxidants and antioxidants and has been associated with a wide range of diseases. Thiols are the most important compounds in antioxidant defense. There is an equilibrium between thiols and their oxidized forms, disulfides, known as dynamic thiol-disulfide homeostasis (TDH). In 2014, Erel and Neselioglu developed a novel automated assay to measure thiol and disulfide levels. Subsequently, many researchers have used this simple, inexpensive and fast method for evaluating TDH in various disorders. We have reviewed the literature on the role of TDH in skin diseases. We identified 26 studies that evaluated TDH in inflammatory diseases (psoriasis, seborrheic dermatitis, atopic dermatitis, vitiligo, acne vulgaris and rosacea), allergic diseases (acute and chronic urticaria) and infectious diseases (warts, pityriasis rosea and tinea versicolor). The results are heterogeneous, but in most cases indicate changes in TDH that shifted toward disulfides or toward thiols, depending on the extent of oxidative damage.

Synthetic Secoisolariciresinol Diglucoside Attenuates Established Pain, Oxidative Stress and Neuroinflammation in a Rodent Model of Painful Radiculopathy.

Painful cervical radiculopathy is characterized by chronic neuroinflammation that lowers endogenous antioxidant responses leading to the development of oxidative stress and pain after neural trauma. Therefore, antioxidants such as secoisolariciresinol diglucoside (SDG), that promote antioxidant signaling and reduce oxidative damage may also provide pain relief. This study investigated if repeated systemic administration of synthetic SDG after a painful root compression reduces the established pain, oxidative stress and spinal glial activation that are typically evident. SDG was administered on days 1–3 after compression and the extent of oxidative damage in the dorsal root ganglia (DRG) and spinal cord was measured at day 7 using the oxidative stress markers 8-hydroxguanosine (8-OHG) and nitrotyrosine. Spinal microglial and astrocytic activation were also separately evaluated at day 7 after compression. In addition to reducing pain, SDG treatment reduced both spinal 8-OHG and nitrotyrosine, as well as peripheral 8-OHG in the DRG. Moreover, SDG selectively reduced glial activation by decreasing the extent of astrocytic but not microglial activation. These findings suggest that synthetic SDG may attenuate existing radicular pain by suppressing the oxidative stress and astrocytic activation that develop after painful injury, possibly identifying it as a potent therapeutic for painful radiculopathies.

Protective effects of vitamin E on aluminium chloride-induced liver and kidney damage in rats

Aluminium is present in many manufactured foods and medicines and is also used in water purification. It is known that aluminium causes oxidative stress. Therefore, the present study was undertaken to determine the effectiveness of vitamin E (VE) in modulating the toxicity of aluminium chloride (AlCl3) on biochemical parameters, antioxidant enzymes and lipid peroxidation in serum and different organs (liver and kidney) of male Wistar rats. 24 rats (150-180g) were divided into four groups of six animals each : control ; Al was administered intraperitoneally (50 mg/kg/bw, one times a week) ; VE was given orally at a daily dose (100 mg/kg/bw) and Al+VE group. The experiment during for 90 days. AlCl3 caused a decreased in body weight consumption along with increased in the absolute and relative liver and kidney weights. TBARS level was increased, and the enzymes activities of CAT and SOD were decreased in liver and kidney of rats treated with AlCl3. While, TBARS was decreased and the antioxidant enzymes were increased in rats treated with VE. The hepatic and renal damage induced by Al was evidenced by a increase in the levels of serum AST, ALT, LDH, ALP, γGT, glucose, urea, creatinine and bilirubin, while total protein and albumin were decreased due to AlCl3 administration. These parameters indicated the extent of oxidative damage in liver and kidney, thus confirming the histology results in these organs. It can be concluded in this study that presence of VE effectively atte-nuated AlCl3 induced hepatotoxicity and nephrotoxicity in rats. It has benefi-cial influences and protective effect against AlCl3 toxicity.

P1146ENHANCED EXPRESSION OF THIOREDOXIN-INTERACTING-PROTEIN (TXNIP) MAY REGULATE OXIDATIVE DAMAGE IN PERITONEAL DIALYSIS PATIENTS

Abstract Background and Aims Glucose-based solutions used as peritoneal dialysis fluids influence the peritoneal membrane. Exposure to high glucose-based peritoneal dialysis solutions induces reactive oxygen species (ROS) production due to upregulation of TXNIP as shown by several studies in rats as well as in human primary cells. Enhanced expression of TXINP also regulates oxidative damage. Therefore the aim of this study was to investigate the expression of TXNIP and the extent of oxidative damage in human peritoneal biopsies. Method Human peritoneal biopsies of healthy controls, PD patients and patients with EPS were collected. TXNIP and thioredoxin-1 (TRX) mRNA expression was determined by qPCR. Protein expression and the extent of oxidative damage were examined by immunohistochemistry. Results Biopsies from the peritoneum of 7 healthy controls, 36 patients on PD without signs of EPS as well as of 12 patients with EPS were collected. The age of the healthy controls was higher (median 64.00 years, IQR: 53.00-70.00) than in the other subgroups (PD: median 60.50 years, IQR: 46.00-69.00 and EPS: median 51.00 years, IQR: 38.00-58.75). Furthermore, compared to the PD- (39 %) and EPS-group (33 %), there were more female participants in the control-group (86 %). Time on PD was longer in EPS patients (median 70.00 months) than in PD patients (median 33.50 months). In a preliminary study, exposure to high glucose-based peritoneal dialysis solutions did not markedly influence the mRNA expression of TXNIP and TRX. However, on protein level a significant glucose-related upregulation of TXNIP could be observed especially in PD patients. Interestingly, there was no glucose-related change in protein expression of its interacting partner and cellular anti-oxidant TRX. To study the effect of TXNIP expression on the generation of oxidative damage, pH2AX positive nuclei were counted on peritoneal membrane sections. A slight increase of pH2AX positive nuclei upon exposure to dialysis solutions could be observed in the cohort analysed. Conclusion Here, we show for the first time a clear tendency for upregulation TXNIP in human peritoneal tissue after exposure to high glucose-based peritoneal dialysis solutions especially in PD patients. This increase in TXNIP expression may correlate with the accumulation of oxidative damage of macromolecules. Therefore, manipulation of TXNIP expression may be a promising therapeutic target to improve peritoneal membrane function.

Malaysian macroalga Padina australis Hauck attenuates high dose corticosterone-mediated oxidative damage in PC12 cells mimicking the effects of depression.

Oxidative damage has been associated with the pathophysiology of depression. Macroalgae are equipped with antioxidant defense system to counteract the effects of free radicals. We explored the use of Malaysian Padina australis to attenuate high dose corticosterone-mediated oxidative damage in a cellular model mimicking depression. Fresh specimen of P. australis was freeze-dried and extracted sequentially with hexanes, ethyl acetate and ethanol. The extracts were screened for their phytochemical contents and antioxidant activities. Ethanol extract demonstrated the most potent antioxidant capacity and was selected for subsequent assays against high dose corticosterone of 600µM-mediated oxidative damage in the rat pheochromocytoma (PC12) cells. The corticosterone reduced the cell viability, glutathione (GSH) level, aconitase activity, and mitochondrial membrane potential (MMP); and increased the lactate dehydrogenase (LDH) release, intracellular reactive oxygen species (ROS) level and apoptosis. However, the extent of oxidative damage was reversed by 0.25-0.5mg/mL ethanol extract suggesting a possible role of P. australis-based antioxidants in the mitochondrial defense against constant ROS generation and regulation of antioxidant pathway. The effects were similar to that of desipramine, a tricyclic antidepressant. Our findings indicate that P. australis can be developed as a mitochondria-targeted antioxidant to mitigate antidepressant-like effects.

Experimental warming induces oxidative stress and immunosuppression in a viviparous lizard, Eremias multiocellata.

Reptiles are especially vulnerable to climate warming because their behavior, physiology, and life history are highly dependent on environmental temperature. In this study, we envisaged new probable mechanisms underlying the high vulnerability of lizards, wherein heat exposure induces oxidative stress and leads to immunosuppression. To test this hypothesis, we conducted a warming experiment on a lizard (Eremias multiocellata) from a desert steppe in Inner Mongolia from May to September using open-top chambers set up in their natural habitat and compared the components of oxidative stress (antioxidant ability [Superoxide dismutase (SOD) activity], extent of oxidative damage [malondialdehyde (MDA) content]), and immunocompetence (white blood cells [WBC] counts and immunoglobulin M [IgM] expression) between the warming and control groups. At the end of the experiment, the warming treatment did not affect the survival rate of the lizards. However, MDA content, but not SOD activity, was significantly higher in the warming group than in the control group. The WBC counts and IgM expression were significantly lower in the warming group than in the control group. Our results verified our hypothesis and provided novel cues and methods for the investigation of the mechanisms behind the high probability of extinction of other ectotherms under warming conditions.

Comparative Evaluation of Oxidative Stress in Type-2 Diabetes Mellitus in Relation to Controlled Vs Uncontrolled Diabetes

Background: Type 2 Diabetes Mellitus (T2DM) is associated with the production of excess free radicals which are not neutralised by available antioxidants thereby, leading to oxidative stress (OS). The extent of oxidative damage and resulting diabetic complications may be determined by the degree of hyperglycemia viz; controlled vs uncontrolled T2DM. Aim: To evaluate and compare oxidative stress in T2DM patients with good glycemic control vs uncontrolled T2DM, by estimating malondialdehyde (MDA, index of lipid peroxidation), ferric acid reducing ability of plasma (FRAP as total antioxidant capacity, TAC). Methods: The study included 50 healthy controls (Gp I) and 100 T2DM patients which were further divided into: Gp II having good glycemic control (HbA1c ≤ 7.0%) and Gp III with uncontrolled T2DM (HbA1c >7.0%)(n=50 each). Fasting & post-prandial plasma glucose, HbA1c, MDA, FRAP & hsCRP were estimated using standard methods. Result: MDA was significantly higher and FRAP was significantly lower in T2DM patients as compared to healthy controls. Further, T2DM patients (Gp III) with uncontrolled hyperglycemia had higher degree of oxidative stress vs Gp II patients with good glycemic control. Moreover there was: i) A significant positive correlation between HbA1c & MDA (p<0.001),& ii) Significant negative correlation between HbA1c & FRAP and MDA & FRAP (p<0.001) in T2DM patients. Conclusion: Oxidative stress in T2DM patients is directly proportional to the degree of hyperglycemia measured as HbA1c.Therefore it is important to maintain tight glycemic control in T2DM patients (HbA1c ≤ 7%), to decrease oxidative stress and thereby delay the onset of diabetic complications.

Pre-treatment with Meloxicam Prevents the Spinal Inflammation and Oxidative Stress in DRG Neurons that Accompany Painful Cervical Radiculopathy

Painful neuropathic injuries are accompanied by robust inflammatory and oxidative stress responses that contribute to the development and maintenance of pain. After neural trauma the inflammatory enzyme cyclooxygenase-2 (COX-2) increases concurrent with pain onset. Although pre-treatment with the COX-2 inhibitor, meloxicam, before a painful nerve root compression prevents the development of pain, the pathophysiological mechanisms are unknown. This study evaluated if pre-treatment with meloxicam prior to painful root injury prevents pain by reducing spinal inflammation and peripheral oxidative stress. Glial activation and expression of the inflammatory mediator secreted phospholipase A2 (sPLA2) in the spinal cord were assessed at day 7 using immunohistochemistry. The extent of oxidative damage was measured using the oxidative stress marker, 8-hydroxyguanosine (8-OHG) and localization of 8-OHG with neurons, microglia and astrocytes in the spinal cord and peripherally in the dorsal root ganglion (DRG) at day 7. In addition to reducing pain, meloxicam reduced both spinal microglial and astrocytic activation at day 7 after nerve root compression. Spinal sPLA2 was also reduced with meloxicam treatment, with decreased production in neurons, microglia and astrocytes. Oxidative damage following nerve root compression was found predominantly in neurons rather than glial cells. The expression of 8-OHG in DRG neurons at day 7 was reduced with meloxicam. These findings suggest that meloxicam may prevent the onset of pain following nerve root compression by suppressing inflammation and oxidative stress both centrally in the spinal cord and peripherally in the DRG.

Exposure to the insecticide endosulfan induces liver morphology alterations and oxidative stress in fruit-eating bats (Artibeus lituratus).

Exposure to pesticides may increase the generation of reactive oxygen species (ROS), leading to oxidation of cell membrane lipids and proteins. Although fruit bats are potentially exposed to pesticides during their entire lifespan, the impacts of this exposure are still poorly investigated. We examined the effects of low, commercially recommended concentrations (0, 1.05 and 2.1g/l) of an organochlorine insecticide endosulfan (EDS) formulation on oxidative responses in the liver and kidneys of Neotropical fruit bats (Artibeus lituratus), as well as possible liver morphological alterations following a 35-day oral exposure. Superoxide dismutase activity was significantly decreased upon exposure to 1.05g/l of EDS in the liver and kidneys, catalase was decreased in the liver of 2.1g/l EDS-exposed bats, while glutathione S-transferase was increased in the liver of 2.1g/l EDS-exposed bats. Protein carbonyls increased following the exposure to the highest EDS dose tested. Endosulfan-induced morphological alterations in the liver included cell degeneration and cell death, with apparent cytoplasm lipid accumulation (steatosis) and pyknotic nuclei, karyolysis and deposit of collagen fibres. Our findings suggest that exposure to low concentrations of EDS induced a certain extent of oxidative damage in fruit bats, which may have led to liver morphological alterations.

Ex vivo analyses of formulated bio-elicitors from a phytopathogen in the improvement of innate immunity in host

Three different bio-elicitors viz. BE 1, BE 2 and BE 3 were formulated from Fusarium oxysporum f. sp. lycopersici. All three elicitors were screened for defence regulating capacity in an ex vivo system where Lycopersicum esculentum was used as a model host plant. Application of bio-elicitors on detached leaves showed varied degrees of defence induction and antioxidative enzymes and total phenol accumulation after 24 h incubation. Among all, BE 3 (2%) was found to be the most effective. Furthermore, production of nitric oxide (NO) was measured in treated leaves, and concurrently, the extent of oxidative damage was evaluated by measuring reactive oxygen species (ROS), malondialdehyde (MDA), proline and total chlorophyll content. All bio-elicitors except BE 3, which was effective at concentrations as low as 2%, showed enhanced production of MDA and proline and reduction in total chlorophyll at higher concentrations. These results suggest that among three elicitors tested, BE 3 (2%) can be used as a potential bio-elicitor in organic tomato farming.

English

Aluminium is present in some manufactured medicines and foods. It is known that aluminium causes oxidative stress. Therefore, the present study was undertaken to determine the effectiveness of Haloxylon salicornicum extract in modulating aluminium chloride (AlCl3) induced oxidative stress in rats. Male rats (40 to 50 g) were divided into four groups of six animals each. The experimental protocol was based on the administration of AlCl3 (30 mg/kg/body weight) intraperitoneally (ip) every 5 days for 15 days. The groups treated with the plant receive daily dose of 0.05 g/kg/body weight. Increased level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), urea, and creatinine in serum indicated hepatic and renal dysfunction. The variation of catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH), and lipid peroxidation (thiobarbituric acid reactive substances, TBARS) were assessed. These parameters indicated the extent of oxidative damage in liver and kidney, thus confirming the histology results in liver and kidney. It was found that the consumption of H. salicornicum extract protects the liver and kidney against aluminium chloride toxicity. The aim of the present study was to evaluate the protective effect of the H. salicornicum extract on the damages caused by administration of aluminium chloride (AlCl3) in young rats. Key words: Aluminum chloride, Wistar rats, Haloxylon salicornicum, lipid peroxidation, superoxide dismutase (SOD), reduced glutathione, catalase.

Estabilización oxidativa del aceite de Sacha inchi (Plukenetia volubilis Linneo) con suspensiones de mortiño (Vaccinium meridionale SW)

&lt;p&gt;El aceite de Sacha inchi (Plukenetia volubilis Linneo)ha sido reconocido a nivel mundial por su alto&lt;br /&gt;contenido de omegas; sin embargo, la presencia en él de ácidos grasos poliinsaturados hace que sea&lt;br /&gt;sustancialmente propenso al deterioro oxidativo. En este trabajo se evaluó el efecto de suspensiones de&lt;br /&gt;mortiño (Vaccinium meridionale SW) a 1000, 1500 y 2000 mg L−1 sobre la estabilidad oxidativa del aceite de Sacha inchi (Plukenetia volubilis Linneo)sometido a condiciones de oxidación aceleradas durante 12 horas (60 °Cy flujo de aire a 1700 mL.min−1). La magnitud del deterioro oxidativo fue monitoreada midiendo la formación de compuestos polares (CP), trienos conjugados (TC) y valor peróxido (VP) del aceite, en presencia y ausencia de la suspensión. Los resultados revelaron que el aditivo es eficaz en la estabilización del aceite de Sacha inchi (Plukenetia volubilis Linneo), de tal manera que concentraciones de 2000 mg L−1 reducen el contenido de compuestos polares, trienos conjugados y valor peróxido en un 92,3%, 71,4% y 47,8%, respectivamente. De otro lado, se determinó el contenido de fenoles totales, flavonoides, taninos condensados y antocianinas de la suspensión de mortiño (Vaccinium meridionale SW), de modo que se caracterizara el poder antioxidante; los resultados demuestran que la suspensión es una fuente excepcional de antioxidantes naturales que serían los responsables de prevenir la oxidación del aceite de Sacha inchi (Plukenetia volubilis Linneo).&lt;/p&gt;

Oxidative stress induced by cadmium in the plasma, erythrocytes and lymphocytes of rats: Attenuation by grape seed proanthocyanidins.

The present study has been designed to investigate the ameliorative effect of grape seed proanthocyanidins (GSP) on cadmium (Cd)-induced oxidative damage in rat erythrocytes. Twenty four male Wistar rats were divided into four groups: control, GSP-treated group (100 mg kg(-1) body weight (BW)), Cd-treated group (cadmium chloride, 5 mg kg(-1) BW), and GSP + Cd-treated group in which GSP was orally pre-administered 90 min before Cd intoxication for 4 weeks. At the end of the experimental period, blood samples were collected by cardiac puncture and were processed for various biochemical estimations. The extent of oxidative damage in isolated rat erythrocyte membrane was assessed by measuring lipid peroxidation, enzymatic and non-enzymatic content, calcium ion (Ca(2+))/magnesium ion (Mg(2+))-ATPase and sodium ion (Na(+))/potassium ion (K(+))-ATPase activities, free iron, calcium, hydrogen peroxide (H2O2) concentration, and osmotic fragility. Our results unveiled that Cd intoxication significantly increased the erythrocyte lipid peroxidation markers and decreased the activity of enzymatic and non-enzymatic markers in erythrocytes. Conversely, GSP pretreatment significantly prevented the decrease in the activities of antioxidant enzymes and membrane-bound ATPases. GSP also restored the levels of iron, calcium, and H2O2 in Cd-treated rats. Conformational changes in erythrocytes of various groups were also determined using morphological and ultrastructural electron microscopic analysis. The findings of our study clearly revealed that GSP affords superior protection against Cd-induced reactive oxygen species generation, lipid peroxidation, and free radical generation in Cd-treated rats, which presumably reflects the ability of this flavonoid to protect erythrocytes and lymphocytes of rats from the toxic effects of Cd.

Chromium toxicity induces oxidative stress in turnip

Effect of chromium (both CrIII and CrVI) were studied on the oxidative damages and the induction of antioxidant defence in turnip. For this purpose turnip (Brassica rapa L.) plants were grown in refined sand under three different sources of chromium, i.e., chromium sulphate (CrIII), potassium chromate (CrVI) and potassium dichromate (CrVI) supplied at 250 µM concentrations for 4, 24 and 168 h (7 days) after 50 days of growth in normal nutrition. The extent of oxidative damage was most in dichromate as it caused a maximum increase in lipid peroxidation and H2O2 concentration in leaves of turnip plants. The growth and biomass of plants decreased, while the levels of chloroplastic pigment and iron increased in plants supplied CrVI (both potassium chromate and potassium dichromate). Exposure of plants to Cr led to increase in Cr concentration, more in the roots than in shoots. Excess supply of Cr (chromium sulphate, potassium chromate and potassium dichromate), though inhibited peroxidase activity (at 4 and 168 h exposure), stimulated catalase, ascorbate peroxidase and superoxide dismutase activities. Localization of different isoforms of APX and SOD on native gels revealed activation of certain isoform in the Cr-treated plants.

Copper-induced intra-specific oxidative damage and antioxidant responses in strains of the brown alga Ectocarpus siliculosus with different pollution histories

Inter- and intra-specific variation in metal resistance has been observed in the ecologically and economically important marine brown macroalgae (Phaeophyceae), but the mechanisms of cellular tolerance are not well elucidated. To investigate inter-population responses of brown seaweeds to copper (Cu) pollution, the extent of oxidative damage and antioxidant responses were compared in three strains of the filamentous brown seaweed Ectocarpus siliculosus, the model organism for the algal class Phaeophyceae that diverged from other major eukaryotic groups over a billion year ago. Strains isolated from locations with different pollution histories (i.e. LIA, from a pristine site in Scotland; REP and Es524 from Cu-contaminated sites in England and Chile, respectively) were exposed to total dissolved Cu concentrations (CuT) of up to 2.4μM (equivalent to 128nM Cu2+) for 10d. LIA exhibited oxidative stress, with increases in hydrogen peroxide (H2O2) and lipid peroxidation (measured as TBARS levels), and decreased concentrations of photosynthetic pigments. Es524 presented no apparent oxidative damage whereas in REP, TBARS increased, revealing some level of oxidative damage. Adjustments to activities of enzymes and antioxidant compounds concentrations in Es524 and REP were strain and treatment dependent. Mitigation of oxidative stress in Es524 was by increased activities of superoxide dismutases (SOD) at low CuT, and catalase (CAT) and ascorbate peroxidase (APX) at all CuT, accompanied by higher levels of antioxidants (ascorbate, glutathione, phenolics) at higher CuT. In REP, only APX activity increased, as did the antioxidants. For the first time evidence is presented for distinctive oxidative stress defences under excess Cu in two populations of a species of brown seaweed from environments contaminated by Cu.

Myocardial creatine levels do not influence response to acute oxidative stress in isolated perfused heart.

BackgroundMultiple studies suggest creatine mediates anti-oxidant activity in addition to its established role in cellular energy metabolism. The functional significance for the heart has yet to be established, but antioxidant activity could contribute to the cardioprotective effect of creatine in ischaemia/reperfusion injury.ObjectivesTo determine whether intracellular creatine levels influence responses to acute reactive oxygen species (ROS) exposure in the intact beating heart. We hypothesised that mice with elevated creatine due to over-expression of the creatine transporter (CrT-OE) would be relatively protected, while mice with creatine-deficiency (GAMT KO) would fare worse.Methods and ResultsCrT-OE mice were pre-selected for creatine levels 20–100% above wild-type using in vivo 1H–MRS. Hearts were perfused in isovolumic Langendorff mode and cardiac function monitored throughout. After 20 min equilibration, hearts were perfused with either H2O2 0.5 µM (30 min), or the anti-neoplastic drug doxorubicin 15 µM (100 min). Protein carbonylation, creatine kinase isoenzyme activities and phospho-PKCδ expression were quantified in perfused hearts as markers of oxidative damage and apoptotic signalling. Wild-type hearts responded to ROS challenge with a profound decline in contractile function that was ameliorated by co-administration of catalase or dexrazoxane as positive controls. In contrast, the functional deterioration in CrT-OE and GAMT KO hearts was indistinguishable from wild-type controls, as was the extent of oxidative damage and apoptosis. Exogenous creatine supplementation also failed to protect hearts from doxorubicin-induced dysfunction.ConclusionsIntracellular creatine levels do not influence the response to acute ROS challenge in the intact beating heart, arguing against creatine exerting (patho-)physiologically relevant anti-oxidant activity.

Does Inoculation with Glomus mosseae Improve Salt Tolerance in Pepper Plants?

A pot experiment was conducted to determine the effects of Glomus mosseae inoculation on growth and some biochemical activities in roots and shoots of pepper (Capsicum annuum L. cv. Zhongjiao 105) plants subjected to four levels of NaCl [0 (control), 25 (low), 50 (medium), and 100 (high) mM] for 30 days, after 30 days of establishment under non-saline conditions. In mycorrhizal (M) plants, root colonization varied from 48 to 16 %. M plants had higher root and shoot dry weight and leaf area compared with non-mycorrhizal (NM) plants. Under salinity stress, M plants accumulated higher amounts of leaf photosynthetic pigments as well as soluble sugar, soluble protein, and total free amino acids in roots and shoots than those of NM plants. In contrast, the accumulation of proline was less intense in M plants than NM plants. Salt stress induced oxidative stress by increasing malondialdehyde (MDA) content; however, the extent of oxidative damage in M plants was less compared with NM plants due to G. mosseae-enhanced activity of superoxide dismutase (SOD) and peroxidase (POD). We concluded that inoculation with G. mosseae improved growth performance and enhanced salt tolerance of pepper plants via improving photosynthetic pigments and the accumulation of organic solutes (except proline), reducing oxidative stress, and enhancing antioxidant activities of the SOD-POD system.