Mn-superoxide Dismutase Activity Research Articles

Oxidative Stress Markers and Histopathological Changes in Selected Organs of Mice Infected with Murine Norovirus 1 (MNV-1).

This paper describes the effects of murine norovirus (MNV) infection on oxidative stress and histopathological changes in mice. This study uses histopathological assays, enzymatic and non-enzymatic antioxidant markers, and total oxidative status and capacity (TOS, TAC). The results suggest that MNV infection can lead to significant changes with respect to the above-mentioned parameters in various organs. Specifically, reduced superoxide dismutase (SOD), Mn superoxide dismutase (MnSOD), catalase (CAT), and glutathione reductase (GR) activities were observed in liver tissues, while higher MnSOD activity was observed in kidney tissues of MNV-infected mice when compared to the control. GR activity was lower in all tissues of MNV-infected mice tested, with the exception of lung tissue. This study also showed that norovirus infection led to increased TOS levels in the brain and liver and TAC levels in the brain, while TOS levels were significantly reduced in the kidneys. These changes may be due to the production of reactive oxygen species (ROS) caused by the viral infection. ROS can damage cells and contribute to oxidative stress. These studies help us to understand the pathogenesis of MNV infection and its potential effects on oxidative stress and histopathological changes in mice, and pave the way for further studies of the long-term effects of MNV infection.

Effects of dietary manganese supplementation on the growth performance, tissue manganese content and antioxidant capacity of coho salmon (Oncorhynchus kisutch) post-smolts

A 10-week growth trial was carried out to study the impact of dietary manganese (Mn) level on growth, tissue Mn content and anti-oxidative capacity of coho salmon (Oncorhynchus kisutch) post-smolts (186.51 ± 1.43 g). Six iso-nitrogenous (42.40% Protein) and iso-lipidic (10.27% Lipid) purified diets based on casein-gelatin were formulated to contain varied graded (MnSO4·H2O as a Mn source) levels of 0.40, 9.50, 16.80, 25.80, 33.40 and 41.20 Mn mg/kg. Fish were reared in a freshwater flow-through rearing system and fed to apparent satiation 3 times daily. No significant effects were found on the survival rate, morphological indices, whole-body proximate composition (p > .05) among the groups. However, higher dietary Mn supplementation level than 25.80 mg/kg improved the growth performance, increased the deposition of Mn in whole-body and vertebral, improved hepatic digestive enzyme activity, enhanced anti-oxidative enzyme activities, and decreased the malondialdehyde content in liver and serum (p < .05). Hepatic and serum total antioxidant capacity, glutathione peroxidase, glutathione reductase, total superoxide dismutase, Mn-superoxide dismutase and catalase activities were enhanced with increasing level of dietary Mn, and then stabilized when dietary Mn level up to 25.80 mg/kg. Using the cubic analysis (based on specific growth rate and feed conversion ratio), the optimal dietary Mn levels were 33.25 and 29.55 mg/kg, respectively. Using the broken-line analysis (based on the deposition of Mn, Mn-superoxide dismutase in liver and serum), the dietary Mn requirements of coho salmon post-smolts were estimated to be 24.52, 26.34, 24.74 and 26.05 mg/kg, respectively.

Effects of a manganese complex with lysine and glutamic acid on growth performance, manganese deposition, and emission, antioxidant capacity and metacarpal strength in weaned piglets.

The present study sought to assess the effects of manganese complexes with lysine and glutamic acid (Mn-LG) as manganese (Mn) sources on growth performance, trace element deposition, antioxidant capacity, and metacarpal strength in weaned piglets. The study involved 288 healthy Duroc × Landrace × Yorkshire piglets that were weaned at 25 to 28 d of age and weighed 8.66 ± 0.96kg. These piglets were randomly divided into six groups: a control group (Mn-LG-0, receiving a basal diet without Mn supplementation), a Mn sulfate group (basal diet supplemented with 40 mg·kg-1 diet of Mn, Mn-S-40 group), and four Mn-LG groups (Mn-LG-20, Mn-LG-40, Mn-LG-60, Mn-LG-80, supplemented with 20, 40, 60, and 80 mg·kg-1 Mn from Mn-LG in the basal diet). Grouping began at weaning on the 0th day of the experiment. The corn-soybean-based basal diet during the early (days 0 to 14) and late (days 15 to 42) phases of the experiment contained 20.88 and 30.12 mg·kg-1 Mn, respectively. Blood samples were collected on days 14 and 42, and pigs were sacrificed for sample collection on day 42. The results indicated no significant differences in average daily gain, average daily feed intake, or feed-to-gain ratio among the groups (P > 0.05). The diarrhea rates of all Mn-LG groups and the Mn-S-40 group were significantly lower in the 0 to 14 d and during the entire experimental period than in the Mn-LG-0 group (P < 0.001). The Mn-LG-40 group exhibited a significant increase in liver Mn concentration and serum Mn superoxide dismutase (Mn-SOD) activity on day 42 (P < 0.01), as well as a significant decrease in fecal Mn concentration (P < 0.05), compared to those of the Mn-S-40 group. Significant differences (P < 0.05) were detected in the serum, liver, and fecal Mn concentrations, as well as in the serum and liver Mn-SOD activity, across the different Mn-LG groups. The serum and fecal Mn concentrations and serum Mn-SOD activity increased linearly or quadratically (P < 0.01) with increasing Mn-LG supplementation. No significant differences (P > 0.05) were found in kidney, heart, or metacarpal bone Mn concentrations or in bone strength indices. In summary, compared with the Mn-LG-0 diet, dietary supplementation with Mn-LG enhanced serum Mn deposition and Mn-SOD activity and decreased the incidence of diarrhea. Additionally, the fecal Mn concentration was lower in the Mn-LG group than in the inorganic group at equivalent dosages.

Evaluation of the Effect of Dietary Manganese on the Intestinal Digestive Function, Antioxidant Response, and Muscle Quality in Coho Salmon.

Manganese (Mn) is a nutritional element required for fish growth and physiology functions. In this study, we examined the effect of Mn on the intestinal digestive function, antioxidant response, and muscle quality in coho salmon (Oncorhynchus kisutch). Nine hundred salmons with initial weight approximately 0.35 g were fed with six isoproteic and isoenergetic diets formulated to contain 2.4, 8.5, 14.8, 19.8, 24.6, and 33.7 mg/kg Mn for 84 days. The result showed that the activity of trypsin and lipase was elevated, whereas α-amylase activity was not affected by various Mn diets in intestine. Dietary Mn elevated the activity of Mn-superoxide dismutase (Mn-SOD), total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-PX), and catalase (CAT), but had no influence on copper/zinc-superoxide dismutase (Cu/Zn-SOD) in intestine. Dietary Mn at 8.5, 14.8, 19.8, 24.6, and 33.7 mg/kg enhanced the gene expression level of protein kinase B (Akt) and mammalian target of rapamycin (mTOR). In addition, the accumulation of Mn in muscle was enhanced with increasing levels of dietary Mn. Dietary Mn elevated the content of sodium (Na), potassium (K), magnesium (Mg), and calcium (Ca), but the content of iron (Fe) and Zn was decreased by dietary Mn in the salmon muscle. The content of fatty acids and amino acids was enhanced by various levels of dietary Mn in muscle. Moreover, a significant quadratic effect was observed on the texture of salmon muscle. The dietary Mn requirement was 16.9-25.7 mg/kg Mn to acquire the highest value of muscle texture using the quadratic regression model. The diets at 14.8 and 19.8 mg/kg Mn had a higher score of sensory evaluation for raw muscle. Our result showed that dietary Mn affected the intestinal digestion function and antioxidant response, which may further result in the change of muscle quality in coho salmon. The result will provide reference for detecting the effect of dietary micronutrients on the muscle quality of salmons.

PD98059 protects SH-SY5Y cells against oxidative stress in oxygen-glucose deprivation/reperfusion.

Mitochondria play a key role in the cerebral ischemia-reperfusion injury. Although the extracellular signal-regulated kinase 1/2 inhibitor PD98059 (PD) is a selective and reversible flavonoid that can protect the mitochondria in a rat model of cardiac arrest/cardiopulmonary resuscitation, its role requires further confirmation. In this study, we investigated whether PD could maintain mitochondrial homeostasis and decrease reactive oxygen species (ROS) production in neuroblastoma (SH-SY5Y) cells exposed to oxygen-glucose deprivation/reperfusion (OGD/R). PD improved the mitochondrial morphology and function, reversed the increase in ROS production and cell apoptosis, and reduced total-superoxide dismutase and Mn-superoxide dismutase activities induced by OGD/R. PD decreases ROS production and improves mitochondrial morphology and function, protecting SH-SY5Y cells against OGD/R-induced injury.

Antioxidant and drought-acclimation responses in UV-B-exposed transgenic Nicotiana tabacum displaying constitutive overproduction of H2O2.

Hydrogen peroxide (H2O2) is an important molecule that regulates antioxidant responses that are crucial for plant stress resistance. Exposure to low levels of ultraviolet-B radiation (UV-B, 280-315nm) can also activate antioxidant defenses and acclimation responses. However, how H2O2 and UV-B interact to promote stress acclimation remains poorly understood. In this work, a transgenic model of Nicotiana tabacum cv Xanthi nc, with elevated Mn-superoxide dismutase (Mn-SOD) activity, was used to study the interaction between the constitutive overproduction of H2O2 and a 14-day UV-B treatment (1.75kJm-2 d-1 biologically effective UV-B). Subsequently, these plants were subjected to a 7-day moderate drought treatment to evaluate the impact on drought resistance of H2O2- and UV-dependent stimulation of the plants' antioxidant system. The UV-B treatment enhanced H2O2 levels and altered the antioxidant status by increasing the epidermal flavonol index, Trolox Equivalent Antioxidant Capacity, and catalase, peroxidase and phenylalanine ammonia lyase activities in the leaves. UV-B also retarded growth and suppressed acclimation responses in highly H2O2-overproducing transgenic plants. Plants not exposed to UV-B had a higher drought resistance in the form of higher relative water content of leaves. Our data associate the interaction between Mn-SOD transgene overexpression and the UV-B treatment with a stress response. Finally, we propose a hormetic biphasic drought resistance response curve as a function of leaf H2O2 content in N. tabacum cv Xanthi.

The role of manganese in morphogenesis and pathogenesis of the opportunistic fungal pathogen Candida albicans.

Metals such as Fe, Cu, Zn, and Mn are essential trace nutrients for all kingdoms of life, including microbial pathogens and their hosts. During infection, the mammalian host attempts to starve invading microbes of these micronutrients through responses collectively known as nutritional immunity. Nutritional immunity for Zn, Fe and Cu has been well documented for fungal infections; however Mn handling at the host-fungal pathogen interface remains largely unexplored. This work establishes the foundation of fungal resistance against Mn associated nutritional immunity through the characterization of NRAMP divalent metal transporters in the opportunistic fungal pathogen, Candida albicans. Here, we identify C. albicans Smf12 and Smf13 as two NRAMP transporters required for cellular Mn accumulation. Single or combined smf12Δ/Δ and smf13Δ/Δ mutations result in a 10-80 fold reduction in cellular Mn with an additive effect of double mutations and no losses in cellular Cu, Fe or Zn. As a result of low cellular Mn, the mutants exhibit impaired activity of mitochondrial Mn-superoxide dismutase 2 (Sod2) and cytosolic Mn-Sod3 but no defects in cytosolic Cu/Zn-Sod1 activity. Mn is also required for activity of Golgi mannosyltransferases, and smf12Δ/Δ and smf13Δ/Δ mutants show a dramatic loss in cell surface phosphomannan and in glycosylation of proteins, including an intracellular acid phosphatase and a cell wall Cu-only Sod5 that is key for oxidative stress resistance. Importantly, smf12Δ/Δ and smf13Δ/Δ mutants are defective in formation of hyphal filaments, a deficiency rescuable by supplemental Mn. In a disseminated mouse model for candidiasis where kidney is the primary target tissue, we find a marked loss in total kidney Mn during fungal invasion, implying host restriction of Mn. In this model, smf12Δ/Δ and smf13Δ/Δ C. albicans mutants displayed a significant loss in virulence. These studies establish a role for Mn in Candida pathogenesis.

Physiological and biochemical responses to caffeine and microplastics in Mytilus galloprovincialis

Caffeine (Caff) is one of the most widely used substances in the human diet and a well-recognized drug. Its input into surface waters is remarkable, but biological effects on aquatic organisms are unclear, particularly in combination with pollutants of suspected modulatory activity, like microplastics (MP). The aim of this study was to reveal the impact on the marine mussel Mytilus galloprovincialis (Lamark, 1819) of Caff (20.0 μg L−1) in the environmentally relevant combination (Mix) with MP 1 mg L−1 (size 35–50 μm) after the exposure for 14 days. Untreated and exposed to Caff and MP separately groups were also examined. Cell viability and cell volume regulation in hemocytes and digestive cells, as well as the indexes of oxidative stress, glutathione (GSH/GSSG) and metallothioneins levels, and caspase-3 activity in digestive gland were assessed. MP and Mix reduced Mn-superoxide dismutase, catalase, and glutathione S-transferase activities and level of lipid peroxidation, but increased the digestive gland cell viability, GSH/GSSG ratio (by 1.4–1.5-fold), metallothioneins level and their Zn content, while Caff did not affect oxidative stress indexes and metallothionein-related Zn chelation. Protein carbonyls were not targeted in all exposures. The distinguishing feature of the Caff group was the decline (2-fold) in caspase-3 activity and low cell viability. The multi-stress effect of Mix was shown by the worsening of the volume regulation of digestive cells and confirmed by discriminant analysis of biochemical indexes. The special capabilities of M. galloprovincialis as a sentinel organism make it an excellent bio-indicator reflecting the multi-stress effects in sub-chronic exposures to potentially harmful substances. The identification of the modulation of individual effects in combined exposure increases the need to base monitoring programs on studies of multi-stress effects in sub-chronic exposures.

GSK-3β inhibition alleviates arthritis pain via reducing spinal mitochondrial reactive oxygen species level and inflammation.

Pain is the main symptom of osteoarthritis, which severely reduces the patients' quality of life. Stimulated neuroinflammation and elevated mitochondrial oxidative stress are associated arthritis pain. In the present study, arthritis model was established by intra-articular injection of complete Freund's adjuvant (CFA) on mice. Knee swelling, pain hypersensitivity and motor disability were observed in CFA-induced mice. In spinal cord, neuroinflammation was triggered and presented as severe infiltration of inflammatory cells and up-regulated expressions of glial fibrillary acidic protein (GFAP), nuclear factor-kappaB (NF-κB), PYD domains-containing protein 3 (NLRP3), cysteinyl aspartate specific proteinase (caspase-1) and interleukin-1 beta (IL-1β). Mitochondrial function was disrupted and characterized as elevated expressions of B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), dihydroorotate dehydrogenase (DHODH) and cytochrome C (Cyto C), and reduced expressions of Bcl-2 and Mn-superoxide dismutase (Mn-SOD) activity. Meanwhile, as a potential target for pain management, glycogen synthase kinase-3 beta (GSK-3β) activity was up-regulated in CFA induced mice. To explore potential therapeutic options for arthritis pain, GSK-3β inhibitor TDZD-8 was intraperitoneally injected for three days on CFA mice. Animal behavioral tests found that TDZD-8 treatment elevated mechanical pain sensitivity, suppressed spontaneous pain and recovered motor coordination. Morphological and protein expression analysis indicated that TDZD-8 treatment decreased spinal inflammation score and inflammatory related protein levels, recovered mitochondrial related protein levels, and increased Mn-SOD activity. In summary, TDZD-8 treatment inhibits GSK-3β activity, reduces mitochondrial mediated oxidative stress, suppresses spinal inflammasome response, and alleviates arthritis pain.

Protective effect of manganese treatment on insulin resistance in HepG2 hepatocytes.

manganese (Mn) is closely related to type 2 diabetes mellitus and insulin resistance (IR), but the exact mechanism is unclear. This study aimed to explore the regulatory effects and mechanism of Mn on IR using hepatocyte IR model induced by high palmitate (PA), high glucose (HG) or insulin. HepG2 cells were exposed to PA (200 μM), HG (25 mM) or insulin (100 nM) respectively, alone or with 5 μM Mn for 24 hours. The expression of key proteins in insulin signaling pathway, intracellular glycogen content and glucose accumulation, reactive oxygen species (ROS) level and Mn superoxide dismutase (MnSOD) activity were detected. compared with control group, the expression of phosphorylated protein kinase B (Akt), glycogen synthase kinase-3β (GSK-3β) and forkhead box O1 (FOXO1) in the three IR groups was declined, and this decrease was reversed by Mn. The reduction of intracellular glycogen content and increase in glucose accumulation in IR groups were also inhibited by Mn. Additionally, the production of ROS was increased in IR models, compared with normal control group, while Mn reduced the excessive production of ROS induced by PA, HG or insulin. However, Mn did not alter the activity of MnSOD in the three IR models. this study demonstrated that Mn treatment can improve IR in hepatocytes. The mechanism is probably by reducing the level of intracellular oxidative stress, enhancing the activity of Akt/GSK-3β/FOXO1 signal pathway, promoting glycogen synthesis, and inhibiting gluconeogenesis.

Manganese alleviates heat stress of primary cultured chick embryonic myocardial cells via enhancing manganese superoxide dismutase expression and attenuating heat shock response

Manganese (Mn) is an essential trace element that has been shown to attenuate the adverse effects of heat stress in the heart of broiler breeders and embryos. However, the underlying molecular mechanisms involving this process remain unclear. Therefore, two experiments were conducted to investigate the possible protective mechanisms of Mn on primary cultured chick embryonic myocardial cells exposed to heat challenge. In experiment 1, the myocardial cells were exposed to 40 °C (normal temperature, NT) and 44 °C (high temperature, HT) for 1, 2, 4, 6 or 8 h. In experiment 2, the myocardial cells were preincubated with no Mn supplementation (CON), 1 mmol/L of Mn as the inorganic MnCl2 (iMn) or organic Mn proteinate (oMn) under NT for 48 h, and then continuously incubated under NT or HT for another 2 or 4 h. The results from experiment 1 showed that the myocardial cells incubated for 2 or 4 h had the highest (P < 0.0001) heat-shock protein 70 (HSP70) or HSP90 mRNA levels than those incubated for other incubation times under HT. In experiment 2, HT increased (P < 0.05) the heat-shock factor 1 (HSF1) and HSF2 mRNA levels as well as Mn superoxide dismutase (MnSOD) activity of myocardial cells compared with NT. Furthermore, supplemental iMn and oMn increased (P < 0.02) HSF2 mRNA level and MnSOD activity of myocardial cells compared with the CON. Under HT, the HSP70 and HSP90 mRNA levels were lower (P < 0.03) in iMn group than in the CON group, in oMn group than in iMn group; and the MnSOD mRNA and protein levels were higher (P < 0.05) in oMn group than in the CON and iMn groups. These results from the present study indicate that supplemental Mn, especially oMn, could enhance the MnSOD expression and attenuate heat shock response to protect against heat challenge in primary cultured chick embryonic myocardial cells.

PSVII-9 The Impact of Increasing Dietary Manganese on the Reproductive Performance of Sows

Abstract The objective of this study was to determine the effect of dietary manganese (ProPath Mn, Zinpro Corporation) on the reproductive performance of sows. Sows (N = 39; 231 ± 8 kg) were randomly assigned to 1 of three dietary levels of Mn (CON: 0 ppm Mn; PRO20: 20 ppm Mn; PRO40: 40 ppm Mn). Experimental treatments were initiated at breeding and continued through 2 parities. Sows were blocked by parity within each farrowing group and dietary treatments were represented within each block. Data were analyzed as a randomized complete block design using the MIXED procedure of SAS with diet as a fixed effect and block as a random effect. Dietary treatment did not affect sow body weights (P &amp;gt; 0.10). Lactation feed intake was increased in PRO20 sows compared with CON and PRO40 sows (P &amp;lt; 0.05). PRO20 and PRO40 sows farrowed heavier piglets (CON 1.23 kg; PRO20 1.57 kg; PRO40 1.40 kg; P = 0.001) with improved average daily gain to weaning (CON 213 g/day; PRO20 237 g/day; 220 g/day; P &amp;lt; 0.05), compared with CON sows. Milk fat content (average from d 7 and 14 of lactation) was reduced in PRO20 (5.5%) and PRO40 sows (6.1%; P &amp;lt; 0.05) compared with CON sows (7.8%), possibly due to increased milk demand from the piglets. There were no significant differences in milk mineral concentrations during lactation or piglet tissue Mn-superoxide dismutase (MnSOD) activity at weaning (P &amp;gt; 0.10). On day 3 of lactation, prolactin concentrations were similar across treatments (P &amp;gt; 0.10), whereas progesterone concentrations tended to differ in response to Mn level (CON 23.70 ng/mL; PRO20 26.15 ng/mL; PRO40 22.10 ng/ml; P = 0.09). Supplementary dietary Mn throughout 2 gestation and lactation cycles led to increased birth weights and pre-weaning growth of piglets.

THE IMPACT OF SUCCINATE DERIVATIVE PHENSUCCINAL ON MITOCHONDRIAL FUNCTION AND REDOX STATUS IN THE HEART OF RATS WITH TYPE 2 DIABETES

Dysfunction of cardiac mitochondria appears to play a substantial role in cardiomyopathy and is a promising therapeutic target for many cardiovascular diseases. Persistent hyperglycaemia and hyperlipidemia are believed to be the main causes of increased oxidative stress, mitochondrial dysfunctions, fibrosis and apoptosis of cardiomyocytes in diabetes. We have previously shown that the low-toxic succinate derivative – Phensuccinal (beta-phenylethylamide-2 hydroxy-succinanylic acid, Phe) possesses antioxidant and anti-inflammatory properties. The aim of this study was to assess the effects of Phe on the mitochondrial function and oxidative status in the heart of rats with T2DM. Materials and Methods. T2DM was induced in Wistar rats by a high-caloric diet during 14 weeks combined with intraperitoneal injections of 25 mg/kg streptozotocin twice per week. All diabetic animals were divided into two groups: treated with vehicle or with Phe (in dose 50 mg/kg/day) for four weeks after diabetes induction. Redox status of rats’ heart mitochondria was estimated by determination of reactive oxygen species (ROS) production, GSH level and activity of antioxidant enzymes (Mn-superoxide dismutase, glutathione peroxidase and glutathione reductase). Mitochondrial function was determined by activity of aconitase, succinate dehydrogenase and cytochrome C oxidase in rats’ cardiomyocytes. Results. It was established that Phe inhibited oxidative stress in isolated heart mitochondria of rats with T2DM, which was confirmed by decreasing ROS production and increasing GSH level compared to diabetic rats. The use of Phe led to a normalization of antioxidant enzymes (Mn-superoxide dismutase and glutathione peroxidase) activity in the heart of diabetic rats. In addition, Phe improved metabolic activity of the heart mitochondria activating aconitase and succinate dehydrogenase in cardiomyocytes. We can suggest that Phe ameliorate mitochondrial dysfunction decreasing oxidative stress and preventing deficiency in complex II of ETC in the heart of rats with type 2 diabetes. Conclusion. The data of the present study confirmed the positive effect of Phe on redox homeostasis and functional state of the heart mitochondria in diabetic rats. We suggest that the use of Phe may contribute to the amelioration of cardiovascular risk in type 2 diabetes

2-Fluorofucose Attenuates Hydrogen Peroxide-Induced Oxidative Stress in HepG2 Cells via Nrf2/keap1 and NF-κB Signaling Pathways.

Fucosylation is one of the most important glycan terminal modifications that affects multiple biological activities of proteins. 2-Fluorofucose (2FF), its specific inhibitor, has recently been reported to reveal numerous biological effects by blocking fucosylation both in vitro and in vivo. The current study aimed to evaluate the effect of 2FF on hydrogen peroxide (H2O2)-induced oxidative damage in vitro. In our study, treatment with H2O2 increased the level of fucosylation, and 2FF improved the cell viability in H2O2-treated HepG2 cells. Our study also showed that 2FF significantly decreased the overproduction of reactive oxygen species (ROS) induced by H2O2 and the activities of catalase, glutathione and Mn-superoxide dismutase were remarkably increased by 2FF pretreatment. Furthermore, 2FF attenuated H2O2-induced early mitochondria dysfunction. The second part of the study revealed that 2FF enhanced antioxidant capacity by affecting Nrf2/keap1 and NF-κB signaling pathways in HepG2 cells. Being pretreated with 2FF significantly increased the nuclear translocation of Nrf2 and simultaneously promoted the expression of downstream proteins, such as HO-1 and NQO1. Moreover, 2FF remarkably suppressed the expression of inflammation-associated proteins. Taken together, these data suggest that 2FF might have a potential therapeutic effect for oxidative stress.

Yeast Fermentation Product Improves Pre-transit Antioxidant Defense and Post-transit Performance of Beef Steers

Steers supplemented Diamond V NaturSafe, a yeast fermentation product, at the manufacturer’s current recommended dose for receiving cattle (12 g/steer/d) during a 19-d preconditioning period exhibited greater antioxidant (glutathione) capacity prior to a 19-h transit event. Regardless of treatment, activity of the antioxidant enzyme Mn-superoxide dismutase was increased post-transit, suggesting more antioxidants may be needed to combat transit-induced stress. Supplementing NaturSafe at 12 g/steer/d during both preconditioning and receiving also improved feedlot performance early in the receiving period (d 0 to 30). These data suggest increasing antioxidant status may be an effective strategy to help cattle prepare for and recover from a stressful event, such as long-distance transit.

Homocysteine-induced neural tube defects in chick embryos via oxidative stress and DNA methylation associated transcriptional down-regulation of miR-124.

Although moderate homocysteine (HCY) elevation is associated with neural tube defects (NTDs), the underlying mechanisms have not been elucidated. In this study, we aimed to investigate that whether HCY-induced NTDs were associated with oxidative stress and methyl metabolism in chick embryos. The potential role of miR-124 in neurogenesis was also investigated. In this study, increased intracellular oxidative species and alterations in DNA methylation were observed following HCY treatment. This alteration coincided with decreases of Mn superoxide dismutase and glutathione peroxidase activities, as well as the expression of anti-rabbit DNA methyltransferase (DNMT) 1 and 3a. In addition, HCY induced significant decreases of S-adenosylmethionine (SAM)/S-adenosylhomocysteine (SAH) (P<0.05). N-acetyl-L-cysteine and choline ameliorated global DNA hypomethylation induced by HCY. MiR-124 levels were significantly suppressed by HCY (P<0.05), while elevated by 5-aza-2'-deoxycytidine (5-aza-dC). MiR-124 knockdown resulted in spina bifida occulta. Our research suggests that HCY-induced NTDs were associated with oxidative stress and methyl metabolism in chick embryos. MiR-124 down-regulation may occur via epigenetic mechanisms and contribute to HCY-induced NTDs in chick embryo models.

The Protective Biochemical Properties of Arbuscular Mycorrhiza Extraradical Mycelium in Acidic Soils Are Maintained throughout the Mediterranean Summer Conditions

In acidic soils with manganese (Mn) toxicity, arbuscular mycorrhizal fungi (AMF) can improve plant host growth by enhancing nutrition and protecting against environmental stress. The intact extraradical mycelium (ERM) of AMF is able to survive Mediterranean summer conditions and provide an earlier colonization of winter crops. This study evaluated if summer season conditions hindered the beneficial effects of wheat colonization by the intact ERM associated with a native plant, in acidic soil. Wheat was grown in soil with intact or disrupted ERM associated with Ornithopus compressus (ORN), developed for 7 or 24 weeks, to simulate ERM summer survival. The activity of antioxidant enzymes was determined, and the quantitative analysis of Mn and macronutrients was performed by inductively coupled plasma mass spectrometry (ICP-MS), in wheat shoots and respective subcellular fractions. Wheat colonization by intact ERM decreased shoot Mn concentration but increased the proportion of Mn in the apoplast. Overall, antioxidant enzymatic activity decreased but the proportion of Mn-superoxide dismutase activity over the remaining isoforms increased, suggesting its important role in the AMF-mediated mitigation of Mn toxicity. Summer conditions did not substantially reduce the benefits provided by ORN ERM. A no-till strategy allied to the development of native microbiota can contribute to the sustainable optimization of acidic soil use.

Alleviation Effects of Diosmetin on H2O2-Induced Oxidative Damage in Human Erythrocytes

Free radicals (FRs) are formed in the high amounts result of the metabolic imbalance in cells and tissue. These radicals-induced oxidative damages constitute the basis of many diseases. Organisms have antioxidant defence systems (ADS) to eliminate the destructive effects of the oxidative damage. In addition to these antioxidant systems, dietary flavonoids have the antioxidant effect and the protective role against oxidative damage. In the present study, it was investigated whether a flavonoid derived diosmetin (10, 50, and 100 µM) have the elimination potential on hydrogen peroxide (H2O2)-induced oxidative damage in erythrocyte culture by using biomarkers such as lipid peroxidation (LP) level, catalase (CAT), total superoxide dismutase (SOD) activity and changes of SOD isozymes containing the manganese SOD (Mn SOD) and the cupper-zinc SOD (CuZn SOD). CAT, total SOD, Mn SOD and CuZn SOD activities showed a serious decline with H2O2 treatment, but diosmetin addition significantly increased their activities. While the H2O2 application critically increased LP products in erythrocytes, diosmetin considerably reduced these oxidative damage products. In conclusion, it has been determined that diosmetin can moderate oxidative damage in human erythrocytes by activating or protecting the ADS.

Quercetin treatment increases H2O2 removal by restoration of endogenous antioxidant activity and blocks isoproterenol-induced cardiac hypertrophy.

Oxidative stress, characterized by the accumulation of reactive oxygen species (ROS), is implicated in the pathogenesis of several diseases, including cardiac hypertrophy. The flavonoid quercetin is a potent ROS scavenger, with several beneficial effects for the cardiovascular system, including antihypertrophic effects. Oxidative imbalance has been implicated in cardiac hypertrophy and heart failure. In this work, we tested whether quercetin could attenuate cardiac hypertrophy by improving redox balance and mitochondrial homeostasis. To test this hypothesis, we treated a group of mice with isoproterenol (30mg/kg/day) for 4 or 8 consecutive days. Another group received quercetin (10mg/kg/day) from day 5th of isoproterenol treatment. We carried out the following assays in cardiac tissue: measurement of cardiac hypertrophy, protein sulfhydryl, catalase, Cu/Zn and Mn-superoxide dismutase (SOD) activity, detection of H2O2, and opening of the mitochondrial permeability transition pore. The animals treated with isoproterenol for the initial 4days showed increased cardiac weight/tibia length ratio, decreased protein sulfhydryl content, compromised SOD and catalase activity, and high H2O2 levels. Quercetin was able to attenuate cardiac hypertrophy, restore protein sulfhydryl, and antioxidant activity, in addition to efficiently blocking the H2O2. We also observed that isoproterenol decreases mitochondrial SOD activity, while quercetin reverses it. Strikingly, quercetin also protects mitochondria against the opening of mitochondrial permeability transition pore. Taken together, these results suggest that quercetin is capable of reversing established isoproterenol-induced cardiac hypertrophy through the restoration of cellular redox balance and protecting mitochondria.

Age-Associated Changes in Antioxidants and Redox Proteins of Rat Heart.

Oxidative stress and decline in cellular redox regulation have been hypothesized to play a key role in cardiovascular aging; however, data on antioxidant and redox regulating systems in the aging heart are controversial. The aim of the present study was to examine the effect of aging on critical antioxidant enzymes and two major redox-regulatory systems glutathione (GSH) and thioredoxin (Trx) system in hearts from adult (6-month-old), old (15-month-old), and senescent (26-month-old) rats. Aging was associated with a non-uniform array of changes, including decline in contents of reduced GSH and total mercaptans in the senescent heart. The activities of Mn-superoxide dismutase (SOD2), glutathione peroxidase (GPx), glutathione reductase (GR), and thioredoxin reductase (TrxR) exhibited an age-related decline, whereas catalase was unchanged and Cu,Zn-superoxide dismutase (SOD1) displayed only slight decrease in old heart and was unchanged in the senescent heart. GR, Trx, and peroxiredoxin levels were significantly reduced in old and/or senescent hearts, indicating a diminished expression of these proteins. In contrast, SOD2 level was unchanged in the old heart and was slightly elevated in the senescent heart. Decline in GPx activity was accompanied by a loss of GPx level only in old rats, the level in senescent heart was unchanged. These results indicate age-related posttranslational protein modification of SOD2 and GPx. In summary, our data suggest that changes are more pronounced in senescent than in old rat hearts and support the view that aging is associated with disturbed redox balance that could alter cellular signaling and regulation.