Superoxide Dismutase Activity Research Articles

Parthenolide alleviates indomethacin-induced gastric ulcer in rats via antioxidant, anti-inflammatory, and antiapoptotic activities.

Parthenolide (PTL) is a sesquiterpene lactone that occurs naturally. It demonstrates a variety of beneficial effects, such as antioxidant, anti-inflammatory, and antiapoptotic properties. The study investigated the potential protective impact of PTL on indomethacin (INDO) induced stomach ulcers in rats. The rats were classified into 5 distinct categories. Group 1 served as the "control" group. Rats in the second group received a single oral dosage of INDO (50 mg kg-1). Rats inGroups three and four received 20 and 40 mg kg-1 oral PTL 1 h before INDO. Omeprazole (30mgkg-1) was given orally to Group 5 rats 1h before INDO. Pretreatment with PTL increased stomach pH and decreased gastric volume as well as reduced the morphological and histological changes induced by INDO. Analysis of probable pathways showed that pre-treatment with PTL successfully reduced oxidative, inflammatory, and apoptotic consequences caused by INDO. The ingestion of PTL leads to a notable increase in the levels of glutathione reduced (GSH) and the activities of superoxide dismutase (SOD) and catalase (CAT). Furthermore, PTL decreased the concentration of malondialdehyde (MDA). In contrast, it was shown that PTL increased both cyclooxygenase-1 (COX-1) and prostaglandin E2 (PGE2). PTL shows a significant decrease in the expression of interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), inducible nitric oxide synthase (iNOS), and nuclear factor kappa B (NF-κB). PTL therapy resulted in a decrease in Bcl-2-associated X protein (Bax) levels and an increase in B-cell lymphoma 2 (Bcl2) levels. In conclusion, PTL offers gastroprotection by its antioxidant, anti-inflammatory, and anti-apoptotic qualities.

35 Role and mechanism of supplemental methionine in metabolic stress of broilers raised at high ambient temperature or stock density

Abstract Current poultry production practices may render fast-growing broilers prone to metabolic stresses induced by high ambient temperatures and(or) high stocking densities. As the first limiting amino acid of broilers fed corn-soy diets, methionine also serves as a free radical scavenger. Our laboratory has explored metabolic effects and biochemical mechanisms of supplemental methionine in grower and finisher diets for broilers raised at high temperature or high stock density. In Experiment 1, a total of 360 male, 1 d-old Cornish cockerel chicks were fed four diets (10 pens/treatment, 9 chicks/pen): 100 or 130% required methionine in the diets as DL-methionine (DL-MET) or 2-hydroxy-4-(methylthio)butanoate (HMTBA). The room was maintained at 4 to 13oC above the suggested thermoneutral temperature. The 130% DL-MET and HMTBA diets enhanced (P < 0.05) hepatic GSH concentrations of growers and plasma ferric reducing ability of finishers than the 100% diets. The DL-MET-fed growers had greater (P < 0.05%) muscle GSH and hepatic unsaturated fatty acid concentrations than those fed HMTBA. The methionine form and concentration exerted an interaction effect (P < 0.05) on the expression of inflammation-related genes in the liver of finishers. In Experiment 2, we determined if 30% extra DL-MET alleviated adverse effects of a greater stocking density on broilers. A total of 560 male, 1 d-old Cornish cockerels were housed at two stocking densities (9 and 12 birds/m2) and fed two concentrations of DL-MET (grower: 2.90 or 3.77 g/kg and finisher: 2.60 or 3.38 g/kg). The high stocking density decreased (P < 0.05) body weight and growth performance of growers and(or) finishers. Those differences were largely removed or attenuated by the 130% DL-MET diet. There were interaction effects (P < 0.05) between dietary DL-MET concentrations and stocking densities on activities of glutathione S-transferase in the liver of growers and the breast, thigh, and adipose tissue of finishers as well as on activities of glutathione peroxidase and superoxide dismutase in the thigh of growers. The 130% DL-MET diet decreased (P < 0.05) hepatic gene expression of heat shock protein 90 (18%) and malondialdehyde concentrations in the thigh and breast of finishers (35%). In summary, the high ambient temperature-induced metabolic responses of broilers were mediated by the extra methionine supplementation. That function varied with the chicken age and(or) tissue and the methionine form. Meanwhile, the 30% extra DL-MET addition partially reversed adverse effects caused by the greater stocking density, partially via improving tissue redox status. (This research was supported in part by Evonik Nutrition & Care GmbH, and was published: J. Anim. Sci. 97:4883-4894; J. Anim. Sci. 98:skaa092. doi: 10.1093/jas/skaa092).

Rosmarinic acid ameliorated oxidative stress, neuronal injuries, and mitochondrial dysfunctions mediated by polyglutamine and ɑ-synuclein in Caenorhabditis elegans models.

Numerous natural antioxidants have been developed into agents for neurodegenerative diseases (NDs) treatment. Rosmarinic acid (RA), an excellent antioxidant, exhibits neuroprotective activity, but its anti-NDs efficacy remains puzzling. Here, Caenorhabditis elegans models were employed to systematically reveal RA-mediated mechanisms in delaying NDs from diverse facets, including oxidative stress, the homeostasis of neural and protein, and mitochondrial disorders. Firstly, RA significantly inhibited reactive oxygen species accumulation, reduced peroxide malonaldehyde production, and strengthened the antioxidant defense system via increasing superoxide dismutase activity. Besides, RA reduced neuronal loss and ameliorated polyglutamine and ɑ-synuclein-mediated dyskinesia in NDs models. Further, in combination with the data and molecular docking results, RA may bind specifically to Huntington protein and ɑ-synuclein to prevent toxic protein aggregation and thus enhance proteostasis. Finally, RA ameliorated mitochondrial dysfunction including increasing adenosine triphosphate and mitochondrial membrane potential levels and rescuing mitochondrial membrane proteins' expressions and mitochondrial structural abnormalities via regulating mitochondrial dynamics genes and improving the mitochondrial kinetic homeostasis. Thus, this study systematically revealed the RA-mediated neuroprotective mechanism and promoted RA as a promising nutritional intervention strategy to prevent NDs.

Superoxide Dismutase and Clopidogrel: A Potential Role in Peripheral Arterial Disease Treatment.

Oxidative stress plays a crucial role in the pathogenesis of peripheral artery disease (PAD). This study aimed to investigate the effect of clopidogrel on oxidative stress in PAD patients. Seventy subjects were divided into three groups: PAD patients before treatment (B-PAD), PAD patients after treatment with clopidogrel (A-PAD), and healthy controls. Serum levels of superoxide dismutase (SOD), copper (Cu), zinc (Zn), manganese (Mn), and oxidized protein were measured. SOD activities were also determined. The results showed that SOD activities, and SOD specific activities were significantly decreased in PAD patients compared to healthy individuals. After treatment with clopidogrel, SOD activities, and SOD specific activities were continuously decrease in PAD patients. The SOD and oxidized protein concentrations were significantly increased in PAD patients compared to healthy individuals. After treatment with clopidogrel, the oxidized protein concentration was significantly decreased, while SOD concentration was significantly increased in PAD patients. These findings suggest that the treatment by clopidogrel stimulated the production of the enzyme but the ratio of active enzyme remained low. The decrease in oxidized protein can be explained by the treatment having antioxidant efficacy that may have compensated for the deficiency in enzyme activity and led to a decrease in oxidized protein. Additionally, the results of this study provide promising evidence that oxidative stress biomarkers including SOD concentration, T-SOD activity, Mn-SOD activity, and oxidized protein levels have potential utility in the diagnosis and management of PAD.

Assessment of single and combined administration of ubiquinone and lactoferrin on histopathology, ultrastructure, oxidative stress, and WNT4 expression gene induced by thioacetamide on hepatorenal system of adult male rats

BackgroundHepatorenal syndrome is a life-threatening medical complication of liver cirrhosis. Hepatic cirrhosis is commonly accompanied by rapid failure of renal functions. Thioacetamide (TAA) is a potent hepatotoxin and a class 2-type carcinogen. Ubiquinone (Coq10) and lactoferrin (LF) are potent antioxidants with antifibrotic and antiinflammatory effects. However, whether Coq10 and LF reduce the hepatorenal injury induced by TAA remains unclear. Here, we investigated the potential protective effect of both/or Coq10 and LF in ameliorating TAA-induced hepatorenal injury and the role of WNT4 gene expression in detecting TAA-induced renal injury in rats. Seventy healthy and mature male Sprague Dawley rats, weighting (200 g ± 20 g) and aging (4–6) weeks were randomly divided into seven groups (n = 10): control, Coq10, LF, TAA, TAA + Coq10, TAA + LF, and TAA + Coq10 + LF. The hepatorenal injury was induced through intraperitoneal (i.p.) injection of TAA (150 mg/kg/twice/weekly) for nine weeks. Coq10 (10 mg/kg/day) and LF (200 mg/kg/day) were orally administered for nine weeks.ResultsTAA induced marked hepatorenal damage, evident by the significant increase in the alanine aminotransferase (ALT), aspartate transaminase (AST), serum creatinine (SCr) activities, and the blood urea nitrogen (BUN) level. Besides, the significant increases in concentrations of malondialdehyde (MDA) and nitric oxide (NOx) together with significant decreases in the activities of catalase (CAT) and superoxide dismutase (SOD). The histopathological analysis of the TAA group showed obvious fibrosis, steatosis, and inflammation of the hepatic parenchyma as well as severe glomerular and tubular damage of the renal parenchyma. In addition, TAA induced marked ultrastructural alterations and up-regulation in the expression of the WNT4 gene in the kidney. Meanwhile, the biochemical, histopathological, and ultrastructural alterations were significantly decreased with significant down-regulation in the expression of WNT4 in the groups exposed to TAA and treated with Coq10 and LF.ConclusionOur data suggested that Coq10 and LF could have protective effects on TAA hepatorenal damage, through improving the hepatic and renal functions, reduction of oxidative stress, structural and ultrastructural alterations, besides down-regulation in the expression of WNT4.

Ion channel Piezo1 activation aggravates the endothelial dysfunction under a high glucose environment

BackgroundVasculopathy is the most common complication of diabetes. Endothelial cells located in the innermost layer of blood vessels are constantly affected by blood flow or vascular components; thus, their mechanosensitivity plays an important role in mediating vascular regulation. Endothelial damage, one of the main causes of hyperglycemic vascular complications, has been extensively studied. However, the role of mechanosensitive signaling in hyperglycemic endothelial damage remains unclear.MethodsVascular endothelial-specific Piezo1 knockout mice were generated to investigate the effects of Piezo1 on Streptozotocin-induced hyperglycemia and vascular endothelial injury. In vitro activation or knockdown of Piezo1 was performed to evaluate the effects on the proliferation, migration, and tubular function of human umbilical vein endothelial cells in high glucose. Reactive oxygen species production, mitochondrial membrane potential alternations, and oxidative stress-related products were used to assess the extent of oxidative stress damage caused by Piezo1 activation.ResultsOur study found that in VECreERT2;Piezo1flox/flox mice with Piezo1 conditional knockout in vascular endothelial cells, Piezo1 deficiency alleviated streptozotocin-induced hyperglycemia with reduced apoptosis and abscission of thoracic aortic endothelial cells, and decreased the inflammatory response of aortic tissue caused by high glucose. Moreover, the knockout of Piezo1 showed a thinner thoracic aortic wall, reduced tunica media damage, and increased endothelial nitric oxide synthase expression in transgenic mice, indicating the relief of endothelial damage caused by hyperglycemia. We also showed that Piezo1 activation aggravated oxidative stress injury and resulted in severe dysfunction through the Ca2+-induced CaMKII-Nrf2 axis in human umbilical vein endothelial cells. In Piezo1 conditional knockout mice, Piezo1 deficiency partially restored superoxide dismutase activity and reduced malondialdehyde content in the thoracic aorta. Mechanistically, Piezo1 deficiency decreased CaMKII phosphorylation and restored the expression of Nrf2 and its downstream molecules HO-1 and NQO1.ConclusionIn summary, our study revealed that Piezo1 is involved in high glucose-induced oxidative stress injury and aggravated endothelial dysfunction, which have great significance for alleviating endothelial damage caused by hyperglycemia.

Potassium fertilizer promotes the thin-shelled Tartary buckwheat yield by delaying senescence and promoting grain filling

The application rate of potassium fertilizer is closely related to the yield of crops. Thin-shelled Tartary buckwheat is a new variety of Tartary buckwheat with the advantages of thin shell and easy shelling. However, little is known about application rate of potassium fertilizer on the yield formation of thin-shelled Tartary buckwheat. This study aimed to clarify the effect of potassium fertilizer on the growth and yield of thin-shelled Tartary buckwheat. A field experiment to investigate the characteristics was conducted across two years using thin-shelled Tartary buckwheat (Miku 18) with four potassium fertilizer applications including 0 (no potassium fertilizer, CK), 15 (low-concentration potassium fertilizer, LK), 30 (medium-concentration potassium fertilizer, MK), and 45 kg·ha−1 (high-concentration potassium fertilizer, HK). The maximum and average grain filling rates; starch synthase activity; superoxide dismutase and peroxidase activities in leaves; root morphological indices and activities; available nitrogen, phosphorus, and organic matter content in rhizosphere soil; urease and alkaline phosphatase activities in rhizosphere soil; plant height, main stem node number, main stem branch number, leaf number; grain number per plant, grain weight per plant, and 100-grain weight increased first and then decreased with the increase in potassium fertilizer application rate and reached the maximum at MK treatment. The content of malondialdehyde was significantly lower in MK treatment than in other three treatments. The yields of thin-shelled Tartary buckwheat treated with LK, MK, and HK were 1.22, 1.37, and 1.07 times that of CK, respectively. In summary, an appropriate potassium fertilizer treatment (30kg·ha−1) can delay the senescence, promote the grain filling, and increase the grain weight and final yield of thin-shelled Tartary buckwheat. This treatment is recommended to be used in production to achieve high-yield cultivation of thin-shelled Tartary buckwheat.

Effects of swimming activity and feed restriction on antioxidant and digestive enzymes in juvenile rainbow trout: Implications for nutritional and exercise strategies in aquaculture.

In this study, we investigated the effects of swimming activity and feed restriction on digestion and antioxidant enzyme activities in juvenile rainbow trout (average body weight of 26.54±0.36g). The stomach, liver and kidney tissues were obtained from four distinct groups: the static water group (fish were kept in static water and fed to satiation), the feeding restricted group (fish were kept in static water with a 25% feed restriction), the swimming exercised group (fish were forced to swimming at a flow rate of 1 Body Length per second (BL/s)) and the swimming exercised-feed restricted group (subjected to swimming exercise at a 1BL/s flow rate along with a 25% feed restriction). We determined the levels of glutathione, lipid peroxidation and the activities of catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase and lactate dehydrogenase, as well as the presence of reactive oxygen species in the tissues obtained from the fish. Additionally, the activities of pepsin, protease, lipase and arginase in these tissues were measured. Swimming activity and feed restriction showed different effects on the enzyme activities of the fish in the experimental groups. It can be concluded that proper nutrition and exercise positively influence the antioxidant system and enzyme activities in fish, reducing the formation of free radicals. This situation is likely to contribute to the fish's development.

Eco-endocrinological dynamics: Unraveling dexamethasone's influence on the interrenal axis in juvenile carp Cyprinus carpio

This study delves into the eco-endocrinological dynamics concerning the impact of dexamethasone (DXE) on the interrenal axis in juvenile carp, Cyprinus carpio. Through a comprehensive analysis, we investigated the effects of DXE exposure on oxidative stress, biochemical biomarkers, gene expression, and bioaccumulation within the interrenal axis. Results revealed a concentration-dependent escalation of cellular oxidation biomarkers, including 1) hydroperoxides content (HPC), 2) lipid peroxidation level (LPX), and 3) protein carbonyl content (PCC), indicative of heightened oxidative stress. Concurrently, the activity of critical antioxidant enzymes, superoxide dismutase (SOD), and catalase (CAT), significantly increased, underscoring the organism's response to oxidative insult. Notable alterations were observed in biochemical biomarkers, particularly Gamma-glutamyl-transpeptidase (GGT) and alkaline phosphatase (ALP) activity, with GGT displaying a significant decrease with increasing DXE concentrations. Gene expression analysis revealed a significant upregulation of stress and inflammation response genes, as well as those associated with sensitivity to superoxide ion presence and calcium signaling, in response to DXE exposure. Furthermore, DXE demonstrated a concentration-dependent presence in interrenal tissue, with consistent bioconcentration factors observed across all concentrations tested. These findings shed light on the physiological and molecular responses of juvenile carp to DXE exposure, emphasizing the potential ecological implications of DXE contamination in aquatic environments. Understanding these dynamics is crucial for assessing the environmental impact of glucocorticoid pollutants and developing effective management strategies to mitigate their adverse effects on aquatic ecosystems.

Aflatoxin B1 inhibited the development of primary myoblasts of grass carp (Ctenopharyngodon idella) by degrading extracellular matrix

According to the International Agency for Research on Cancer (IARC), aflatoxin B1 (AFB1) has been recognized as a major contaminant in food and animal feed and which is a common mycotoxin with high toxicity. Previous research has found that AFB1 inhibited zebrafish muscle development. However, the potential mechanism of AFB1 on fish muscle development is unknown, so it is necessary to conduct further investigation. In the present research, the primary myoblast of grass carp was used as a model, we treated myoblasts with AFB1 for 24h. Our results found that 5μM AFB1 significantly inhibited cell proliferation and migration (P < 0.05), and 10μM AFB1 promoted lactate dehydrogenase (LDH) release (P < 0.05). Reactive oxygen species (ROS), protein carbonyl (PC) and malondialdehyde (MDA) levels were increased in 15, 5 and 10μM AFB1 (P < 0.05), respectively. Catalase (CAT), glutathione peroxidase (GPx) and total superoxide dismutase (T-SOD) activities were decreased in 10, 10 and 15μM AFB1 (P < 0.05), respectively. Furthermore, 15μM AFB1 induced oxidative damage by Nrf2 pathway, also induced apoptosis in primary myoblast of grass carp. Meanwhile, 15μM AFB1 decreased MyoD gene and protein expression (P < 0.05). Importantly, 15μM AFB1 decreased the protein expression of collagen Ⅰ and fibronectin (P < 0.05), and increased the protein levels of urokinase plasminogen activator (uPA), matrix metalloproteinase 9 (MMP-9), matrix metalloproteinase 2 (MMP-2), and p38 mitogen-activated protein kinase (p38MAPK) (P < 0.05). As a result, our findings suggested that AFB1 damaged the cell morphology, induced oxidative damage and apoptosis, degraded ECM components, in turn inhibiting myoblast development by activating the p38MAPK/urokinase-type plasminogen activator (uPA)/matrix metalloproteinase (MMPs)/extracellular matrix (ECM) signaling pathway.

Kefir mitigates renal damage caused by zearalenone in female Wistar rats by reducing oxidative stress

The estrogen-like mycotoxin zearalenone (ZEA) was popularly occurred in several food and feeds, posing threats to human and animal health. ZEA induced renal toxicity and caused oxidative stress. In the current study, the protecting effect of kefir administration against ZEA-induced renal damage in rats was explored. Rats were divided into 4 groups, each consisting of 5 animals. For the initial 7 days, they were orally administered sterile milk (200 μL/day). Subsequently, during the second week, the groups were exposed to kefir (200 μL/day), ZEA (40 mg/kg b.w./day) and a combination of kefir and ZEA. The biochemical parameters, kidney histological changes and ZEA residue were assessed. Kefir supplementation enhanced the antioxidant enzymes in the kidney, such as superoxide dismutase, catalase and glutathione peroxidase activities, which increased by 1.2, 4 and 20 folds, respectively, relative to the ZEA group. Remarkably, the concomitant administration kefir+ZEA suppressed ZEA residues in both serum and kidney. Additionally, serum levels of blood urea nitrogen, uric acid and renal malondialdehyde decreased by 22, 65 and 54%, respectively, in the kefir+ZEA group; while, the creatinine content increased by around 60%. Rats co-treated with kefir showed a normal kidney histological architecture contrary to tissues alterations mediated in the ZEA group. These results suggest that kefir may showed a protective effect on the kidneys, mitigating ZEA-induced acute toxicity in rats.

Reducing the injury of hippocampal vascular endothelial cells after stroke via targeting SIRT1 by butylphthalide

Butylphthalide (NBP) can inhibit various pathological processes of ischemic stroke. This experiment explored the mechanism of NBP and SIRT1 on damage of hippocampal vascular endothelial cells after stroke. The neurons in the hippocampus of rats were stained with HE, and morphology and density of neurons were observed. Flow cytometry, commercial kits and Western blotting detected apoptosis of endothelial cells, levels of antioxidant enzymes and apoptotic proteins, intracellular calcium level and activity of Ca2+-ATPase. The damage to rat nerve cells was alleviated by butylphthalide to varying degrees, and the lost parts of rat nerve cells were recovered with decreased Bax and cleaved caspase-3 expression after butylphthalide treatment, and increased Bcl-2 (P &lt;0.05), as well as decreased serum malondialdehyde (MDA) content and activity of catalase (CAT) decreased and elevated Superoxide dismutase (SOD) activity (P &lt;0.05). The concentration of calcium ion also decreased but activity of Ca2+-ATPase increased (P &lt;0.05) and mitochondria in the model group appeared with severe vacuolation and swelling. The vacuolation and swelling of mitochondria in the treatment group were improved. Additionally, mitochondrial membrane fluidity, potential and rat hippocampal ATPase activity in butylphthalide group were also increased. Compared to normal control group, model group, SIRT1 inhibitor group and butylphthalide+SIRT1 inhibitor group had lower levels of SIRT1 and higher p-NF-kB p65/p-IkBα levels. Butylphthalide has a protective effect on hippocampal neurons in stroke rats and can alleviate the damage degree of rat nerve cells.

Integrated transcriptome and metabolome analysis provide insights into the mechanism of saponin biosynthesis and its role in alleviating cadmium-induced oxidative damage in Ophiopogon japonicum.

Zhe-Maidong, a cultivar of Ophiopogon japonicus is a prominent traditional herbal medicine rich in saponins. This study explored the mechanism of saponin biosynthesis and its role in alleviating Cd-induced oxidative damage in the Zhe-Maidong cultivar using three experimental groups undergoing Cd stress. In the Cd-contaminated soil treatment, total saponins were 1.68 times higher than those in the control. The saponin content in the Cd-2 and Cd-3 treatments was approximately twice as high as that in the Cd-CK treatment. These findings revealed that Cd stress leads to total saponin accumulation. Metabolomic analysis identified the accumulated saponins, primarily several monoterpenoids, diterpenoids, and triterpenoids. The increased saponins exhibited an antioxidant ability to prevent the accumulation of Cd-induced reactive oxygen species (ROS). Subsequent saponin application experiments provided strong evidence that saponin played a crucial role in promoting superoxide dismutase (SOD) activity and reducing ROS accumulation. Transcriptome analysis revealed vital genes for saponin synthesis under Cd stress, including SE, two SSs, and six CYP450s, positively correlated with differentially expressed metabolite (DEM) levels in the saponin metabolic pathway. Additionally, the TF-gene regulatory network demonstrated that bHLH1, bHLH3, mTERF, and AUX/IAA transcript factors are crucial regulators of hub genes involved in saponin synthesis. These findings significantly contribute to our understanding of the regulatory network of saponin synthesis and its role in reducing oxidative damage in O. japonicum when exposed to Cd stress.

Effectiveness of manganese foliar spraying to mitigate salt stress in ornamental cabbage: Insights into morphological, physiological biochemical adaptations and mTERF gene responses

Salinity has been the subject of research for many years. However, salt stress studies on ornamental plants have increased recently. It is very important to determine the responses of bedding flowers, which are widely used in landscaping, to salt stress, and to strengthen the defense against stress. Ornamental cabbage (Brassica oleareacea L.) is widely used bedding flower in winter. The aim of this study was determining the effects of foliar application of manganese (Mn) on morphological, physiological, biochemical, and molecular parameters in ornamental cabbage ('Pigeon Purple F1′) under salt stress. Plants were irrigated with 4 different irrigation solutions which containing 0 [control], 75, 150 and 300 mM NaCl concentrations and Mn (4000 ppm) was sprayed to the leaves on 0, 7th and 14th days of the salt stress application. The application of manganese did alleviate the negative effects of salinity on shoot fresh weight and shoot dry weight in 75 mM NaCl plants. Ion leakage for 0 and 75 mM NaCl decreased with foliar spraying of Mn, but relative water content of plants did not change with Mn application. Lipid peroxidation (7.6 %) and H2O2 (hydrogen peroxide) (21.3 %) contents increased with Mn foliar spraying. Superoxide dismutase (SOD) and peroxidase activity did not change with Mn application under salinity. The highest catalase activity obtained from 150 mM (13.81 Unit g−1 leaf) and 300 mM NaCl (16.00 Unit g−1 leaf) which treated with Mn. Root Na content was lower with Mn-treated plants when compared control plants under salt stress. Foliar spraying of Mn significantly increased the K content of the plants. Furthermore, Na/K and Na/Ca ratios which are important indicators for salt stress also decreased by Mn application under saline conditions. In addition, m TERF genes were measured by using the q-RT PCR. In most cases, mTERF expression was slightly induced by salinity, while manganese application generally led to downregulation of mTERFs.

Cadmium promoted LPS-induced inflammation through TLR4/IκBα/NFκ-B signaling by increasing ROS-mediated incomplete autophagy

Cadmium (Cd) exposure is considered as non-infectious stressor to human and animal health. Recent studies suggest that the immunotoxicity of low dose Cd is not directly apparent, but disrupts the immune responses when infected with some bacteria or virus. But how Cd alters the adaptive immunity organ and cells remains unclear. In this study, we applied lipopolysaccharide (LPS, infectious stressor) to induced inflammation in spleen tissues and T cells, and investigated the effects after Cd exposure and the underlying mechanism. Cd exposure promoted LPS-induced the expressions of the inflammatory factors, induced abnormal initiation of autophagy, but blocked autophagic flux. The effects Cd exposure under LPS activation were reversed by the autophagy promoter Rapamycin. Under LPS activation conditions, Cd also induced oxidative stress by increasing the levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and reducing total antioxidant capacity (T-AOC) activity. The increased superoxide dismutase (SOD) activity after Cd exposure might be a negative feedback or passive adaptive regulation of oxidative stress. Cd-increased autophagic flux inhibition and TNF-α expression were reversed by ROS scavenger α-tocopherol (TCP). Furthermore, under LPS activation condition, Cd promoted activation of toll-like receptor 4 (TLR4)/IκBα/NFκ-B signaling pathway and increased TLR4 protein stability, which were abolished by the pretreatment of Rapamycin. The present study confirmed that, by increasing ROS-mediated inhibiting autophagic degradation of TLR4, Cd promoted LPS-induced inflammation in spleen T cells. This study identified the mechanism of autophagy in Cd-aggravated immunotoxicity under infectious stress, which could arouse public attention to synergistic toxicity of Cd and bacterial or virus infection.

Dietary lysophospholipid improves growth performance, antioxidant capacity and immunity response of red tilapia (Oreochromis niloticus × O. mossambicus)

Lysophospholipids (LPL) are usually used as emulsifiers in fish nutrition because of their ability to ameliorate nutrient digestibility and lipid metabolism. The present study aims to assess the effects of a commercial dietary lysophospholipid on growth performance, feed utilization, antioxidant activity, innate immunity and biochemical indices of red tilapia (Oreochromis niloticus x O. mosambicus) fingerlings. Five isonitrogenous (35.8 % CP) and isocaloric (18.7 MJ kg−1) diets were prepared as follows: two control diets coded as C1 and C2, containing 2 and 1 % soybean oil, respectively. The other three diets were coded as LPL1, LPL2 and LPL3, and were formulated by supplementing the C2 diet with 0.1, 0.2 and 0.3 % lysophospholipid. The fingerlings of red tilapia (2.13 ± 0.42 g fish−1) were fed the diets for 70 days. The highest significant (p < 0.05) final weight and weight gain were recorded in LPL2. The best values of feed efficiency and protein efficiency (PER)were in all fish groups fed LPL in their diets (p < 0.05). Protein productive value (PPV) showed the highest result in LPL3 (p < 0.05). Lysozyme activity showed the best result in LPL3 (p < 0.05). The highest values of alternative complement activity (ACH50) and total immunoglobulin (Ig) were in LPL3 and LPL2 (p < 0.05). The best results of superoxide dismutase (SOD) and catalase activity were recorded in LPL3 (p < 0.05). Triglycerides (TG) and total cholesterol (CHO) showed significantly low values at (p < 0.05) in LPL1 and LPL2. Thus, the inclusion of 0.2 % of the commercial lysophospholipid in red tilapia diets enhanced the growth performance, feed utilization, innate immunity, antioxidant activity and lipase activity, and reduced CHO and TG of red tilapia fingerlings.

Vincamine alleviates brain injury by attenuating neuroinflammation and oxidative damage in a mouse model of Parkinson's disease through the NF-κB and Nrf2/HO-1 signaling pathways.

Parkinson's disease (PD)is a neurodegenerative disease featured by progressive loss of nigrostriatal dopaminergic neurons, the etiology of which is associated with the existence of neuroinflammatory response and oxidative stress. Vincamine is an indole alkaloid that was reported to exhibit potent anti-inflammatory and antioxidant properties in many central and/or peripheral diseases. Nevertheless, the specific role of vincamine in PD development remains unknown. In our study, dopaminergic neuron loss was determined through immunohistochemistry staining and western blot analysis of tyrosine hydroxylase (TH)expression in the substantia nigra (SN)of PD mice. Reactive oxygen species (ROS)production and malondialdehyde (MDA),superoxide dismutase (SOD),and glutathione (GSH)levels were detected through DHE staining and commercially available kits to assess oxidative stress. Pro-inflammatorycytokine (TNF-α,IL-1β, and IL-6)levels in the SN were measured via RT-qPCRand western blot analysis. Microglial and astrocyte activation was examined through immunofluorescence staining of Iba-1 (microglia marker) and GFAP (astrocyte marker) in the SN. The regulation of vincamine on the NF-κBand Nrf2/HO-1pathway was estimated through western blot analysis. Our results showed that vincamine treatment decreased TNF-α,IL-1β,and IL-6 mRNA and protein levels, reduced GFAP and Iba-1 expression, decreased ROS production and MDA level, and increased SOD activity and GSH level in the SN of PD mice. Mechanically, vincamine repressed the phosphorylation levels of p65, IKKβ, and IκBα but enhanced the protein levels of Nrf2 and HO-1 in PD mice. Collectively, vincamine plays a neuroprotective role in PD mouse models by alleviating neuroinflammation and oxidative damage via suppressing the NF-κBpathway and activating the Nrf2/HO-1pathway.

Oxidative Coupling Assembly Induced Bio-engineered Quercetin Microspheres for the Gastrosparing Delivery of Diclofenac Sodium.

The study aimed to develop microspheres of quercetin by oxidative coupling assembly and these microspheres were used to deliver diclofenac sodium without causing gastrotoxicity. The oxidative coupling assembly of quercetin was carried out in the presence of copper sulfate to yield quercetin microspheres. The microsphere of quercetin was loaded with diclofenac sodium (QP-Diclo). The carrageenan induced paw edema in rats was used for anti-inflammatory action was studied by using and acetic acid-induced writhing in mice was used to study the analgesic potential of the QP loaded microspheres. The ulcerogenecity and gastrotoxicity comparison was made between diclofenac and QP-Diclo. The oxidative coupling assembly of quercetin resulted in microspheres of 10-20 μm in size, which were loaded with diclofenac sodium (QP-Diclo). The marked anti-inflammatory activity was observed by QP-Diclo treatment using carrageenan induced paw edema (in rats) and better analgesic activity than diclofenac sodium in mice. The administration of QP-Diclo significantly elevated the diminished overall nitrite/nitrate extent and thiobarbituric acid reactive and significantly increased the diminished superoxide dismutase activity in comparison to diclofenac sodium in gastric mucosa. The results suggested that dietary polyphenol quercetin can be converted to microspheres by oxidative coupling assembly and can be used to deliver diclofenac sodium without causing gastrotoxicity.

Effect of changing the proportion of C16:0 and cis-9 C18:1 in fat supplements on rumen fermentation, glucose and lipid metabolism, antioxidation capacity, and visceral fatty acid profile in finishing Angus bulls

This study evaluated the effects of different proportions of palmitic (C16:0) and oleic (cis-9 C18:1) acids in fat supplements on rumen fermentation, glucose (GLU) and lipid metabolism, antioxidant function, and visceral fat fatty acid (FA) composition in Angus bulls. The design of the experiment was a randomized block design with 3 treatments of 10 animals each. A total of 30 finishing Angus bulls (21 ± 0.5 months) with an initial body weight of 626 ± 69 kg were blocked by weight into 10 blocks, with 3 bulls per block. The bulls in each block were randomly assigned to one of three experimental diets: (1) control diet without additional fat (CON), (2) CON + 2.5% palmitic calcium salt (PA, 90% C16:0), (3) CON + 2.5% mixed FA calcium salts (MA; 60% C16:0 + 30% cis-9 C18:1). Both fat supplements significantly increased C18:0 and cis-9 C18:1 in visceral fat (P < 0.05) and up-regulated the expression of liver FA transport protein 5 (FATP5; P < 0.001). PA increased the concentrations of insulin (P < 0.001) and aspartate aminotransferase (AST; P = 0.030) in bull’s blood while reducing GLU (P = 0.009) concentrations. PA increased the content of triglycerides (TG; P = 0.014) in the liver, the content of the C16:0 in visceral fat (P = 0.004), weight gain (P = 0.032), and up-regulated the expression of liver diacylglycerol acyltransferase 2 (DGAT2), stearoyl-CoA desaturase 1 (SCD1; P < 0.05). MA increased blood superoxide dismutase activity (SOD; P = 0.011), reduced the concentration of acetate and total volatile FA (VFA) in rumen fluid (P < 0.05), and tended to increase non-esterified FA (NEFA; P = 0.069) concentrations in blood. Generally, high C16:0 fat supplementation increased weight gain in Angus bulls and triggered the risk of fatty liver, insulin resistance, and reduced antioxidant function. These adverse effects were alleviated by partially replacing C16:0 with cis-9 C18:1.

Serum Total Superoxide Dismutase Activity as a Predictive Factor in Patients with Hepatocellular Carcinoma

Objectives: This study aimed to determine the cutoff value for diagnosis and predict mortality in hepatocellular carcinoma (HCC) based on serum total superoxide dismutase (SOD) activity. Methods: A retrospective case-control study of the SOD Model was conducted using data from a single-center dataset at Shandong Provincial Hospital Affiliated with Shandong First Medical University, China. Serum total SOD activity was analyzed in HCC patients (n = 124) and control subjects (n = 117). Receiver operating characteristic (ROC) curves were used to determine cutoff values of serum total SOD activity for HCC diagnosis. Overall survival (OS) was assessed using the Kaplan-Meier method. Results: In the model groups, the cutoff level of total SOD activity for HCC was 169.2 U/mL (sensitivity: 87.23%, specificity: 91.95%), while for HCC [alpha fetoprotein (AFP) &lt; 20 ng/mL], it was 173.4 U/mL (sensitivity: 86.79%, specificity: 88.51%). Additionally, in the validation groups, the true positive rate, true negative rate, and accuracy rate were all above 90%. Based on the cutoff value of SOD, HCC patients were assigned to an H-SOD and L-SOD group depending on their serum total SOD activity at admission before operation. The 5-year OS rate of the H-SOD group was 75.00%, and that of the L-SOD group was 36.59% in HCC patients (P = 0.0245). With a decrease in SOD activity, serum levels of Zn (t = 3.890, P = 0.0003) and Se (t = 7.694, P &lt; 0.0001) were also significantly decreased and positively correlated with SOD activity (both P &lt; 0.05) in HCC patients. Conclusions: Low serum total SOD activity may also be a risk factor for HCC. The decrease of SOD activity in HCC patients was partly related to a lack of Zn and Se.