Decreased Superoxide Dismutase Activity Research Articles

Impact of Physically and Chemically Dispersed Crude Oil on the Antioxidant Defense Capacities and Non-Specific Immune Responses in Sea Cucumber (Apostichopus japonicus)

Currently, oil spill pollution is one of the major environmental concerns for sea cucumber (Apostichopus japonicus) aquaculture. During oil spills, spraying chemical dispersants is generally considered an efficient oil spill response. However, the impact of chemical dispersant deployment during oil spills on sea cucumbers is still less known. In this study, we treated sea cucumbers with physically and chemically (by GM-2 chemical dispersant) dispersed Oman crude oil for 24 h. For antioxidant defense capacities, our results showed that physically dispersed crude oil caused a significant elevation on superoxide dismutase (SOD) and catalase (CAT) activities, and glutathione (GSH) content, while chemically dispersed crude oil caused a significant decrease in SOD activity and GSH content with no apparent change in CAT activity. As for non-specific immune responses, our results indicated that physically dispersed crude oil up-regulated acid phosphatase (ACP) and lysozyme (LZM) activities but had no obvious impact on alkaline phosphatase (ALP) activity. Differently, chemically dispersed crude oil down-regulated ACP and LZM activities while up-regulating ALP activity. Based on the integrated biomarker response analysis, the overall impact of chemically dispersed crude oil on antioxidant defense capacities and non-specific immune responses of sea cucumbers was more severe than physically dispersed crude oil.

Effect of high glucose supplementation on pulmonary fibrosis involving reactive oxygen species and TGF-β

This study explored the profibrotic impact of high glucose in the lung and potential mechanisms using latent TGF-β1-induced human epithelial cell pulmonary fibrosis and bleomycin (BLM)-induced pulmonary fibrosis models. Results demonstrated that high glucose administration induced epithelial–mesenchymal transition (EMT) in human epithelial cells in a dose-dependent manner via activating latent TGF-β1, followed by increased expression of mesenchymal-related proteins and decreased expression of epithelial marker protein E-cadherin. Further mechanism analysis showed that administration of high glucose dose-dependently promoted total and mitochondrial reactive oxygen species (ROS) accumulation in human epithelial cells, which promoted latent TGF-β1 activation. However, N-acetyl-L-cysteine, a ROS eliminator, inhibited such effects. An in vivo feed study found that mice given a high-glucose diet had more seriously pathological characteristics of pulmonary fibrosis in BLM-treated mice, including increasing infiltrated inflammatory cells, collagen I deposition, and the expression of mesenchymal-related proteins while decreasing the expression of the epithelial marker E-cadherin. In addition, high glucose intake further increased TGF-β1 concentration and upregulated p-Smad2/3 and snail in lung tissues from BLM-treated mice when compared to BLM-treated mice. Finally, supplementation with high glucose further increased the production of lipid peroxidation metabolite malondialdehyde and decreased superoxide dismutase activity in BLM-treated mice. Collectively, these findings illustrate that high glucose supplementation activates a form of latent TGF-β1 by promoting ROS accumulation and ultimately exacerbates the development of pulmonary fibrosis.

Heparin-Binding Protein Aggravates Acute Lung Injury in Septic Rats by Promoting Macrophage M1 Polarization and NF-κB Signaling Pathway Activation.

Objective Heparin-binding protein (HBP) plays an important role in sepsis and is a prognostic biomarker in patients with sepsis, but the role of HBP in the pathogenesis of sepsis-associated acute lung injury (ALI) remains unclear. This study aimed to investigate the role of HBP in sepsis-induced ALI and its underlying molecular mechanisms. Methods The cecal ligation and puncture (CLP) model was used to induce ALI in mice and randomly divided into 4 groups: control group, CLP (rats treated with cecal ligation and puncture), HBP (rats treated with CLP and HBP injection), and HBP + UFH (rats treated with CLP and injection of HBP and unfractionated heparin). Subsequently, HBP expression in rat serum and lung tissues was detected by qRT-PCR, edema and pathological changes in lung tissue by lung wet-to-dry weight ratio (W/D) and HE staining, myeloperoxidase (MPO) and superoxide dismutase (SOD) activities in lung tissues by detection kits. Additionally, ELISA and western blot were applied for the determination of IL-6, TNF-α, and IL-1β expression in rat bronchoalveolar lavage fluid, and iNOS, Arg-1, Mrc1, NF-κBp65, IKKα, IκBα, and p-IκBα expression in lung tissues. Results The expression levels of HBP in serum and lung tissues of rats in the HBP group were significantly increased, the lung tissues were severely injured, accompanied by a significant increase in MPO activity but a significant decrease in SOD activity, and the levels of IL-6, TNF-α, and IL-1β in bronchoalveolar lavage fluid were significantly increased. In addition, the expression levels of iNOS, NF-κB p65, IKKα, and p-IκBα in the lung tissues of rats in the HBP group were significantly increased, while the addition of unfractionated heparin reversed the above results. Conclusion HBP aggravates ALI in septic rats, and its mechanism may be related to the promotion of macrophage M1 polarization and activation of the NF-κB signaling pathway.

Fluoride subacute testicular toxicity in Wistar rats: Benchmark dose analysis for the redox parameters, essential elements and DNA damage

Excessive fluoride (F−) levels in the environment could induce different pathological changes, including comorbidities in reproductive functions. Hence, the aim of the present in vivo study was to explore F− subacute toxicity mechanisms via Benchmark dose (BMD) methodology on rat's testicles. The experiment was conducted on thirty male Wistar rats for 28 days, divided into six groups (n = 5): 1) Control (tap water); 2) 10 mg/L F−; 3) 25 mg/L F−; 4) 50 mg/L F−; 5) 100 mg/L F−; 6) 150 mg/L F−. Testicles were dissected out and processed for the determination of F− tissue concentrations, redox status parameters, essential elements level, and DNA damage. PROASTweb 70.1 software was used for determination of external and internal dose-response relationship. The results confirmed a significant increase in superoxide anion (O2.-), total oxidative status (TOS), copper (Cu), zinc (Zn), iron (Fe), DNA damage levels, and decrease in superoxide dismutase activity (SOD1) and total thiol (SH) groups. The dose-dependent changes were confirmed for SOD1 activity and DNA damage. The most sensitive parameters were SOD1 activity and DNA damage with the lowest BMDLs 0.1 μg F−/kg b. w. Since human and animal populations are daily and frequently unconsciously exposed to F−, this dose-response study is valuable for further research regarding the F− health risk assessment.

Metabolome and transcriptome association analysis revealed key factors involved in melatonin mediated cadmium-stress tolerance in cotton.

Cadmium (Cd), a non-essential element for plant, is a ubiquitous and highly toxic heavy metal, seriously endangering agricultural production and human health. As a nonedible economic crop, cotton (Gossypium hirsutum L.) has great potential in remediation of Cd contaminated soil, but its underlying mechanism is still unknown. Melatonin (MT), as a plant growth regulator, is involved in alleviating Cd toxicity in some plants, but the molecular mechanisms of MT-mediated Cd detoxification in cotton are largely unknown. This study investigated the possible molecular mechanisms of the MT-mediated Cd detoxification in cotton seedlings by comparative transcriptomic and metabolomic analyses. The results showed that the cotton seedlings were dwarfed and the leaves were wilted and yellow under Cd stress. The application of 50 µmol L−1 MT significantly increased the superoxide dismutase (SOD) activity and malondialdehyde (MDA) content under Cd stress, but 100 µmol L−1 MT significantly decreased SOD activity, while increased ascorbate peroxidase (APX) activity significantly. The addition of 100 μmol L−1 MT significantly increased Cd concentration in the shoots and roots under Cd stress. RNA-seq analysis showed that 5573, 7105, 7253, 25, 198, 9 up-regulated and 6644, 7192, 7404, 9, 59, 0 down-regulated differentially expressed genes (DEGs) were identified in the comparisons of CK vs T1, CK vs T2, CK vs T3, T1 vs T2, T1 vs T3 and T2 vs T3, respectively. It was revealed that MT promoted the expression of certain related genes under Cd stress, and the effect of 100 µmol L−1 MT was better. Moreover, UPLC-MS/MS widely targeted metabolites analyses showed that 195, 150, 150, 12, 24, 59 up-regulated and 16, 11, 23, 38, 127, 66 down-regulated differentially accumulated metabolites (DAMs) were changed in the CK vs T1, CK vs T2, CK vs T3, T1 vs T2, T1 vs T3 and T2 vs T3, respectively. It was revealed that MT induced the synthesis of alkaloids and flavonoids, and inhibited or reduced the synthesis of lipids, amino acids and their derivatives. The comprehensive analyses of transcriptomic and metabolic data showed that 33 DEGs and 4 DAMs, 46 DEGs and 16 DAMs, and 1 DEGs and 1 DAMs were dominantly involved in the pathways of valine, leucine and isoleucine degradation, ABC transporter, alpha-linolenic acid metabolism, respectively. It was revealed that there were three major mechanisms involved in MT-mediated Cd detoxification in cotton, including the enhancement of antioxidant capacity regulated by APX, flavonoids and alkaloids; accumulation of secondary metabolites related to Cd chelation, such as amino acids and derivatives; and regulation of cadmium ion transportation, such as ABC transporter activation. In conclusion, this study provides new insights into the MT-mediated Cd stress response.

Physiological and Metabolic Responses of Gac Leaf (Momordica cochinchinensis (Lour.) Spreng.) to Salinity Stress.

Gac is a carotenoid-rich, healthful tropical fruit; however, its productivity is limited by soil salinity, a growing environmental stress. This study aimed to evaluate the effects of salinity stress on key physiological traits and metabolites in 30-day-old gac seedling leaves, treated with 0, 25-, 50-, 100-, and 150-mM sodium chloride (NaCl) for four weeks to identify potential alarm, acclimatory, and exhaustion responses. Electrolyte leakage increased with increasing NaCl concentrations (p < 0.05) indicating loss of membrane permeability and conditions that lead to reactive oxygen species production. At 25 and 50 mM NaCl, superoxide dismutase (SOD) activity, starch content, and total soluble sugar increased. Chlorophyll a, and total chlorophyll increased at 25 mM NaCl but decreased at higher NaCl concentrations indicating salinity-induced thylakoid membrane degradation and chlorophyllase activity. Catalase (CAT) activity decreased (p < 0.05) at all NaCl treatments, while ascorbate peroxidase (APX) and guaiacol peroxidase (GPX) activities were highest at 150 mM NaCl. GC-MS-metabolite profiling showed that 150 mM NaCl induced the largest changes in metabolites and was thus distinct. Thirteen pathways and 7.73% of metabolites differed between the control and all the salt-treated seedlings. Salinity decreased TCA cycle intermediates, and there were less sugars for growth but more for osmoprotection, with the latter augmented by increased amino acids. Although 150 mM NaCl level decreased SOD activity, the APX and GPX enzymes were still active, and some carbohydrates and metabolites also accumulated to promote salinity resistance via multiple mechanisms.

Efficacy of low extra-abdominal aortic block in cesarean section for placenta accreta spectrum disorders and its effect on the expression of MDA and SOD.

Placenta accreta spectrum disorders (PAS) refers to a group of abnormalities in placental adhesion and invasion, which may lead to serious complications such as intractable postpartum hemorrhage. The use of low-level extra-abdominal aortic temporary block during cesarean section may reduce intraoperative bleeding in patients with PAS, but it may also cause ischemia-reperfusion injury. In this study, we intend to investigate the efficacy of low extra-abdominal aortic block in cesarean section for placental implantation disease and its effect on malondialdehyde (MDA) level and superoxide dismutase (SOD) activity, and analyze the severity of ischemia-reperfusion injury caused by them. Pregnant women with invasive placenta accreta spectrum disorders who delivered in the Department of Obstetrics and Gynecology of the Third Xiangya Hospital of Central South University from July 2017 to July 2021, were selected, and they were divided into 2 groups. Group A consisted of those who underwent low extra-abdominal aortic block during cesarean section (n=15) and group B consisted of those who did not undergo extra-abdominal aortic block (n=15). The intraoperative bleeding, blood transfusion, hysterectomy and complication rate, postoperative hospital stay and hospitalization expenses were compared between the 2 groups to analyze the efficacy of abdominal aortic block. The biochemical indexes related to ischemia-reperfusion, MDA content and total superoxide dismutase (T-SOD) activity, were measured at the corresponding time points in both groups. The time points of each test were: in group A, before the block of the low extra-abdominal aorta after delivery (A0), 0 h (A1, when the myometrium was started to be sutured), 0.5 h (A2), 2 h (A3), and 4 h (A4) after the open block; in group B, after delivery of the fetus (B0), 0 h (B1), 0.5 h (B2), 2 h (B3), and 4 h (B4) after the myometrium was started to be sutured. Total duration of abdominal aortic block in group A was also recorded. Both groups were observed for sings of edema, ischemia, necrosis and infection in the limbs after surgery. The severity of ischemia-reperfusion injury caused by abdominal aortic block were determined by detecting the relevant biochemical indexes at different moments of reperfusion. The intraoperative bleeding and blood transfusion in group A were less than those in group B, and the difference was statistically significant (P<0.05). There was no significant difference in postoperative hospital stay and hospitalization expenses between the 2 groups (P>0.05). Surgical complications: in group A, the uterus was preserved in all cases, there was 1 bladder injury and 2 pelvic infections; while in group B, there was 1 hysterectomy, 3 bladder injuries, and 3 pelvic infections. Changes in T-SOD and MDA values: compared with A0 before block, the MDA level was significantly elevated in blood at time points A1, A2, and A3, while SOD activity was significantly decreased (P<0.05), and the 2 observed indexes basically returned to A1 level (ischemic period) at 4 h after open block (A4). There was no significant difference in the changes of T-SOD and MDA in group B (P>0.05). Comparison of T-SOD and MDA levels between group A and B: the difference of the 2 indexes was not statistically significant between A0 and B0 (P>0.05), MDA level was not statistically significant between A1 and B1, T-SOD activity at A1 was lower than B1, the difference was statistically significant, at the rest of the same time point, MDA level in group A were higher than that in group B, T-SOD activity in group A were lower than that in group B, the difference was statistically significant (P<0.05). No postoperative limb edema, ischemia, necrosis, or infection occurred in both groups. Low-level extra-abdominal aortic block effectively reduces bleeding and transfusion during cesarean section for placenta accreta spectrum disorders, resulting in a transient MDA elevation and a decrease of SOD activity, which means causing transient ischemia-reperfusion injury without complications such as limb edema, ischemia, necrosis, and infection.

Inorganic Nitrogen-Containing Aerosol Deposition Caused "Excessive Photosynthesis" of Herbs, Resulting in Increased Nitrogen Demand.

The amount of atmospheric nitrogen-containing aerosols has increased dramatically due to the globally rising levels of nitrogen from fertilization and atmospheric deposition. Although the balance of carbon and nitrogen in plants is a crucial component of physiological and biochemical indexes and plays a key role in adaptive regulation, our understanding of how nitrogen-containing aerosols affect this remains limited; in particular, regarding the associated mechanisms. Using a fumigation particle generator, we generated ammonium nitrate solution (in four concentrations of 0, 15, 30, 60 kg N hm−2 year−1) into droplets, in 90% of which the diameters were less than 2.5 μm, in the range of 0.35–4 μm, and fumigated Iris germanica L. and Portulaca grandiflora Hook. for 30 days in April and August. We found that the weight percentage of nitrogen in the upper epidermis, mesophyll tissue, and bulk of leaves decreased significantly with the N addition rate, which caused a decrease of carbon:nitrogen ratio, due to the enhanced net photosynthetic rate. Compared with Portulaca grandiflora Hook., Iris germanica L. responded more significantly to the disturbance of N addition, resulting in a decrease in the weight percentage of nitrogen in the roots, due to a lower nitrogen use efficiency. In addition, the superoxide dismutase activity of the two plants was inhibited with a higher concentration of nitrogen sol; a reduction of superoxide dismutase activity in plants means that the resistance of plants to various environmental stresses is reduced, and this decrease in superoxide dismutase activity may be related to ROS signaling. The results suggest that inorganic nitrogen-containing aerosols caused excessive stress to plants, especially for Iris germanica L.

Shenmai Injection Attenuates Myocardial Ischemia/Reperfusion Injury by Targeting Nrf2/GPX4 Signalling-Mediated Ferroptosis.

To examine the effect of Shenmai Injection (SMJ) on ferroptosis during myocardial ischemia reperfusion (I/R) injury in rats and the underlying mechanism. A total of 120 SPF-grade adult male SD rats, weighing 220-250 g were randomly divided into different groups according to a random number table. Myocardial I/R model was established by occluding the left anterior descending artery for 30 min followed by 120 min of reperfusion. SMJ was injected intraperitoneally at the onset of 120 min of reperfusion, and erastin (an agonist of ferroptosis), ferrostatin-1 (Fer-1, an inhibitor of ferroptosis) and ML385 (an inhibitor of nuclear factor erythroid-2 related factor 2 (Nrf2)) were administered intraperitoneally separately 30 min before myocardial ischemia as different pretreatments. Cardiac function before ischemia, after ischemia and after reperfusion was analysed. Pathological changes in the myocardium and the ultrastructure of cardiomyocytes were observed, and the myocardial infarction area was measured. Additionally, the concentration of Fe2+ in heart tissues and the levels of creatine kinase-MB (CK-MB), troponin I (cTnl), malondialdehyde (MDA) and superoxide dismutase (SOD) in serum were measured using assay kits, and the expressions of Nrf2, glutathione peroxidase 4 (GPX4) and acyl-CoA synthetase long-chain family member 4 (ACSL4) were examined by Western blot. Compared with the sham group, I/R significantly injured heart tissues, as evidenced by the disordered, ruptured and oedematous myocardial fibres; the increases in infarct size, serum CK-MB, cTnI and MDA levels, and myocardial Fe2+ concentrations; and the decreases in SOD activity (P<0.05). These results were accompanied by ultrastructural alterations to the mitochondria, increased expression of ACSL4 and inhibited the activation of Nrf2/GPX4 signalling (P<0.05). Compared with I/R group, pretreatment with 9 mL/kg SMJ and 2 mg/kg Fer-1 significantly reduced myocardial I/R injury, Fe2+ concentrations and ACSL4 expression and attenuated mitochondrial impairment, while 14 mg/kg erastin exacerbated myocardial I/R injury (P<0.05). In addition, cardioprotection provided by 9 mL/kg SMJ was completely reversed by ML385, as evidenced by the increased myocardial infarct size, CK-MB, cTnI, MDA and Fe2+ concentrations, and the decreased SOD activity (P<0.05). Ferroptosis is involved in myocardial I/R injury. Pretreatment with SMJ alleviated myocardial I/R injury by activating Nrf2/GPX4 signalling-mediated ferroptosis, thereby providing a strategy for the prevention and treatment of ischemic heart diseases.

Trehalose Attenuates Oxidative Stress and Endoplasmic Reticulum Stress-Mediated Apoptosis in IPEC-J2 Cells Subjected to Heat Stress.

Simple SummaryAs global warming continues, the increased frequency and intensity of high ambient temperatures imposes heat stress (HS) on farm animals and human beings. Pigs are susceptible to heat exposure; decreased performance and increased morbidity due to HS give rise to economic losses for the swine industry. HS induces oxidative stress and apoptosis, both of which are associated with compromised intestinal barrier integrity. Trehalose (Tre) is a natural disaccharide that is considered a health-promoting food owing to its antioxidant and anti-inflammatory effects and its molecular chaperone ability to inhibit protein denaturation. The present study aimed to determine the optimum trehalose level for alleviating HS-induced intestinal porcine epithelial cell (IPEC-J2) insults and to uncover the molecular mechanism of the protective effects of Tre. This study demonstrated that 10 mM trehalose can significantly attenuate HS-induced IPEC-J2 cell impairment and that the mechanism is related to trehalose alleviating oxidative stress and endoplasmic reticulum stress-mediated apoptosis.This study was carried out to investigate the effects of trehalose (Tre) on antioxidant capacity, endoplasmic reticulum stress (ERS) response and apoptosis of heat-stressed intestinal porcine epithelial cells (IPEC-J2). IPEC-J2 cells were cultured at 37 °C until the end of the experiment (control, CON); exposed to heat stress for 2 h (43 °C, HS); or pretreated with 0.1, 1, 5, 10, and 15 mM trehalose at 37 °C for 4 h prior to heat stress exposure for 2 h. The optimum level of trehalose for protecting against HS-induced cell injuries was determined to be 10 mM, as evidenced by the highest cellular viability and lowest malondialdehyde (MDA) content and lactate dehydrogenase (LDH) activity. Based on these, IPEC-J2 cells were divided into three groups: the first group was cultured at 37 °C until the end of the experiment (control, CON); the second group was exposed to heat stress for 2 h (43 °C, HS); the third group was pretreated with 10 mM trehalose for 4 h at 37 °C prior to heat stress exposure for 2 h (Tre + HS). The reactive oxygen species (ROS) content, superoxide dismutase (SOD) activity, mitochondrial membrane potential (MMP) changes, and expressions of the manganese superoxide dismutase (SOD2), ERS and apoptosis-related proteins were determined. Compared to the CON group, HS significantly increased ROS generation (p < 0.01), decreased SOD activity (p < 0.05), and downregulated protein expression of SOD2 (p < 0.01). Compared to the HS group, Tre supplementation reduced ROS levels and increased SOD activity and SOD2 expression to the levels that were comparable to the control (p < 0.05). The HS-induced ERS response was evidenced by the increased protein expressions of glucose-regulated protein 78 (GRP78) (p < 0.01), eukaryotic translation initiation factor 2α (p-eif2α) (p < 0.01), transcription activator 4 (ATF4) (p < 0.01), and the protein expression of C/EBP homologous protein (CHOP) (p < 0.01), which were the four hallmarks of ERS. The Tre + HS group showed lower expressions of GRP78 (p < 0.01), p-eif2α (p < 0.01), ATF4 (p < 0.01), and CHOP (p < 0.01) than that of the HS group. Tre pretreatment attenuated HS-induced mitochondrial apoptosis in IPEC-J2 cells, demonstrated by the increased MMP and decreased proapoptotic proteins active caspase 3, Bax, and cytochrome c (Cyt c). Taken together, trehalose can protect against HS-induced oxidative damage and endoplasmic reticulum stress-mediated apoptosis in IPEC-J2 cells. These data may provide a nutritional strategy for alleviating heat stress in pig production.

Cdc42 upregulation under high glucose induces podocyte apoptosis and impairs β-cell insulin secretion.

ObjectivesThe progressive impairment of β-cell function results in prolonged deterioration in patients with type 2 diabetes mellitus (T2DM). Interestingly, the finding on pancreatitis secondary to renal injury suggests that potential communication exists between kidney and pancreas. Therefore, we aimed to investigate cell division cycle 42 (Cdc42)-mediated podocyte apoptosis and its effect on insulin secretion in islet β-cells.MethodsType 2 diabetic nephropathy mouse models were established to identify the expression of Cdc42 in podocytes by immunohistochemistry. An in vitro co-culture of mouse podocyte MPC5 and β-TC6 cells was preliminarily established. Subsequently, podocyte apoptosis induced by high glucose and Cdc42 was detected by TUNEL staining and western blotting. In addition, the JNK pathway was examined to determine the mechanism of apoptosis in MPC5 cells. Finally, insulin secretion and expression in β-TC6 cells as well as malondialdehyde (MDA) and superoxide dismutase (SOD) levels in both cell types were examined after the regulation of Cdc42 in MPC5 cells.ResultsCdc42 was highly expressed in the podocytes of diabetic nephropathy mice. Exposure to 25 mM glucose for 48 h induced a significant upregulation of Cdc42, Bax, and cleaved caspase-3 as well as a decreased Bcl-2 expression. In addition, marked apoptosis of MPC5 cells was observed compared to normal glucose treatment. After transfection with Cdc42 plasmid, apoptosis of MPC5 cells was enhanced with an increased expression of p-JNK, whereas inhibition of Cdc42 significantly alleviated podocyte apoptosis accompanied by a downregulation of p-JNK. The glucose-stimulated insulin secretion level of β-TC6 cells decreased after the upregulation of Cdc42 in MPC5 cells. Immunofluorescence staining for insulin showed that co-culture with MPC5 cells carrying the Cdc42 plasmid significantly reduced insulin expression, whereas inhibition of Cdc42 in MPC5 cells alleviated the above-mentioned abnormality of β-TC6 cells. The expression of Cdc42 and p-p38 in β-TC6 cells increased following the upregulation of Cdc42 in MPC5 cells; this was concurrent with augmented MDA levels and decreased SOD activity. The opposite result was observed for Cdc42 knockdown in MPC5 cells.ConclusionsCdc42 in podocytes plays a crucial role in insulin secretion by β-cells, which may provide a new therapeutic target to prevent the vicious cycle of β-cell dysfunction in T2DM.

The regulatory effect and molecular mechanism of lncRNA Gm10451 on islet cell dysfunction in children with diabetes.

The dysfunction of islet β-cells is one of the causes of diabetes, and lncRNA Gm10451 is also a participant in the occurrence and the development of various diseases. This study was carried out to reveal the correlation within β-cells and Gm10451. Our study was started with the cellular cultivation of MIN6 cells in vitro, where this islet β-cell line was randomly divided into the groups of control, hyperglycemia, Gm10451 siRNA tansfection, and Gm10451 tansfection. Of all these treatments, cells in the groups of Gm10451 siRNA tansfection and Gm10451 tansfection were given with lentiviral transfection under hyperglycemia condition. Further explorations were established using PCR assay and MTT method to evaluate Gm10451 expression and estimate cellular proliferation. It ended up with the enzyme-linked immunosorbent assay (ELISA) to assess Caspase 3 activity, superoxide dismutase (SOD) activity, and reactive oxygen species (ROS) content and the secretion of IL-10 and IL-1. It was found that Gm10451 expression in MIN6 cells under hyperglycemia cultivation was notably higher than the control group; likewise, a transfection with the lentivirus of Gm10451 also resulted in the upregulation of Gm10451 expression, succeeded with inhibiting cellular proliferation, enhancing Caspase 3 activity, and decreasing SOD activity. In the lentivirus transfection groups, transfection of Gm10451 elevated the ROS content and promoted IL-1 expression, and it also decreased both IL-10 expression and insulin secretion, leading to a consequence of statistically significant difference in contrast to the high-glucose group; on the contrary, transfection of Gm10451 siRNA in a high-glucose environment downregulated the expression of Gm10451 and inversed those change before, whose results were statistically significant when compared with the high-glucose group. Hyperglycemia promotes the expression of Gm10451. Targeting inhibition toward Gm10451 alleviates cellular apoptosis and the oxidative stress of islet cells, promoting proliferation and insulin secretion of islet cells.

Antioxidant status of fish with inflammation of the swim bladder in yearling carp

The literature data on the etiology and pathogenesis of swim bladder inflammation (SBI) in various fish species have been highlighted in the paper. The main goal of this work was to analyze the impact of the disease on the physiological status of the body of the yearling carp, the state of the antioxidant defense system, and the content of lipid peroxidation products (LPP). The yearling Liubyn scaly carps, with an average weight of 40 g, which were grown in the ponds of the Rivne fish and reclamation station, were selected for experimental research. During control catches and ichthyopathological examination of forty fish, inflammation of the swim bladder was detected with an intensity of 35 %. During the pathological autopsy of this yearling carp, thickening of the walls of the swim bladder with purulent exudate, atrophy of the posterior lobe, and hyperemia of internal organs was found. Data on the content of lipid peroxidation products (LPP) and the state of the antioxidant system (AOS) in the cells of the hepatopancreas and skeletal muscles of this year's carp with SPM have been presented. It was determined that in the hepatopancreas of fish with the swim bladder inflammation, primary and secondary LPP products accumulate, and the activity of AOS enzymes decreases. The increase of diene conjugates in the hepatopancreas of the diseased fish was revealed by 11.8 % compared to the control group, and the content of TBC-active products by 29.8 %. The level of SOD activity is 13.5 % lower in the fish affected by SMP than in the control group. Catalase activity in the hepatopancreas of the diseased fish increases by 11.7 % compared to the control group. There was a 45.5 % decrease in superoxide dismutase activity in the skeletal muscles of fish affected by SBI and a significant increase in the level of catalase (Р &lt; 0.01) compared to the control group. Pathogens that cause diseases of the swim bladder cause also have an inhibitory effect on the activity of enzymes of the antioxidant system, and the content of products of lipid peroxidation increases.

ANTI-LITHIATIC EFFECT OF LYCOPENE IN CHEMICALLY INDUCED NEPHROLITHIASIS IN RATS

Objective: The search for anti-calculi drugs from natural sources has been believed of greater importance. Hence, the present study explored the effectiveness of lycopene against experimentally induced nephrolithiasis. Methods: The experimental study lasted for 28 days. Adult male Wistar rats were divided into six groups. Group I (Normal control) received drinking water. Group II (Disease control) received 0.75% ethylene glycol and 1% ammonium chloride in drinking water to induce nephrolithiasis. Group III–V was treated with lycopene (50 mg/kg, 100 mg/kg, and 200 mg/kg, p.o.) along with 0.75% ethylene glycol and 1% ammonium chloride. Group VI treated standard (750 mg/kg, p.o.) along with 0.75% ethylene glycol and 1% ammonium chloride. Results: The study results showed significantly high levels of urinary and serum creatinine, urea, calcium, and uric acid levels and a decrease in magnesium levels in Group II (Disease control) compared with Group I (Normal control). Treatment with lycopene (50 mg/kg, 100 mg/kg, and 200 mg/kg) restored the elevated urinary and serum parameters in Group III–VI compared with Group II. Ethylene glycol administrations lead to the production of oxidative stress and decrease superoxide dismutase, reduced glutathione, and catalase activity. Lycopene treatment restored the elevated oxidative stress parameters to normal. Histologically, lycopene has alleviated the damaged integrity of the renal structure. Conclusion: Supplementation with lycopene (100 mg/kg and 200 mg/kg) reduces and prevents the toxicity caused by ethylene glycol administration and protects the renal cells from damage.

A zinc finger suppressor involved in stress resistance, cell wall integrity, conidiogenesis, and autophagy in the necrotrophic fungal pathogen Alternaria alternata

The tangerine pathotype of Alternaria alternata can withstand high-level reactive oxygen species (ROS). By analyzing loss- and gain-of-function mutants, this study demonstrated that a Cys2His2 zinc finger-containing transcription regulator, A. alternata Stress Response Regulator 1 (AaSRR1), plays a negative role in resistance to peroxides and singlet-oxygen-generating compounds. AaSRR1 plays no role in cellular susceptibility or resistance to superoxide-producing compounds. AaSRR1 also negatively regulates conidiogenesis, maintenance of cell wall and membrane integrities, and chitin biosynthesis. Some wild-type hyphae displayed necrosis after exposure to 30 mM H2O2, whereas AaSRR1 deficient mutant (ΔAaSRR1) hyphae had visible granules and vacuoles. sGFP-AaATG8 proteolysis assays revealed that H2O2 and starvation could trigger autophagy formation in both wild type and ΔAaSRR1. Autophagy occurred at higher rates in ΔAaSRR1 than wild type under both conditions, particularly after H2O2 treatments, indicating that autophagy might contribute to ROS resistance. Upon exposure to H2O2 or under starvation, AaSRR1 was translocated into the nucleus, even though the expression of AaSRR1 was decreased. AaSRR1 is required for vegetative growth but is dispensable for fungal virulence as assayed on detached calamondin leaves. AaSRR1 suppressed the expression of the gene encoding a HOG1 mitogen-activated protein (MAP) kinase implicated in ROS resistance. Mutation of AaSRR1 increased catalase activity but decreased superoxide dismutase activity, leading to fewer ROS accumulation in the cytosol. Nevertheless, our results indicated that AaSRR1 is a transcription suppressor for ROS resistance. This study also revealed tradeoffs between stress responses and hyphal growth in A. alternata.

Chronic toxic effects of polystyrene microplastics on reproductive parameters of male rats.

Microplastics have become a significant environmental concern. However, information on toxicity of microplastics in terrestrial organisms is limited. In this study, the chronic toxic effects of polystyrene microplastics (PS-MPs) on the reproductive system and serum antioxidants of male albino Wistar rats fed for 90 days with standard rat feed containing 1–10% granules of crushed polystyrene disposable plates were evaluated. Significant reductions in volume, motility, epididymal sperm count and serum testosterone level were observed. Histological examination of testicular architecture showed distorted testes with vacuolated seminiferous tubules at the highest percentage, together with increased catalase and decreased superoxide dismutase activities. This study showed that ingestion of PS-MPs caused reproductive dysfunction in male rats and contributes to understanding the potential toxicity of microplastics in terrestrial animals.

MAP 산소 농도가 세절한 쇠고기의 SOD 활성 및 산화안정성에 미치는 영향

This study estimated the effect of oxygen (O2) concentration in modified atmosphere packaging (MAP) on the superoxide dismutase (SOD) activity and oxidative stability of ground beef. The samples of Top rounds from Hanwoo (Korean cattle) were ground, packaged into four O2proportion (0%, 25%, 50%, or 75%), and then stored for 11 days at 11°C. SOD activity was significantly (p&lt;0.05) lower in the beef stored under 25%, 50%, and 75% O2-MAP than in that stored in 0% O2-MAP after 3 days of storage. After 7 days of storage, total reducing ability (TRA) was the lowest (p&lt;0.05) in the beef stored under 75% O2-MAP, but that stored under 0% O2-MAP had the highest (p&lt;0.05) TRA. Higher O2 proportion remarkably (p&lt;0.05) increased the TBARS content of stored beef, and 25%, 50%, and 75% O2-MAP treatments showed more than 5 times higher TBARS content compared to the 0% O2-MAP treatment at day 11 of storage. Oxymyoglobin concentration greatly (p&lt;0.05) decreased in 25%, 50%, and 75% O2-MAP treatments. The highest (p&lt;0.05) L* and b* values were maintained in 50% and 75% O2-MAP treatments, but 25%, 50%, and 75% O2-MAP drastically (p&lt;0.05) decreased the a* value of stored beef. These findings suggest that high O2-MAP decreases the oxidation stability of stored beef with a decrease in SOD activity.

Ameliorative Effects of EUK-134, a Superoxide Dismutase and Catalase Mimetic, in a Rat Model of D-Galactose-Induced Oxidative Stress and Accelerated Aging

Background and Aim: EUK-134, a synthetic superoxide dismutase/catalase mimetic, is a salen-manganese complex that exhibits the catalytic actions of both superoxide dismutase and catalase, important antioxidant enzymes biosynthesized by cells. In the current study, we evaluated the protection effects of EUK-134 against D-galactose-induced oxidative stress and accelerated aging in rats. Methods: D-galactose was sub-cutaneously injected at a dose of 100 mg/kg on the back of rats once daily for 42 days and simultaneously EUK-134 was administered to the rats by intra-abdominal injection at a dose of 5 mg/kg once daily. As a positive control, donepezil was administered to the rats by oral feeding at a dose of 1 mg/ kg once daily. Following behavioral tests (eight-arm radial maze test and Morris water maze test), animals were sacrificed on day 42, and their brains were used for histopathological and biochemical assessments of oxidative stress. Results: We found that the administration of EUK-134 (5 mg/kg, i.a.) significantly reversed the spatial memory deficits, the brain weight loss, the reduced cerebral cortex thickness, the decreased pyramidal neuron density and the pyramidal layer in brain hippocampus, the decreased superoxide dismutase activity, the decreased catalase activity, the increased malondialdehyde level, the increased acetylcholine esterase activity and the decreased acetylcholine level in the brain hippocampus and prefrontal cortex of D-gal-induced aging rats, as did the administration of donepezil (1 mg/ kg, oral). Conclusion: These results indicated that EUK-134 possesses neuroprotective effects against D-galactose-induced senescence, probably due to its antioxidant enzyme activities and this shows the availability of EUK-134 in the prevention and treatment of neurodegenerative diseases such as Alzheimer’s disease.

THE LEVEL OF OXIDATIVE STRESS METABOLITES IN AN EXPERIMENTAL MODEL WITH PERIODONTITIS

Europäische Wissenschaftliche Gesellschaft Home About the Journal Peer Review Editorial Board For Authors Reviewer Recognition Archiv Kontakt Impressum EWG e.V. indexing in the Clarivate Analytics indexing in the Emerging Sources Citation Index Crossref Member Badge Erfolgreich durch internationale Zusammenarbeit MORPHOLOGY, PATHOLOGY, PHYSIOLOGY Cite as: Archiv EuroMedica. 2022. 12; 3: e1. DOI 10.35630/2199-885X/2022/12/3.2 Received 07 March 2022; Received in revised form 11 April 2022; Accepted 13 April 2022 THE LEVEL OF OXIDATIVE STRESS METABOLITES IN AN EXPERIMENTAL MODEL WITH PERIODONTITIS Tatyana Tarasova1 orcid id logo , Larisa Balykova1 orcid id logo , Dalila Khaydar2 orcid id logo, Olga Gurova2 orcid id logo, Alexey Zakhvatov1 orcid id logo, Elina Korovyakova2 orcid id logo, Larisa Mosina1, Roman Tarasov1, Maria Francisca Alekseeva3 1National Research Ogarev Mordovia State University, Saransk; 2Peoples' Friendship University of Russia, Moscow; 3Pirogov Russian National Research Medical University, Moscow, Russia download article (pdf) 9023060@mail.ru ABSTRACT In people worldwide, chronic periodontitis occurs in 10-15% of cases. Prolonged inflammation of periodontal tissues contributes to the formation of oxidative stress. The purpose of this study was to evaluate the level of malondialdehyde and superoxide dismutase (as indicators of oxidative stress) in periodontitis in rats. For this, in the main group of rats (n=10) a model of ligature periodontitis was created. The control group of rats (n=10) was intact. As a result, in periodontitis, the level of malondialdehyde doubled. We also found an inverse relationship between the level of lipid damage and superoxide dismutase activity. Conclusions. The level of metabolites of redox processes is significantly increased in periodontitis. This confirms a significant increase in the indicators of malondialdehyde. A decrease in superoxide dismutase activity leads to a low antioxidant status in rats.

РЫБИЙ ЖИР ПРЕДУПРЕЖДАЕТ РАЗВИТИЕ АРТЕРИАЛЬНОЙ ГИПОТЕНЗИИ У КРЫС С ПОСТТРАВМАТИЧЕСКИМ СТРЕССОВЫМ РАССТРОЙСТВОМ

Objectives. To evaluate the nature and mechanisms of the protective effect of fish oil (FO) on systemic hemodynamics in rats with an experimental analogue of post-traumatic stress disorder (PTSD). Material and methods. The studies were carried out on 50 outbred white male rats weighing 210-240 g, divided into groups: «Control», «PTSD», «FO», «FO+PTSD». An analogue of PTSD was reproduced by rats contacting with cat feces for 10 days for 15 minutes daily. Fish oil was administered intragastrically in doses of 0.2 ml (100 mg/kg body weight of eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids, CJSC «Biosola», Lithuania) 3 days before modelling PTSD and during 10 days of stressor action. After 2 weeks, systolic, diastolic, mean arterial blood pressure (SBP, DBP, MAP) and heart rate (HR) were measured by a non-invasive method. The concentration of endothelial NO-synthase (eNOS), inducible NO-synthase (iNOS), corticosterone, C-reactive protein (C-RP), interleukin-1β (IL-1β) was determined in blood serum by enzyme-linked immunosorbent assay (ELISA); spectrophotometric method was used to determine the concentration of malondialdehyde (MDA), diene conjugates (DC), as well as the activity of catalase (CAT) and superoxide dismutase (SOD). Results. In animals with PTSD, there was a decrease in SBP, DBP and MAP by 18-23% and an increase in heart rate by 20%. The concentration of eNOS in the blood of rats with PTSD decreased by 28%, and iNOS increased 2.28 times, along with 3.3 and 3.6 times increase in the content of DC and MDA against the background of the decreased SOD activity by 27%, CAT by 59% and 1.6 and 3 times increase in the concentration of C-RP and IL-1β, respectively, compared with the control. The introduction of FO either prevented or significantly limited the severity of the detected changes. Conclusions. The introduction of fish oil to rats prevents the development of arterial hypotension, as well as the changes in the concentration of eNOS and iNOS, it also prevents the disruption of the prooxidant-antioxidant status of blood serum, and reduces the severity of systemic inflammation in animals with PTSD.