Manganese Superoxide Dismutase Gene Research Articles

The Effect of Barley Bran Polyphenol-Rich Extracts on the Development of Nonalcoholic Steatohepatitis in Sprague–Dawley Rats Fed a High-Fat and High-Cholesterol Diet

Oxidative stress and inflammation play a central role in the progression of nonalcoholic steatohepatitis (NASH), which can lead to liver cirrhosis. Barley bran has potential bioactivities due to its high content of functional substances, such as anthocyanins, with anti-inflammatory and anti-oxidative properties. Here, we investigated whether barley bran polyphenol-rich extracts (BP) can prevent NASH in Sprague–Dawley rats fed a high-fat and high-cholesterol diet including 1.25% or 2.5% cholesterol for 9 weeks. In the rat model of NASH with advanced hepatic fibrosis, BP prevented NASH development by ameliorating the histopathological findings of lobular inflammation. The BP also tended to attenuate serum aspartate aminotransferase level in this model. In the rat model of NASH with mild-to-moderate hepatic fibrosis, BP tended to attenuate the serum levels of transaminases. BP-dose-dependent effects were revealed for several parameters, including monocyte chemoattractant protein-1, transforming growth factor-β, and manganese superoxide dismutase gene expressions in the liver. These results suggest that BP may prevent NASH development or progression, presumably due to its anti-inflammatory and anti-oxidative properties.

Enterocytozoon hepatopenaei (EHP) Infection Alters the Metabolic Processes and Induces Oxidative Stress in Penaeus vannamei

Enterocytozoon hepatopenaei (EHP) is highly contagious and can cause hepatopancreatic microsporidiosis (HPM), which is typically characterized by the slow growth of shrimp. In this study, the differences in histology, metabolism, oxidative stress and growth between healthy and EHP-infected Penaeus vannamei were analyzed using an EHP challenge experiment. Histology showed that EHP caused lesions in the hepatic tubules of P. vannamei, such as hepatic tubular atrophy and epithelial cell shedding, with mature spores. Meanwhile, white feces may appear when the infection is severe. Furthermore, the content of total protein, glycogen, ATP and glucose in the EHP challenge group was significantly reduced. The qPCR results showed that EHP infection changed the expression of key genes in glucose metabolism, among which hexokinase (HK), phosphofructokinase (PFK), pyruvatekinase (PK), citrate synthase (CS) and isocitric dehydrogenase (IDH) were significantly down-regulated, while phosphoenolpyruvate carboxykinase (PEPCK), fructose bisphosphatase (FBP) and glucose-6-phosphatase (G6P) were significantly up-regulated. Obviously, the expression of growth-related genes was disordered. Simultaneously, the antioxidant genes manganese superoxide dismutase (MnSOD), catalase (CAT), glutathione peroxidase (GPX), glutathione-S-transferases (GST) and nuclear factor E2-related factor2 (Nrf2) were up-regulated to varying degrees in the EHP challenge group, and EHP infection induced significant increases in the oxidative damage products lipid peroxide (LPO) and malondialdehyde (MDA). Ultimately, the shrimp weight of the challenge group was 6.85 ± 0.86 g, which was significantly lower than that of the control group (8.95 ± 0.75 g). Taken together, we speculate that EHP changes the substance metabolism and growth process by causing oxidative damage to the hepatopancreas, which may lead to the growth retardation of P. vannamei.

An integrated approach for the assessment of the electrochemical oxidation of diclofenac: By-product identification, microbiological and eco-genotoxicological evaluation

Diclofenac (DCF), a contaminant of emerging concern, is a non-steroidal anti-inflammatory drug widely detected in water bodies, which demonstrated harmful acute and chronic toxicity toward algae, zooplankton and aquatic invertebrates, therefore its removal from impacted water is necessary. DCF is recalcitrant toward traditional treatment technologies, thus, innovative approaches are required. Among them, electrochemical oxidation (EO) has shown promising results. In this research, an innovative multidisciplinary approach is proposed to assess the electrochemical oxidation (EO) of diclofenac from wastewater by integrating the investigations on the removal efficiency and by-product identification with the disinfection capacity and the assessment of the effect on environmental geno-toxicity of by-products generated through the oxidation.The electrochemical treatment successfully degraded DCF by achieving >98 % removal efficiency, operating with NaCl 0.02 M at 50 A m−2. By-product identification analyses showed the formation of five DCF parental compounds generated by decarboxylic and CN cleavage reactions.The disinfection capacity of the EO technique was evaluated by carrying out microbiological tests on pathogens generally found in aquatic environments, including two rod-shaped Gram-negative bacteria (Pseudomonas aeruginosa and Escherichia coli), one rod-shaped Gram-positive bacterium (Bacillus atrophaeus), and one Gram-positive coccus (Enterococcus hirae).Eco-toxicity was evaluated in freshwater organisms (algae, rotifers and crustaceans) belonging to two trophic levels through acute and chronic tests. Genotoxicity tests were carried out by Comet assay, and relative expression levels of catalase, manganese and copper superoxide dismutase genes in crustaceans. Results highlight the effectiveness of EO for the degradation of diclofenac and the inactivation of pathogens; however, the downstream mixture results in being harmful to the aquatic ecosystem.

Patient Characteristics and Prevalence of Single Nucleotide Polymorphism (SNP) V16A MnSOD Gene in Diabetic Retinopathy Patients at RSUP Prof. Dr. I.G.N.G. Ngoerah Denpasar Bali

Diabetic Retinopathy (DR) is a microvascular complication of Diabetes Mellitus (DM) caused by hyperglycemia and oxidative stress that is prevalent to the blindness risk. Manganese superoxide dismutase (MnSOD) gene affect the oxidative damage and progression of DR severity. This study aims to determine the association of patient characteristics on the severity and prevalence of Single Nucleotide Polymorphism (SNP) V16A in the MnSOD gene in DR patients at Prof. Dr. I.G.N.G. Ngoerah Denpasar Bali. Twelve (12) subjects with Non-Proliferative DR and 21 subjects with Proliferative DR were enrolled. Patient characteristics (age, T2DM duration, BMI, blood pressure) were associated to the DR severity using cross-sectional analytic study. While to detect the status of the SNP V16A MnSOD gene using descriptive experimental study. DNA segment amplification was performed using the PCR method, sequencing was performed to detect the base pattern at the location of the SNP. A domination of the VV genotype in the SNP V16A MnSOD gene was present in all subjects (100%). The majority of subjects were female (51,5%), age range 40-65 years (84,9%), T2DM duration <10 years (60,6%), normal BMI (60,6%). Blood pressure was dominated with non hypertension 60,6%, with a history of oral anti hypertensive. No significant association was found between patient characteristics and the DR severity (p<0,05). We may conclude that wildtype variant (VV) SNP V16A MnSOD gene was dominated in this finding. There is no significant association between patient characteristics and the severity of DR in Prof. Dr. I.G.N.G. Ngoerah Denpasar Bali. Keywords: Diabetic Retinopathy, MnSOD gene, SNP V16A

SOD2 in platelets: with age comes responsibility

SOD2 in platelets: with age comes responsibility

Expression Changes of SIRT1 and FOXO3a Significantly Correlate with Oxidative Stress Resistance Genes in AML Patients.

The increased metabolism in acute myeloid leukemia (AML) malignant cells resulted in the production of high levels of free radicals, called oxidative stress conditions. To avoid this situation, malignant cells produce a considerable amount of antioxidant agents, which will lead to the release of a continuous low level of reactive oxygen species (ROS), causing genomic damage and subsequent clonal evolution. SIRT1 has a key role in driving the adaptation to this condition, mainly through the deacetylation of FOXO3a that affects the expression of oxidative stress resistance target genes such as Catalase and Manganese superoxide dismutase (MnSOD). The aim of this study is to simultaneously investigate the expression of SIRT1, FOXO3a, and free radical-neutralizing enzymes such as Catalase and MnSOD in AML patients and measure their simultaneous change in relation to each other. The gene expression was analyzed using Real Time-PCR in 65 AML patients and 10 healthy controls. Our finding revealed that expression of SIRT1, FOXO3a, MnSOD and Catalase was significantly higher in AML patients in comparison to healthy controls. Also, there was a significant correlation between the expression of SIRT1 and FOXO3a, as well as among the expression of FOXO3a, MnSOD and Catalase genes in patients. According to the results, the expression of genes involved in oxidative stress resistance was higher in AML patients, which possibly contributed to the development of malignant clones. Also, the correlation between the expression of SIRT1 and FOXO3a gene reflects the importance of these two genes in increased oxidative stress resistance of cancer cells.

An accidental discovery of mannan-oligosaccharide's protection effect against air exposure and its potential mechanism in hybrid grouper (Epinephelus lanceolatus ♂ × Epinephelus fuscoguttatus ♀).

The original objective was to explore the potential benefiting effects of three prebiotics in hybrid grouper (Epinephelus lanceolatus♂ × Epinephelus fuscoguttatus♀). Therefore, three experimental diets (basal diet + 1% fructooligosaccharide, Diet F; basal diet + 1% inulin, Diet I; basal diet + 0.3% mannan-oligosaccharide, Diet M) and one basal diet (Diet C) were prepared and a feeding trial was conducted. However, at the end of the fourth week into the feeding experiment, a water-leaking accident occurred and fishes of all groups went through an unexpected air exposure event. Surprisingly, different prebiotic-supplemented groups showed significantly different air exposure tolerance: the mortality of M group was significantly lower (P ≤ 0.05) than all the other groups. Examination of antioxidant, non-specific immunity, and stress parameters revealed that comparing to control group, M group showed significantly increased catalase (CAT), acid phosphatase (ACP), and alkaline phosphatase (AKP) activities, decreased superoxide dismutase (SOD) activity, and similar cortisol level (P ≤ 0.05). Real-time PCR experiment revealed that M group significantly increased the expression of CAT, glutathione peroxidase (GPx), and manganese superoxide dismutase (MnSOD) genes in head kidney (P ≤ 0.05). Overall, M exhibited the best anti-air exposure/antioxidative stress effects among the three prebiotics and could be considered a promising feed additive to relieve air exposure/oxidative stress in hybrid grouper culture.

Association of the Manganese Superoxide Dismutase (Mn-SOD) Gene C47T Polymorphism with Lung Cancer: A Case-Control Study.

The objective of this study was to determine the association between manganese superoxide dismutase (Mn-SOD) gene C47 T polymorphism and the risk of malignant lung cancer in Iraqi smokers. Blood samples were obtained from 260 lung cancer patients (88 females and 172 males) and 295 healthy individuals (91 females and 204 males). DNA was extracted from blood samples and the SOD2 gene was amplified using specific primers. The nucleotide sequences of the SOD2 gene were analyzed by using BLAST server at National Center for Biotechnology Information (NCBI) and the Raptorx app. TT, CT, and CC genotypes concentrations were 48.1%, 33.2%, and 18.7%, respectively, in the control group. The concentrations of TT, CT, and CC genotypes were 43.5%, 31.5%, and 25%, respectively, in the case group. There were no statistical differences between cases and controls in terms of genotype frequency of SOD2C47T polymorphism. We observed that SOD2C47T polymorphism CT genotype did not increase the risk of lung cancer development compared to those with TT genotype (OR= 0.951, 95% CI = 0.648-1.396; P = 0.798). In addition, it was observed that CC genotype did not increase the risk of lung cancer development in comparison with TT genotype ( OR=0.673, 95% Cl=0.435-1.041: P=0.075). These results indicated that there was no association between SOD2C47T polymorphism and the risk of lung cancer development in Iraqi smokers.

Association of Polymorphisms in Antioxidant Enzyme-Encoding Genes with Diabetic Nephropathy in a Group of Saudi Arabian Patients with Type II Diabetes Mellitus.

IntroductionAn imbalance between reactive oxygen species (ROS) generation and the defence mechanisms underlying the activity of antioxidant enzymes has been demonstrated as the leading pathology in diabetes mellitus (DM)-related microvascular complications.PurposeThis study aims to evaluate the association between polymorphisms in antioxidant enzyme-encoding genes: catalase (CAT); manganese superoxide dismutase (Mn-SOD); glutathione S transferase M1 (GSTM1); and GSTT1 glutathione S transferase T1 (GSTT1), and the risk of type II diabetic nephropathy (DN) in the Saudi population.Patients and MethodsThe present study involved 64 type II DM patients with nephropathy and 64 type II diabetes patients without nephropathy from the King Abdulaziz University (KAU) Hospital. They underwent real-time PCR genotyping for the Mn-SOD and CAT genes. Multiplex PCR was used to detect GSTM1- and GSTT1-null polymorphisms.ResultsA statistically significant difference was observed between the case and control groups with regard to polymorphisms in the CAT gene (P = 0.037), but not for polymorphisms in the Mn-SOD (P = 0.64) gene. In addition, a statistically significant association was observed between null polymorphisms of the GSTT1 and GSTM1 genes and DN in the case and control groups (P = 0.046 and P = 0.035, respectively).ConclusionOur results showed that the genetic ability to combat oxidative stress may play a major role in DN pathogenesis in Saudi type II DM patients. These polymorphisms in antioxidant enzyme-encoding genes could be used as independent genetic markers for the construction of risk prediction models for kidney-related complications in type II DM patients.

Methylation of the Hippo effector YAP by the methyltransferase SETD7 drives myocardial ischaemic injury: a translational study.

Methylation of non-histone proteins is emerging as a central regulatory mechanism in health and disease. The methyltransferase SETD7 has shown to methylate and alter the function of a variety of proteins in vitro; however, its function in the heart is poorly understood. The present study investigates the role of SETD7 in myocardial ischaemic injury. Experiments were performed in neonatal rat ventricular myocytes (NRVMs), SETD7 knockout mice (SETD7-/-) undergoing myocardial ischaemia/reperfusion (I/R) injury, left ventricular (LV) myocardial samples from patients with ischaemic cardiomyopathy (ICM), and peripheral blood mononuclear cells (PBMCs) from patients with ST-elevation MI (STEMI). We show that SETD7 is activated upon energy deprivation in cultured NRVMs and methylates the Hippo pathway effector YAP, leading to its cytosolic retention and impaired transcription of antioxidant genes manganese superoxide dismutase (MnSOD) and catalase (CAT). Such impairment of antioxidant defence was associated with mitochondrial reactive oxygen species (mtROS), organelle swelling, and apoptosis. Selective pharmacological inhibition of SETD7 by (R)-PFI-2 restored YAP nuclear localization, thus preventing mtROS, mitochondrial damage, and apoptosis in NRVMs. In mice, genetic deletion of SETD7 attenuated myocardial I/R injury, mtROS, and LV dysfunction by restoring YAP-dependent transcription of MnSOD and CAT. Moreover, in cardiomyocytes isolated from I/R mice and ICM patients, (R)-PFI-2 prevented mtROS accumulation, while improving Ca2+-activated tension. Finally, SETD7 was up-regulated in PBMCs from STEMI patients and negatively correlated with MnSOD and CAT. We show a methylation-dependent checkpoint regulating oxidative stress during myocardial ischaemia. SETD7 inhibition may represent a valid therapeutic strategy in this setting.

Curcumin protects against manganese-induced neurotoxicity in rat by regulating oxidative stress-related gene expression via H3K27 acetylation

Long-term manganese exposure causes a neurodegenerative disorder referred to as manganese poisoning, but the mechanism remains unclear and no specific treatment is available. Oxidative stress is widely recognised as one of the main causes of manganese-induced neurotoxicity. In recent years, the role of histone acetylation in neurodegenerative diseases has been widely concerned. curcumin is a natural polyphenol compound extracted from the rhizome of turmeric and exhibits both antioxidant and neuroprotective properties. Therefore, we aimed to investigate whether and how curcumin protects against manganese-induced neurotoxicity from the perspective of histone acetylation, based on the reversibility of histone acetylation modification. In this study, rats were treated with or without curcumin and subjected to long-term manganese exposure. Results that treatment of manganese decreased the protein expression of H3K18 acetylation and H3K27 acetylation at the promoters of oxidative stress-related genes and inhibited the expression of these genes. Nevertheless, curcumin increased the H3K27 acetylation level at the manganese superoxide dismutase (SOD2) gene promoter and promoted the expression of SOD2 gene. Oxidative damage in the rat striatum as well as learning and memory dysfunction were ameliorated after curcumin treatment. Taken together, our results suggest that the regulation of oxidative stress by histone acetylation may be a key mechanism of manganese-induced neurotoxicity. In addition, curcumin ameliorates Mn-induced neurotoxicity may be due to alleviation of oxidative damage mediated by increased activation of H3K27 acetylation at the SOD2 gene promoter.

Combined oncolytic adenovirus carrying MnSOD and mK5 genes both regulated by survivin promoter has a synergistic inhibitory effect on gastric cancer.

Gastric cancer (GC) is one of the major causes of cancer-related mortality. The use of oncolytic virus for cancer gene-virotherapy is a new approach for the treatment of human cancers. In this study, a novel Survivin promoter-driven recombinant oncolytic adenovirus carrying mK5 or MnSOD gene was constructed, which was modified after deletion of the E1B gene. Human plasminogen Kringle 5 mutant (mK5) and manganese superoxide dismutase (MnSOD) are both potential tumor suppressor genes. By constructing Ad-Surp-mK5 and Ad-Surp-MnSOD oncolytic adenoviruses, we hypothesized that the combination of the two viruses would enhance the therapeutic efficacy of GC as compared to the one virus alone. The results of the in vitro experiments revealed that the combination of adenovirus carrying mK5 and MnSOD gene exhibited stronger cytotoxicity to GC cell lines as compared to the virus alone. Additionally, the virus could selectively kill cancer cells and human somatic cells. Cell staining, flow cytometry, and western blot analysis showed that the combination of two adenoviruses containing therapeutic genes could promote the apoptosis of cancer cells. In vivo experiments further verified that Ad-Surp-mK5 in combination with Ad-Surp-MnSOD exhibited a significant inhibitory effect on the growth of GC tumor xenograft as compared to the virus alone, and no significant difference was observed in the bodyweight of treatment and the normal mice. In conclusion, the combination of our two newly constructed recombinant oncolytic adenoviruses containing mK5 or MnSOD therapeutic genes could significantly inhibit gastric cancer growth by inducing apoptosis, suggestive of its potential for GC therapy.

Evaluating the expression of key genes involved in resistance to oxidative stress in ALL patients

Background: Leukemia accounts for about 8% of all cancers and causes approximately 7% of mortalities due to malignancies. Acute lymphoblastic leukemia (ALL) is the most common childhood cancer and rare in older subjects. The aim of this study was to evaluate the expression of oxidative stress resistance genes including Catalase, manganese superoxide dismutase (MnSOD), Forkhead Box O3 (Foxo3a), and sirtuin-1 (SIRT1) in ALL patients that may be applied for therapeutic purposes in the future.
 Materials and Methods: In this observational case-control study, blood samples were drawn from 60 newly diagnosed ALL patients and 10 healthy individuals as a control group. After RNA extraction and cDNA synthesis, real-time polymerase chain reaction (RT-PCR) amplification was performed using specific primers for evaluating the expression of Catalase, MnSOD, Foxo3a, and SIRT1 genes.
 Results: The expression of all studied genes were significantly higher in ALL patients than in the control group; catalase gene, FOX gene, MnSOD gene, and SIRT1 gene were expressed 4 times (p =0.04), 4.5 times (p =0.001), 2.2 times (p =0.05) and 4.8 (p =0.01) times higher than healthy individuals in the control group respectively. However, no significant relationship between their expression and the stage of the disease and blast percentage was demonstrated (P>0.05).
 Conclusion: According to these results, the authors believe that the pathways involved in oxidative stress may be one of the most important causes of ALL disease's development and progression. In this regard, targeting the critical genes of these pathways can be considered a potential treatment with fewer side effects.

Cloning of Mn-SOD gene and its mRNA expression difference and antioxidant enzyme activities under hypoxia stress of cobia Rachycentron canadum.

Environmental hypoxia affects the survival and development of organisms. It is also an important environmental factor that leads to oxidative damage. Hypoxia is a condition in which tissues are deprived of oxygen; reoxygenation is the phenomenon in which hypoxic tissues are exposed to oxygen. Hypoxia-reoxygenation is vital in pathogenesis, where the production of reactive oxygen species and antioxidant disparity significantly contribute to disease progression, and it is one of the most common physiological stressors in the aquaculture industry. In this study, the full length of complementary DNA (cDNA) of the manganese superoxide dismutase (Mn-SOD) gene of healthy cobia Rachycentron canadum was analysed using rapid amplification of cDNA ends. The real-time quantitative Polymerase Chain Reaction was used to measure the expression levels of Mn-SOD mRNAs in various tissues (heart, muscle, brain, liver, kidney, gill, intestine, and spleen). The 2-ΔΔCT method was used to performed the expression analysis. The experimental data were analysed using SPSS ver. 19.0 ( https://spss.software.informer.com/19.0/ ). P < 0.05 and P < 0.01 were set as significant differences. The values were articulated as mean ± standard deviation. The Mn-SOD gene cDNA sequence was 1209bp long, including a 684bp open reading frame, 42bp 5'UTR and 483bp 3'UTR, encoding 227 amino acids. Under hypoxia-reoxygen stress, the expression of Mn-SOD in brain tissue was significantly lower than in the control group after 8h of reoxygenation and higher than the control group after 24h. Hypoxia and subsequent reoxygenation triggered a disturbance in antioxidant homeostasis, displayed in the modification of GPx expression/activity in the liver: GPx was improved. These results provide valuable information on the role of Mn-SOD regulation in oxidative stress caused by hypoxia.

Gene Therapy for Systemic or Organ Specific Delivery of Manganese Superoxide Dismutase.

Manganese superoxide dismutase (MnSOD) is a dominant component of the antioxidant defense system in mammalian cells. Since ionizing irradiation induces profound oxidative stress, it was logical to test the effect of overexpression of MnSOD on radioresistance. This task was accomplished by introduction of a transgene for MnSOD into cells in vitro and into organs in vivo, and both paradigms showed clear radioresistance following overexpression. During the course of development and clinical application of using MnSOD as a radioprotector, several prominent observations were made by Larry Oberley, Joel Greenberger, and Michael Epperly which include (1) mitochondrial localization of either manganese superoxide dismutase or copper/zinc SOD was required to provide optimal radiation protection; (2) the time required for optimal expression was 12–18 h, and while acceptable for radiation protection, the time delay was impractical for radiation mitigation; (3) significant increases in intracellular elevation of MnSOD activity were required for effective radioprotection. Lessons learned during the development of MnSOD gene therapy have provided a strategy for delivery of small molecule SOD mimics, which are faster acting and have shown the potential for both radiation protection and mitigation. The purpose of this review is to summarize the current status of using MnSOD-PL and SOD mimetics as radioprotectors and radiomitigators.

The association of manganese superoxide dismutase gene polymorphism (Rs4880) with diabetic macular edema in a cohort of type 2 diabetic Egyptian patients

BackgroundDiabetic retinopathy (DR) and diabetic macular edema (DME) are the leading causes of blindness in patients with diabetes. Increasing numbers of people with diabetes worldwide suggest that DR and DME will continue to be major contributors to vision loss and associated functional impairment for years to come. Oxidative stress is a key participant in the development and progression of diabetes mellitus (DM) and its complications. Antioxidant status can affect vulnerability to oxidative damage, onset and progression of diabetes, and complications of diabetes. Manganese superoxide dismutase (Mn-SOD) is a key mitochondrial enzyme in cell defense against reactive oxygen species (ROS). DR and progression to DME have been associated with polymorphism in the second exon of the Mn-SOD gene at the 16th amino acid (Ala16Val) in the mitochondrial targeting sequence (MTS) of the protein. The study aimed to investigate the association between Ala16Val Mn-SOD gene polymorphism and the susceptibility to DR and DME in type 2 DM (T2DM).ResultsIn this study, 150 patients with type 2 DM were enrolled: 100 patients with DR with and without diabetic macular edema (DME) and 50 patients with type 2 diabetes with a duration of 10 years without DR. Ala16Val SNP of the Mn-SOD gene (rs4880) was detected by TaqMan real-time PCR. The results showed that the homozygous polymorphic variant VV between the DME group is significantly higher than the non-DME group (P 0.018) among the DR group.ConclusionMn SOD A16V polymorphism itself may not be associated with DR; meanwhile, it may be implicated in the pathogenesis of DME.

Relationship between Superoxide Dismutase Manganese Gene Polymorphism and Eye Tumors

ABSTRACT&#x0D; &#x0D; Background: Orbital tumor in Indonesia is one of the eye health problems that can cause blindness. The impact caused by orbital tumors on patients is quite large because it can result in blindness and even death due to its metastatic nature. The role that SOD plays in cancer biology is not well understood, most studies showing a more oxidative state, characterized by increased intracellular ROS, particularly superoxide.&#x0D; Objective: To determine the relationship between Manganese Superoxide Dismutase (SOD2) gene polymorphisms and the incidence of orbital tumors in Medan.&#x0D; Methods: This study is an analytic observational study with a cross-sectional data collection method using controls. Comparisons were made between the control group and the observed group to see the relationship between SOD2 polymorphisms and the risk of orbital tumor incidence in Medan. The ophthalmic examination, anterior and posterior segments, and assessment of CT orbit if deemed necessary for the orbital tumor patients. Histopathological examination was done by the Pathologist. Blood samples was taken for polymorphism examination on extracted DNA using the Polymerase Chain Reaction (PCR) and Restriction Fragment Length Polymorphism (RFLP) methods.&#x0D; Results: About 30 patients that met the inclusion criterias. Laterality, the left eye is more likely to suffer from tumors when compared to the right eye. This study found as many as 16 patients, while malignant tumors was 14 patients. There was a relationship between the MnSOD gene polymorphism and the incidence of orbital tumors (p &lt;0.001), there was a relationship between the MnSOD gene polymorphism and the incidence of orbital tumors in the female sex (p &lt;0.001)&#x0D; Conclusion: There was a relationship between MnSOD gene polymorphisms and the incidence of orbital tumors (p &lt;0.001)

Dietary arsenic supplementation induces oxidative stress by suppressing nuclear factor erythroid 2-related factor 2 in the livers and kidneys of laying hens

This study investigated the effects of dietary arsenic supplementation on laying performance, egg quality, hepatic and renal histopathology, and oxidative stress in the livers and kidneys of laying hens. Furthermore, the nuclear factor erythroid 2-related factor 2 (Nrf2)-Kelch-like ECH-associated protein 1 (Keap1) pathway was explored to reveal the molecular mechanism of the stress. Five hundred and twelve 40-week-old Hyline White laying hens were randomly allocated to 4 groups with 8 pens per group and 16 hens per pen. The doses of arsenic administered to the 4 groups were 0.95, 20.78, 40.67, and 60.25 mg/kg. The results revealed that dietary arsenic supplementation significantly reduced hen-day egg production (P < 0.05), average egg weight (P < 0.05), Haugh units (P < 0.05), albumen height (P < 0.05), and eggshell strength (P < 0.05). Dietary arsenic supplementation also induced the accumulation of arsenic and histopathological damages in the liver and kidney. In accordance, dietary arsenic supplementation significantly enhanced serum alanine aminotransferase (P < 0.05), aspartate aminotransferase (P < 0.05), blood urea nitrogen (P < 0.05), and uric acid (P < 0.05) levels. After arsenic exposure, the activities of superoxide dismutase (SOD) (P < 0.05), catalase (P < 0.01), glutathione reductase (P < 0.05), and glutathione peroxidase (P < 0.05), and glutathione content (P < 0.05) were significantly decreased, while the malondialdehyde level was significantly increased (P < 0.05) in the liver and kidney. Positive correlations occurred between antioxidant enzyme activities and antioxidant enzyme gene expressions in the liver and kidney, except for renal manganese superoxide dismutase gene expression and SOD activity. Additionally, hepatic and renal Nrf2 mRNA expression was positively correlated with antioxidant gene expressions and negatively correlated with Keap1 mRNA expression. In summary, dietary arsenic supplementation induced oxidative stress by suppressing the Nrf2-Keap1 pathway in the livers and kidneys of laying hens.

Extraction, Identification and Gene Cloning of Mn-SOD from Pleurotus tuber-regium

The manganese superoxide dismutase of Pleurotus tuber-regium was extracted and identified. The manganese superoxide dismutase (Mn-SOD) gene of P. tuber-regium was cloned from the mycelium of P.tuber-regium. Mn-SOD of P.tuber-regium was extracted by liquid nitrogen grinding, ultrasound, ammonium sulfate precipitation and dialysis. Mn-SOD activity of P. tuber-regium was determined by WST-8 method. SOD type of P. tuber-regium was identified by H2O2. Mn-SOD gene was cloned from P. tuber-regium by homologous cloning, rapid amplification of cDNA ends, fusion primers and nested PCR. Results showed that the activity of Mn-SOD of P. tuber-regium was 1.66 U. There was no significant difference between the enzyme treated with H2O2 and untreated, indicating that the main SOD in P. tuber-regium was Mn-SOD. PtMn-SOD was cloned and obtained. Its DNA sequence was 1025 bp in total, 663 bp in open reading frame and 220 amino acids were encoded. Sequence analysis and phylogenetic tree showed that PtMn-SOD was closely related to Pleurotus ostreatus (accession number:MH645359.1). It was predicted that the molecular weight of the protein was 24.54 kDa and the isoelectric point of the protein was 7.86. PtMn-SOD protein located in mitochondria and played a role in mitochondria.

FvmnSOD is involved in oxidative stress defence, mitochondrial stability and apoptosis prevention in Fusarium verticillioides

Superoxide dismutases are key enzymes in elimination of the superoxide anion radical (O2 •- ) generated intracellularly or by exogenous oxidative stress eliciting agents, like menadione. In this study, we investigated the physiological role of the manganese superoxide dismutase-encoding gene in Fusarium verticillioides via the construction of a gene deletion mutant, ΔFvmnSOD and comparing its phenotype with that of the wild-type parental strain and a ΔFvmnSOD' C strain, complemented with the functional manganese superoxide dismutase gene. Deletion of FvmnSOD had no effect on the relative intracellular superoxide ratio but increased the sensitivity of the fungus to menadione sodium bisulphite on Czapek-Dox stress agar plates. The lack of FvmnSOD caused changes in mitochondrial morphology and physiology: The volumetric ratio of these cell organelles in the second hyphal segment, as well as the total, the KCN-sensitive cytochrome c-dependent and the KCN+SHAM (salicylhidroxamic acid)-resistant residual respiration rates, were higher in the mutant as compared to the wild-type and the complemented strains. Nevertheless, changes in the respiration rates were attributable to the higher volumetric ratio of mitochondria found in the gene deletion mutant. Changes in the mitochondrial functions also brought about higher sensitivity to apoptotic cell death elicited by the Penicillium chrysogenum antifungal protein. The gene deletion mutant developed significantly thinner hyphae in comparison to the wild-type strain. Deletion of FvmnSOD had no effect on fumonisin B1 and B2 production of the fungus grown in Myro medium as a static culture.