Superoxide Dismutase Gene Polymorphism Research Articles

Role of superoxide dismutase in acute pancreatitis: from antioxidant protection to gene regulation

We present modern data on the role of superoxide dismutase (SOD) in antioxidant protection and gene regulation in acute pancreatitis. Antioxidant enzymes are essential in pathogenesis of numerous diseases. SOD is one of the key enzymes of antioxidant system. In this review, we analyzed activity of this enzyme depending on various factors, mechanisms and role in physiological and pathological processes, in particular, acute pancreatitis. SOD is significantly less active in patients with severe acute pancreatitis accompanied by renal failure, severe circulatory disorders and high mortality. There are some SOD gene polymorphisms, in particular, acute destructive pancreatitis R213G, contributing to acute inflammation. Thus, SOD is not only one of the key antioxidant enzymes, but also potential transcription factor regulating activity of signaling pathways. These aspects can underlie new therapies for diseases.

SOD2 in platelets: with age comes responsibility

SOD2 in platelets: with age comes responsibility

Superoxide Dismutase (SOD1) Gene Polymorphism in Cataract Patients of Karachi, Pakistan

Objective: To investigate the polymorphism superoxide dismutase (SOD1) gene and its relationship with the development of cataracts in patients of Karachi.Methods: This was a case-control study carried out at different centers in Karachi, Pakistan between September 2019 and 2020. A single nucleotide polymorphism (SNP) at rs2070424(SOD1) locus was examined with polymerase chain reaction (PCR) using high resolution melting curve (HRM) technique in 250 cataract patients and 250 healthy control groups of similar age and gender.Results: Of 500 subjects, there were 250 cases and 250 controls. The mean age of the cataract patients (cases) was 43.97± 13.36 years. Among cases, 150 (60.0%) were males and 100 (40.0%) were females whereas in controls, 127 were males (50.8%) and 123 (49.2%) were females. A significant association of cataract was found with age (p value = 0.005), and smoking (p-value = 0.001). AG genotype has a smaller risk (OR=1.77, 95% CI 1.11 – 2.66, p-value= 0.006) associated with cataract while GG has a higher risk (OR = 2.83, 95% CI 1.71 – 4.68, p-value < 0.001). Further, calculation of allelic distribution revealed that the G allele was more prevalent in the cataract group 200 (61.7%) as compared to controls 124 (38.3%) (p-value=0.001). Conclusion: The significantly higher G allele frequency in the SOD1 gene at the rs2070424(SOD1) locus in the cataract group indicates that potential risk factors contribute to cataracts' development. This study contributes to the genetic profiling of cataract patients in the Pakistani population.

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.

Glutathione S-transferase, catalase, and mitochondrial superoxide dismutase gene polymorphisms modulate redox potential in systemic lupus erythematosus patients from Manaus, Amazonas, Brazil.

To investigate the frequency of glutathione S-transferase (GST), catalase, and SOD2 genetic polymorphisms and their correlation with SLE. A total of 290 females (patients = 151; controls= 139) were recruited. Multiplex PCR was performed for genotyping GSTM1 and GSTT1 genes, whereas real-time qPCR was used for determination of SNPs: CAT C262T, SOD2 C47T, GSTP1 A313G and GSTP1 IVS6 -C16T. Thiol levels are decreased in SLE patients (p<0.001), while MDA levels were significantly higher (p<0.001) and those carrying the polymorphisms had higher rates of oxidative stress. Patients with double null deletion GSTT1null/GSTM1null had a frequency almost five times higher than the controls (p<0.001, OR 4.81, CI 1.98-12.11). SLE patients had a lower wild-type frequency of SOD2CC allele compared to controls (12.4% vs 27.3%). Statistical significances were observed on the association between the GSTT1null and GSTM1null with SOD2mut (p<0.001, OR 0.15, CI 0.05-0.47), with GSTP1 A303G (p=0.012, OR 0.19, CI 0.05-0.69), and with GSTP1 IVS6 (p=0.008, OR 0.14, CI 0.03-0.63). The same was observed between SOD2 C47T with GSTP1 A303G (p=0.09, OR 0.27, CI 0.09-0.74) and GSTP1 IVS6 (p=0.036, OR 0.41, CI 0.18-0.92). The deletion GSTT1null/GSTM1null may contribute to the increased of the oxidative stress in SLE patients. Isolated GSTP1 and CAT polymorphisms do not seem to influence the increased oxidative stress, neither SLE clinical manifestations. SOD2 47CT/TT allele may have greater oxidative stress due to structural change in the protein and decreased H2O2 production. The combination of polymorphic genes may be involved in the pathogenesis of the disease. Key points • Major question of our paper: Many studies have shown that the antioxidant status levels are decreased in patients with SLE, especially in severe stages of disease. We believe that this paper will be of interest to the readership of your journal had the involvement of polymorphisms and mutations in several genes that contribute to the genetic etiology of SLE, suggesting that these may influence the mechanisms of disease. • Our results. Thiol level was significantly (p<.001) lower and MDA level significantly increased (p<.001) among SLE patients. Those carrying the polymorphisms hadhigher rates of oxidative stress. SLE Patients had a frequency almost five times higher of double null deletion GSTT1null/GSTM1null than the controls.SLE Patients had a lower wild type frequency of SOD2CC allele compared to controls (12.4% vs 27.3%). We believed the deletion GSTT1null/GSTM1nullmay contribute to the increased of the oxidative stress in SLE patients while carriers of the mutant SOD2 47CT/TT allele may have greater oxidative stressdue to structural change in the protein and decreased H2O2 production. The combination of polymorphic genes may be involved in the pathogenesis of thedisease. • Implications of our results: Evidence for the involvement of genetic factors in severe clinical to lupus is compelling. This manuscript shows genetic insights in pathogenic pathways that may lead to severe clinical implications to LES. Therefore, it is necessary to understand their impact on overall disease pathogenesis and prognosis in these patients. We understand from general consensus about environmental factors can modify disease, however, maybe just in individuals who have a permissive genetic background. Even that no single gene predisposes some individuals to LES, we believe the genetic factors described in this manuscript are important elements in susceptibility to severe clinical to LES.

Superoxide Dismutase Gene Polymorphism is Associated With Ischemic Stroke Risk in the China Dali Region Han Population.

Background:Stroke is a serious cardiovascular disease, a major cause of disability and death in both developed and developing countries. Superoxide dismutases (SODs) are enzymes that catalyze the breakdown of superoxide into oxygen and hydrogen peroxide and play a key role in the antioxidant response. This study explored the relationship between single-nucleotide polymorphisms (SNPs) in SOD genes and the risk of ischemic stroke (IS) in the Chinese Han population of Dali City.Methods:For this case-control study, the authors enrolled 144 patients who had an IS and 128 healthy controls. The SNPs rs17880487 and rs80265967 of the SOD1 gene, rs4880 and rs2842960 of the SOD2 gene, and rs2695232 and rs7655372 of the SOD3 gene were detected through TaqMan polymerase chain reaction. Genotypes and allele frequencies of the 2 groups were compared. Odds ratio and 95% confidence intervals were calculated by unconditional logistic regression, and environmental factors were corrected with multivariate logistic regression analysis.Results:Rs7655372 of SOD3 was associated with a significantly increased risk of IS. Moreover, the A and GA genotypes of SNP rs7655372 were associated with increased risk of IS, whereas the A and GA genotypes were risk factors for IS. Furthermore, multivariate logistic regression analysis showed that the rs7655372 GA genotype is the independent risk factor for IS.Conclusion:The SOD3 gene rs7655372 locus polymorphism is a risk factor for IS in the Dali region.

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)

Role of MnSOD Val16Ala Gene Polymorphism in Changing the Level of Serum Metals in Workers Exposed to Heavy Metals in Al-Nasiriyah City

Low activity of antioxidant enzymes due to polymorphism in antioxidant genes and differences in mineral and metal levels creates oxidative stress that may play a role in advancing many diseases. The aim of this study was to determine the role of Manganese superoxide dismutase (MnSOD) gene polymorphism [rs4880 Val16Ala)] in exposed workers and to compare the levels of metals and minerals among its various genotypes in control group. A total of 80 individuals including age and gender matched workers and control group were genotyped. Detection of rs4880 polymorphism was done using sequencing technique. The blood serum were tested for determination of metals and minerals using Atomic absorption spectrophotometer (AA 6600 Shimadzu). This study indicate that the frequency of T allele was higher than that of C allele in control group as well as in workers. Our results indicate no association between all genotypes in study subjects. The results of present study indicates that Pb and Cd concentration differ significantly between TT genotypes of MnSOD (rs4880) gene polymorphism as compared to CC genotypes in workers and control group (p<0.05). Control group with TT, TC and CC genotypes have high concentration of Fe, Cu and Zn as compared to workers group.

A prospective study on associations between superoxide dismutase gene polymorphisms and antituberculosis drug-induced liver injury in a Chinese Han population.

Antituberculosis drug-induced liver injury (ATDILI) is increasing globally and, hence, it is crucial to predict its risk in the clinical management of antituberculosis therapy. As a major antioxidant, superoxide dismutase (SOD) is mainly responsible for providing defence against oxidative stress, which is involved in ATDILI. The present study aimed to investigate the associations between polymorphisms in SOD genes, including Cu/ZnSOD (SOD1), mitochondrial manganese SOD (MnSOD or SOD2) and extracellular SOD (SOD3), as well as the susceptibility to ATDILI in a Chinese Han population. In total, 1060 Chinese Han subjects highly suspected to have tuberculosis (TB) were prospectively enrolled from West China Hospital of Sichuan University. Overall, 746 subjects comprising 118 ATDILI and 628 ATD-tolerant TB patients were eligible and were genotyped for seven single-nucleotide polymorphisms in three SOD genes (SOD1: rs4816407 and rs1041740; SOD2: rs4880; SOD3: rs699473, rs2536512, rs2855262 and rs8192290). Logistic regression analysis showed that none of the seven genetic variants in the three SOD genes were significantly associated with susceptibility to ATDILI in the Chinese Han population after Bonferroni correction, except for a potential association for the SOD2 rs4880 A>G (G allele, p=0.190, odds ratio=1.53, 95% confidence interval=1.05-2.23; GG genotype, p=0.155). The promising application of single-nucleotide polymorphisms in the SOD1, SOD2 and SOD3 genes as genetic markers for ATDILI is challenged, and further studies are needed with larger sample sizes and different ethnicities, especially for SOD2 rs4880.

Superoxide Dismutase Levels and Polymorphism (Ala16val) In Tuberculosis Patients with Diabetes Mellitus in Medan City.

BACKGROUND:Infectious diseases and metabolic disorders would result in oxidative stress in cells. Superoxide dismutase (SOD) is an antioxidant present inside cells that acts against oxidative stress. SOD gene polymorphism can affect the activity and levels of SOD.AIM:This study aimed to analyse SOD levels and polymorphism of gene (ala16val) that regulated SOD in tuberculosis patients with diabetes mellitus in Medan city.METHODS:A total of 40 tuberculosis patients with diabetes mellitus and 40 healthy subjects participated in the study. The levels of SOD were measured using enzyme-linked immunosorbent assay (ELISA). Analysis of SOD gene polymorphism (ala16val) was done using polymerase chain reaction-restriction fragment lengths polymorphisms (PCR-RFLP) with BsaW1 as the restriction enzyme. The statistical significance was determined using the Mann Whitney test, Fisher’s exact test, and Kruskal Wallis test (p < 0.05).RESULTS:The SOD levels of tuberculosis patients with diabetes mellitus were lower than those of the healthy subjects (102.474 ± 36.07 U/L vs 294.543 ± 58.75 U/L, p < 0.05). Patients of tuberculosis with diabetes mellitus tend to have more value/Val genotypes than the healthy group (57.5% vs 50%, p > 0.05). There was no association between SOD levels and SOD gene polymorphism (ala16val) in tuberculosis patients with diabetes mellitus.CONCLUSION:In this study, there was an association between the levels of SOD and tuberculosis patients with diabetes mellitus, but not for the SOD gene polymorphism (ala16val). The SOD gene polymorphism (ala16val) was not the key role to influence the SOD levels in tuberculosis patients with diabetes mellitus in Medan city.

The Role of Extracellular Superoxide Dismutase (Ec-SOD) Gene Polymorphism in Motor Neuron Damage of Type 2 Diabetic Peripheral Neuropathy Patients of Babylon Province-Iraq

Background: Extracellular superoxide dismutase (EC-SOD) gene polymorphism play an essential role in the progression of diabetic complications. Reactive oxygen species (ROS) were known to damage neurons by enhancing nerve lipid peroxidation, the damaging mitochondrial DNA, break-down the respiratory chain, and the cross-linking of neuron proteins. Aim: the aim of this study was to investigate the relationship between (Ec-SOD) gene polymorphism and the pathogenesis of diabetic peripheral neuropathy in type2 diabetic patients. Arg(213)Gly polymorphism of Ec-SOD gene polymorphism were studied in type2 diabetic patients with (n=30) and without DPN (n=30). Results: Polymerase chain reaction (PCR) technique were used for detection Ec-SOD polymorphisms. This technique included the use of PCR primers (Forward and Reverse) to produce a restriction site in the amplified EC-SOD gene product just with the polymorphic base. Then, the product of (PCR) was digested with Eco52I restriction enzyme to detect Arg(-213)Gly polymorphic position. The results of Arg(-213)Gly polymorphism showed that the frequency of Arg/Arg, Arg/Gly, and Gly/Gly were 70%, 13.3%, and 16.6% in healthy control subject and 53.3%, 16.6%, and 30% in diabetic without neuropathy countered by 23.3%, 26.6%, and 50% in diabetic with neuropathy. This proposed that the Arg (-213)Gly polymorphism in the EcSOD gene is significantly associated with a risk for progression of diabetic peripheral neuropathy. Conclusions: Arg(-213)Gly polymorphism of Ec-SOD gene was associated with diabetic peripheral neuropathy in type2 diabetic patients of Babylon Province

Association of pre-eclampsia with SOD2 Ala16Val polymorphism among mother-father-infant triads.

To determine whether pre-eclampsia is associated with polymorphisms in superoxide dismutase (SOD) genes among mother-father-infant triads. We did this follow-up cohort study at 17 urban hospitals in Canada between October 1, 2008, and September 30, 2010. We recruited Canadian participants who had participated in the International Trial of Antioxidant Supplementation for the Prevention of Pre-eclampsia. Saliva specimens were collected for DNA extraction. The SOD1 +35A/C (rs2234694) and SOD2 Ala16Val C/T (rs4880) single-nucleotide polymorphisms (SNPs) were genotyped. Dual presence of the SOD2 Ala16Val TT variant among mother-father pairs (n=657) was associated with an increased risk of pre-eclampsia when compared with the absence of the TT variant among the mother-father pairs (7/48 [14.6%] vs 11/339 [3.2%]; adjusted odds ratio 6.80, 95% confidence interval 2.32-19.95; P<0.001). By contrast, presence of a single T variant in mother-father pairs (16/270 [5.9%]) or mother-infant pairs (8/179 [4.5%]) was not associated with pre-eclampsia. The SOD1 +35A/CSNP was not associated with pre-eclampsia. The SOD2 Ala16Val SNP might be involved in paternal influence on the maternal predisposition to pre-eclampsia. Genotyping of mother-father pairs could be a promising strategy to identify pre-eclampsia genes.

Manganese superoxide dismutase, glutathione peroxidase and catalase gene polymorphisms and clinical outcomes in acute kidney injury

Introduction The aim of this study was to evaluate the potential association of single gene polymorphisms of manganese superoxide dismutase (MnSOD), glutathione peroxidase 1 (GPX1) and catalase (CAT) with clinical outcomes of acute kidney injury (AKI). Materials and methods Ninety AKI patients and 101 healthy volunteers were included in the study. Determination of MnSOD rs4880, GPX1 rs1050450 and CAT rs769217 polymorphisms was performed using real-time polymerase chain reaction amplification. The duration of hospitalization of AKI patients, dialysis and intensive care requirements, sepsis, oliguria and in-hospital mortality rates were assessed. Results The MnSOD, GPX1 and CAT genotypes and allele frequencies of AKI patients did not differ significantly from those of healthy controls. In patients with a T allele in the ninth exon of the CAT gene, intensive care requirements were greater than those of patients with the CC genotype (p = 0.04). In addition, sepsis and in-hospital mortality were observed significantly more frequently in patients with a T allele in the ninth exon of the CAT gene (p = 0.03). Logistic regression analysis determined that bearing a T allele was the primary determinant of intensive care requirements and in-hospital mortality, independent of patient age, gender, presence of diabetes and dialysis requirements (OR 6.10, 95% CI 1.34–27.81, p = 0.02 and OR 10.25, 95% CI 1.13–92.80, p = 0.04, respectively). Conclusion Among AKI patients in the Turkish population, hospital morbidity and mortality were found to be more frequent in patients bearing a T allele of the rs769217 polymorphism of the CAT gene.

Superoxide Dismutase Gene (SOD1, SOD2, and SOD3) Polymorphisms and Antituberculosis Drug-induced Hepatitis.

PurposeDrug-induced liver injury (DILI) is a serious issue often leading to discontinuation of the proper regimen of antituberculosis drugs (ATD). Previous studies have suggested that antioxidant enzymes play an important role in DILI.MethodsWe explored whether polymorphisms in superoxide dismutase genes, including Cu/Zn superoxide dismutase (SOD1), manganese superoxide dismutase (SOD2) and extracellular superoxide dismutase (SOD3) are associated with ATD-induced hepatitis. Genotype distributions of four single nucleotide polymorphisms (SNPs) in three genes (rs2070424, SOD1; rs4880, SOD2; rs2536512, and rs1799895, SOD3) were compared between 84 patients with ATD-induced hepatitis and 237 patients tolerant to ATD.ResultsIntron SNP rs2070424 of SOD1 showed a significant association with ATD-induced hepatitis. The frequency of genotypes carrying minor alleles (GA or GG) was significantly higher in the case group than that of controls (P=0.019, OR=2.26, 95% CI 1.14-4.49). For the other SNPs of SOD2 and SOD3, there were no differences in genotype frequencies between ATD-induced hepatitis and ATD-tolerant controls.ConclusionsThese findings suggest that rs2070424 of SOD1 is significantly associated with ATD-induced hepatitis. This genetic variant may be a risk factor for ATD-induced hepatitis in individuals from Korea.

Seminal superoxide dismutase activity and its relationship with semen quality and SOD gene polymorphism

Superoxide dismutase (SOD) is an important component of antioxidative defense systems and plays an important role in protecting spermatozoa from oxidative damage. In this study, we assessed seminal SOD activity, its association with semen parameters, and also genetic and non-genetic factors contributing to the determination of SOD activity in infertile men. Semen samples were obtained from 435 male infertility patients. Sperm DNA damage levels were detected with the Tdt-mediated dUTP nick end labelling (TUNEL) assay. Four single nucleotide polymorphisms (SNPs) in SOD2 and SOD3 genes were genotyped using OpenArray platform. We found that seminal SOD activity was positively associated with sperm concentration and overall motility, whereas inversely with sperm DNA fragmentation. In addition, infertile men with SOD2 rs4880 CC variants showed a low level of SOD activity when compared with TT carriers (Mean ± SD: 268.3 ± 102.3 and 342.8 ± 98.2, respectively, P = 0.005). Those who consumed vitamin C/E (≥3 times per week) had a significantly higher SOD activity level than those who did not (mean ± SD: 379.8 ± 93.3 and 332.2 ± 94.9, respectively, P = 0.001). Seminal SOD activity and other factors influencing SOD activity play a role in determining sperm fertilization potential and male infertility.

Analysis of manganese superoxide dismutase (MnSOD: Ala-9Val) and glutathione peroxidase (GSH-Px: Pro 197 Leu) gene polymorphisms in mood disorders.

We investigated the etiopathogenetic role of manganese superoxide dismutase (MnSOD) (Ala-9Val) and glutathione peroxidase (GSH-Px) (Pro 197 Leu) gene polymorphisms in patients diagnosed with major depressive disorder (MDD) and bipolar I disorder (BD). Eighty patients with MDD, 82 patients with BD (total 162 patients) and 96 healthy controls were enrolled in this study and genotyped using a Real Time-Quantitative Polymer Chain Reaction (RT-qPCR)-based method. The patients with BD and MDD and the controls had a similar distribution of the genotypes and alleles in the Ala-9Val MnSOD gene polymorphism. Comparison of the MDD group and control group regarding the Pro 197 Leu GSH-Px gene polymorphism revealed similar genotype distribution but different allele distribution. The BD group and control group were similar both for genotypes and for alleles when compared regarding the Pro 197 Leu GSH-Px gene polymorphism. The combined analysis (MDD plus BD) also failed to find any association between the Ala-9Val MnSOD and Pro 197 Leu GSH-Px gene polymorphism. Although small statistical power of the current study the significant difference between patients with depression and the control group for the Pro 197 Leu GSH-Px polymorphism indicates that the distribution of these alleles may have a contribution in the physiopathogenesis of depression. One of the limitation of the current study is that the sample size is too small. Understanding of the exact role of Pro 197 Leu GSH-Px polymorphism in the development of depression needs to further studies with more sample size and high statistical power.

Molecular and Biochemical Study of Superoxide Dismutase Gene Polymorphisms in Egyptian Patients with Type 2 Diabetes Mellitus with and without Retinopathy

Molecular and Biochemical Study of Superoxide Dismutase Gene Polymorphisms in Egyptian Patients with Type 2 Diabetes Mellitus with and without Retinopathy

Different Association of Manganese Superoxide Dismutase Gene Polymorphisms with Risk of Prostate, Esophageal, and Lung Cancers: Evidence from a Meta-analysis of 20,025 Subjects

Altered expression or function of manganese superoxide dismutase (MnSOD) has been shown to be associated with cancer risk but assessment of gene polymorphisms has resulted in inconclusive data. Here a search of published data was made and 22 studies were recruited, covering 20,025 case and control subjects, for meta- analyses of the association of MnSOD polymorphisms with the risk of prostate, esophageal, and lung cancers. The data on 12 studies of prostate cancer (including 4,182 cases and 6,885 controls) showed a statistically significant association with the risk of development in co-dominant models and dominant models, but not in the recessive model. Subgroup analysis showed there was no statistically significant association of MnSOD polymorphisms with aggressive or nonaggressive prostate cancer in different genetic models. In addition, the data on four studies of esophageal cancer containing 620 cases and 909 controls showed a statistically significant association between MnSOD polymorphisms and risk in all comparison models. In contrast, the data on six studies of lung cancer with 3,375 cases and 4,050 controls showed that MnSOD polymorphisms were significantly associated with the decreased risk of lung cancer in the homozygote and dominant models, but not the heterozygote model. A subgroup analysis of the combination of MnSOD polymorphisms with tobacco smokers did not show any significant association with lung cancer risk, histological type, or clinical stage of lung cancer. The data from the current study indicated that the Ala allele MnSOD polymorphism is associated with increased risk of prostate and esophageal cancers, but with decreased risk of lung cancer. The underlying molecular mechanisms warrant further investigation.

Molecular and Biochemical Study of Superoxide Dismutase Gene Polymorphisms in Egyptian Patients with Type 2 Diabetes Mellitus with and without Retinopathy

Aims: This study aims to determine the antioxidant enzyme EC -SOD polymorphisms in Egyptian patients with type 2 diabe tes mellitus with and without retinopathy, and its association with other biochemical changes to assess whether decreased SOD activity is associated with the development of diabetic complications . Study Design:Cross-sectional study.

Superoxide Dismutase Gene Polymorphisms in Patients with Age-related Cataract

ABSTRACTBackground: Functional polymorphisms in genes encoding antioxidant enzymes may result in reduced enzyme activity and increased levels of reactive oxygen species, such as superoxide radicals, which in turn may contribute to increased risk of age-related disorders. Copper–zinc superoxide dismutases, SOD-1 and SOD-3, and manganese superoxide dismutase, SOD-2, are enzymes involved in the protection against oxidative stress and detoxification of superoxide. In this study, we investigated a number of disease-associated single nucleotide polymorphisms (SNPs) of SOD1, SOD2 and SOD3, in patients with age-related cataract.Materials and methods: The study included an Estonian sample of 492 patients with age-related cataract, subgrouped into nuclear, cortical, posterior subcapsular and mixed cataract, and 185 controls. Twelve SNPs in SOD1, SOD2 and SOD3 were genotyped using TaqMan Allelic Discrimination. Haplotype analysis was performed on the SNPs in SOD2.Results: None of the studied SNPs showed an association with risk of cataract. These results were consistent after adding known risk factors (age, sex and smoking) as covariates in the multivariate analyses and after stratification by cataract subtype. Analysis of SOD2 haplotypes did not show any associations with risk of cataract.Conclusions: If genetic variation in genes encoding SOD-1, SOD-2 and SOD-3 contributes to cataract formation, there is no major contribution of the SNPs analyzed in the present study.