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

Sari, Mayang; Daulay, Milahayati; Wahyuni, Dian

doi:10.3889/oamjms.2019.195

Cited by 8 publications

(6 citation statements)

References 26 publications

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“…Polykretis et al demonstrated that glyoxal, another strong oxidizing dialdehyde capable of forming AGEs, may combine with SOD1 to produce persistent adducts due to the liberation of the positive charge from the Cu, Zn-SOD1 catalytic site. 28 The results show a change in antioxidant enzyme level. Especially in the second withdrawal, due to the glyoxalase pathway primarily responsible for MGO detoxification.…”

Section: Resultsmentioning

confidence: 91%

The Combined Effect of Coenzyme Q10 and Magnesium Ion on Advanced Glycation End Products Formed by Methylglyoxal in Rabbits

2022

TJNPR

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IntroductionMethylglyoxal (MGO) is a toxic and highly reactive alphaoxoaldehyde produced during glycolysis enhanced in disorders characterized by increased oxidative stress. 1 Methylglyoxal is a somewhat viscous clear yellow liquid with a strong odour. It was discovered first as a critical step in mammalian glucose metabolism. Its discovery in 1913 in plants and microorganisms, MGO has been found in a wide range of meals high in carbohydrates (80%), lipids, and fermented drinks. 2 The production of advanced glycation end products (AGEs) has been linked with diabetes and cancer, with MGO serving as a precursor, keeping a vicious loop. Diabetic hyperglycemia promotes the development of MGO and AGEs, which creates an environment conducive to tumour growth and metastasis. On the one hand, it leads to disease progression and therapeutic resistance, and on the other, chronic diabetes complications. 3 MGO has been shown to promote the production of ROS, proinflammatory cytokines, and peroxynitrites. MGO increases oxidative stress by lowering cell antioxidant capacity and detoxification mechanisms. In addition to promoting free radical generation, 4,5 it leads to oxygen poisoning, which affects living cells. Cellular toxicity is enhanced by ROS, superoxide anion radical (O2), hydrogen peroxide (H2O2), and hydroxyl radical (OH) like (OH -). 6

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Section: Resultsmentioning

confidence: 91%

The Combined Effect of Coenzyme Q10 and Magnesium Ion on Advanced Glycation End Products Formed by Methylglyoxal in Rabbits

2022

TJNPR

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“…Previous study showed that there was a decrease of glutathione peroxidase and glutathione in DM patients compared to healthy subjects [30]. The other study showed that decrease of SOD level occurred in tuberculosis patients with DM compared to healthy subjects [31]. Decline of antioxidants levels stimulate oxidative stress in the cell and trigger insulin resistance.…”

Section: Discussionmentioning

confidence: 96%

The Gene Polymorphisms (-308G/A) and the Tumor Necrosis Factor-alpha Levels in Type 2 Diabetic Patients with and Without Tuberculosis Infection

Daulay

Sari

Wahyuni

et al. 2019

Open Access Maced J Med Sci

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BACKGROUND: The gene polymorphism (-308G/A) and tumor necrosis factor-alpha (TNF-α) levels influence development of disease in type 2 diabetic patients and tuberculosis patients. AIM: In this study, we analyze the association between the TNF-α polymorphisms (-308G/A) and the levels of TNF-α in type 2 diabetic patients with and without tuberculosis infection. METHODS: This study was an analytic observational with cross sectional approach consisting 40 type 2 diabetic patients with tuberculosis infection, 40 type 2 diabetic patients without tuberculosis infection and 40 healthy control (HC) subjects. The TNF-α gene polymorphism (-308G/A) was analyzed with polymerase chain reaction-restriction fragment lengths polymorphisms (PCR-RFLP) method. The TNF-α levels were measured using an enzyme-linked immunosorbent assay. The association between gene polymorphism (-308G/A) in study groups was analyzed by Fisher's exact test, tumor necrosis factor-alpha (TNF-α) levels in study groups was carried out using the Kruskal-Wallis test. Hardy-Weinberg Equilibrium also determined genotype deviation and allele frequencies. RESULTS: The GG and GA+AA genotypes frequency in both of patient groups and HC subjects were not differ significantly (95% and 5% vs 95% and 5% vs 92.5% and 7.5%; p > 0.05). The TNF-α levels (pg/ml) of type 2 diabetic without tuberculosis infection were higher than those of type 2 diabetic with tuberculosis infection and HC subjects (7.42 ± 0.78 vs 2.23 ± 0.51 vs 2.57 ± 0.63; p < 0.01). The TNF-α levels in the GA+AA genotypes were higher than the GG wild-type genotype (p > 0.05). There was no significant deviation of genotype frequency and allele from Hardy-Weinberg Equilibrium. CONCLUSION: The gene polymorphism (-308G/A) had no association with type 2 diabetic patients with and without tuberculosis infection and the gene polymorphism (-308G/A) was not influence the TNF-α levels but there was a significant differentiation of TNF-α levels between the groups.

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“…Super-oxide dismutase (SOD) was found to be upregulated in the DM and TBDM patients in comparison to TB only and healthy controls. SOD levels are found to be low in tuberculosis patients and higher in DM patients in comparison to healthy controls (20,21). Upregulated expression of SOD has also been observed in Helicobacter Pylori infection, which supports the fact that the pathogen has developed protective mechanism against immune system (22).…”

Section: D-page Analysismentioning

confidence: 86%

Proteomic profiling of peripheral blood mononuclear cells isolated from patients with tuberculosis and diabetes copathogenesis -A pilot study

Kundu

Bakshi

Joshi

et al. 2020

Preprint

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18Background: Diabetes is an important risk factor for developing tuberculosis. This association 19 leads to exacerbation of tuberculosis symptoms and delayed treatment of both the diseases. 20 Molecular mechanism and biomarkers/drug targets related to copathogenesis of tuberculosis and 2 21 diabetes, however, still remains to be poorly understood. In this study, proteomics based 2D-22 MALDI/MS approach was employed to identify host signature proteins which are altered during 23 copathogenesis of tuberculosis and diabetes. 24 Methods: Comparative proteome of human peripheral blood mononuclear cells (PBMCs) from 25 healthy controls, tuberculosis and diabetes patients in comparison to comorbid diabetes and 26 tuberculosis patients was analyzed. Gel based proteomics approach followed by in gel trypsin 27 digestion and peptide identification by mass spectrometry was used for signature protein 28 identification. 29 Results: Total of 18 protein spots with differential expression in TBDM patients in comparison 30 to other groups were identified. These include Vimentin, tubulin beta chain protein, superoxide 31 dismutase, Actin related protein 2/3 complex subunit 2, PDZ LIM domain protein, Rho-GDP 32 dissociation inhibitor, Ras related protein Rab, dCTPpyrophosphatase 1, Transcription initiation 33 factor TFIID subunit 12, coffilin 1, three isoforms of Peptidylprolylcis-trans isomerase A, three 34 isoforms of Protein S100A9, Protein S100A8 and SH3 domain containing protein. These 35 proteins belonged to four functional categories i.e. structural, cell cycle/growth regulation, 36 signaling and intermediary metabolism.40 42 10million fresh TB cases has been reported worldwide (1). Despite extensive research on the 3 43 biology of M. tuberculosis, exact mechanism of infection and immune evasion still remains 44 elusive. Copathogenesis with HIV and diabetes further complicates the tuberculosis control 45 measures. Although HIV infection is the topmost risk factor for development of active 46 tuberculosis but population attributable risk of diabetes is more than that of HIV infection (2, 3) 47 as diabetes is known to triple the risk of developing active tuberculosis (4). As diabetes is 48 associated with various immunological dysfunctions, diabetic patients fall prey to other co-49 infections like tuberculosis, melioidosis and other conventional hyperglycemia related 50 complications like various cardiovascular disorders, retinopathy, nephropathy and many more. 51 Diabetes mellitus affected 425 million individuals worldwide in 2017 and is predicted to reach 52 629 million by 2045, the time at which 80% of diabetics will be residents of economically 53 challenged countries where active tuberculosis (TB) prevails (5, 6). Countries with highest 54 burden of diabetes are also in the list of WHO's tuberculosis high burden countries and India and 55China for example, have first two positions for the copathogenesis of TB and diabetes (7, 8). The 56 epidemiological data for association between TB and DM is increasing significantly...

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

Cited by 8 publications

References 26 publications

The Combined Effect of Coenzyme Q10 and Magnesium Ion on Advanced Glycation End Products Formed by Methylglyoxal in Rabbits

The Combined Effect of Coenzyme Q10 and Magnesium Ion on Advanced Glycation End Products Formed by Methylglyoxal in Rabbits

The Gene Polymorphisms (-308G/A) and the Tumor Necrosis Factor-alpha Levels in Type 2 Diabetic Patients with and Without Tuberculosis Infection

Proteomic profiling of peripheral blood mononuclear cells isolated from patients with tuberculosis and diabetes copathogenesis -A pilot study

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