Academic literature on the topic 'Diabetes Cataract Oxidative stress'

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Journal articles on the topic "Diabetes Cataract Oxidative stress"

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Bhatia, Geeta, A. N. Sontakke, and Subodhini Abhang. "Role of oxidative stress in cataractogenesis." International Journal of Research in Medical Sciences 5, no. 6 (May 27, 2017): 2390. http://dx.doi.org/10.18203/2320-6012.ijrms20172087.

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Background: Cataract is a multifactorial disease and is a major cause of blindness in india. Oxidative stress is thought to be a major factor to initiate the process of cataractogenesis. It is today well established fact that oxidative stress participates in both age-related (senile) and diabetes-induced cataract (diabetic). Oxidative damage to the lens most likely arises as a consequence of an impaired antioxidant defence system, due to increased generation of ROS both by age and diabetes. The present study was designed to determine role of oxidative stress in cataractogensis and to compare levels of oxidative stress markers in senile and diabetic cataract patients.Methods: Serum malondialdehyde (MDA) and serum protein carbonyl (PC) were measured as indicator of oxidative stress whereas antioxidant status was assessed by estimating serum Total antioxidant capacity (TAC) and dietary antioxidants levels i.e vitamin C and vitamin E in senile and diabetic cataract patients compared with healthy controls.Results: The result reveal that the serum MDA and PC levels were significantly increased in patients with senile and diabetic cataract whereas serum TAC, vitamin C and Vitamin E were significantly reduced in senile and diabetic patients when compared with normal healthy controls.Conclusions: From the result, it is concluded that oxidative stress is in the foreground of cataract formation which includes senile and diabetic cataract. Oxidative stress produced in diabetic cataract patients is more as compared to senile cataract patients.
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Lestari, Indah, and Fifiyahpuahsari Fifiyahpuahsari. "LEVELS OF DIABETES BLOOD SUGAR WITH TYPE OF CATARACT." INTERNATIONAL JOURNAL OF NURSING AND MIDWIFERY SCIENCE (IJNMS) 3, no. 1 (May 11, 2019): 7–13. http://dx.doi.org/10.29082/ijnms/2019/vol3.iss1.211.

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Diabetes mellitus was a disease with macro and micro risk of angiopathy, which includes the impact of causing cataracts. Diabetic patients with high sugar levels have a greater chance of developing cataracts at a younger age and certain tendencies towards cataract type. The aim of the study was to analyze the correlation between diabetes blood sugar levels and cataract type. The research design was correlation analysis with Cross-Sectional approach. Samples in the study were some cataract patients who had a history of diabetes mellitus in Surabaya Undaan Eye Hospital as many as 125 people, it was taken using consecutive sampling technique, and fulfilling the criteria of the study (age range 45 - 65 years, have complete medical records related to the continuity of sugar examination results in blood, the incidence of cataracts is not caused by congenital cataracts, juveniles, due to trauma, chemical exposure to UV radiation). Independent variable was the blood sugar level of Diabetes mellitus and the Dependent variable was cataract type. The instruments used were laboratory tests related to blood sugar levels, and medical diagnosis related to cataract type. Data were analyzed by Spearman rho, with a significant value <0.05. The results showed a close association between diabetes and cataracts, where as many as 47.2% with high blood sugar levels, 40% with nuclear cataract type and from 59 respondents with high blood sugar levels 26 people experienced nuclear cataract type, with rho value = 0.001. The mechanism of glucose toxicity in Diabetes Mellitus which causes cataracts can go through three paths: increased activity of the aldose reductase enzyme which causes the formation of sugar alcohol, sorbitol and galactitol in crystalline lenses; through the non-enzymatic replication process; and at high blood glucose levels a glucose oxidation process will occur which causes oxidative stress conditions. Maintenance of managing blood sugar levels must be a concern for diabetics. Keywords: Blood Sugar Level, Diabetes Mellitus, Type of Cataract
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Lestari, Indah, and Fifiyahpuahsari Fifiyahpuahsari. "LEVELS OF DIABETES BLOOD SUGAR WITH TYPE OF CATARACT." INTERNATIONAL JOURNAL OF NURSING AND MIDWIFERY SCIENCE (IJNMS) 3, no. 1 (May 11, 2019): 7–13. http://dx.doi.org/10.29082/ijnms/2019/vol3/iss1/211.

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Diabetes mellitus was a disease with macro and micro risk of angiopathy, which includes the impact of causing cataracts. Diabetic patients with high sugar levels have a greater chance of developing cataracts at a younger age and certain tendencies towards cataract type. The aim of the study was to analyze the correlation between diabetes blood sugar levels and cataract type. The research design was correlation analysis with Cross-Sectional approach. Samples in the study were some cataract patients who had a history of diabetes mellitus in Surabaya Undaan Eye Hospital as many as 125 people, it was taken using consecutive sampling technique, and fulfilling the criteria of the study (age range 45 - 65 years, have complete medical records related to the continuity of sugar examination results in blood, the incidence of cataracts is not caused by congenital cataracts, juveniles, due to trauma, chemical exposure to UV radiation). Independent variable was the blood sugar level of Diabetes mellitus and the Dependent variable was cataract type. The instruments used were laboratory tests related to blood sugar levels, and medical diagnosis related to cataract type. Data were analyzed by Spearman rho, with a significant value <0.05. The results showed a close association between diabetes and cataracts, where as many as 47.2% with high blood sugar levels, 40% with nuclear cataract type and from 59 respondents with high blood sugar levels 26 people experienced nuclear cataract type, with rho value = 0.001. The mechanism of glucose toxicity in Diabetes Mellitus which causes cataracts can go through three paths: increased activity of the aldose reductase enzyme which causes the formation of sugar alcohol, sorbitol and galactitol in crystalline lenses; through the non-enzymatic replication process; and at high blood glucose levels a glucose oxidation process will occur which causes oxidative stress conditions. Maintenance of managing blood sugar levels must be a concern for diabetics. Keywords: Blood Sugar Level, Diabetes Mellitus, Type of Cataract
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Zoric, Lepsa. "Some parameters of the oxidative stress in lens, humour aqueous and serum of patients with diabetes and age-related cataract." Srpski arhiv za celokupno lekarstvo 131, no. 3-4 (2003): 137–42. http://dx.doi.org/10.2298/sarh0304137z.

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Contemporary hypothesis considers the oxidative stress as a crucial event in age-related processes in the body, as well as in the age-related cataract formation. The secondary aging factors accelerate ageing processes. One of them is diabetes. With the aim of investigation of the noninsulin-dependent diabetes (Type II) influence on cataract genesis here were analyzed contents of the lipid oxidation products (lipid peroxides - LP) and total sulfhydryle groups (TSH) in the lens? corticonuclear blocks and antioxidative capacity in their humour aqueous expressed as percent of induced malondyaldehyde (% iMDA) in 14 samples obtained from patients with cataract and diabetes mellitus type II (without diabetic complications) and compared to 66 samples of patients with cataract without diabetes, as well as some parameters of the oxidative stress in serums (content of vitamin C, acrobat - A dehydroascorbate - DA and their relation, vitamin E, glutathione - GSH peroxidase - P and catalase - Cat activity, content of malondyaldehyde - MDA and % iMDA) of 27 patients with age-related cataract and diabetes mellitus type II (without complications), and compared to the other 135 age-related cataract patients. Also were analyzed frequencies of the secondary senium diseases in a clinical group of 162 patients with cataract and sex and age matched 55 examined people without cataract, as a control group. Patients with diabetes and cataract have lower values of almost all investigated parameters of antioxidative defense in their serum and higher level of the lipid peroxidation products. Level of glutathione in their serums is significantly lower (p<0.05). Intensity of lipid peroxidation in corticonuclear lens blocks is higher in patients with diabetes, whereas their total sulfhydryle groups and % iMDA in humour aqueous shows lower antioxidant capacity in the same group, probably because of higher intensity of oxidative stress. Also, by investigation of frequencies of the secondary ageing diseases in patients with age-related cataract and age and sex matched control subjects, by a logistic regression was found high odds ratio (2.506) for diabetes. Results confirm hypothesis of the oxidative stress role in the age-related cataract genesis, and especially of patients with diabetes mellitus.
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., Ghazala, Syed Liaquat Ali, Jamil Ahmed Siddiqui, Aziza Khanam, and Saleh Memon. "Oxidative stress and antioxidant vitamins in cataract patients." International Journal of Research in Medical Sciences 7, no. 5 (April 26, 2019): 1568. http://dx.doi.org/10.18203/2320-6012.ijrms20191637.

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Background: In Pakistan age related vision disturbances are mainly due to cataract. Various studies have reported relationship of ocular lesion with senile changes and diabetes mellitus resulting in reduced quality of life due to vision. Oxidative stress is an important factor in the process of cataractogenesis. The pathogenesis of the cataract may involve decreased activity of antioxidant scavenging system which includes non-enzymatic natural antioxidants as biomolecules such as carotenoids and vitamins. So, it is planned to investigate the level of serum antioxidant vitamins in diabetic cataract patients and in non-diabetic cataract patients.Methods: The study was conducted at Biochemistry department, Al-Tibri Medical College Karachi from October 2016 to October 2017. Ninety pre diagnosed cataract patients were selected from Al-Ibrahim Eye Hospital Karachi 40 normal control subjects were selected from the same population with same socioeconomic group. The demographic data was analyzed. The random blood sugar, antioxidant vitamins (C, A and E) and malondialdehyde were analyzed in the blood sample of control and cataract patients. The data was analyzed by SPSS version 20.Results: There was no significant difference in the level of vitamin C, A, E and MDA between diabetic and non-diabetic cataract patients, but the blood levels of vitamins of control are higher as compared to the cataract patients. The level of MDA is significantly high in cataract patients as compared to control. Antioxidant vitamin E was negatively correlated with serum malondialdehyde in cataract patients.Conclusions: It is concluded that in diabetic and non-diabetic cataract low level of serum antioxidant vitamins may be a contributory factor for cataractogenesis.
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Wu, Tsung-Tien, Ying-Ying Chen, Hui-Yu Chang, Ya-Hsin Kung, Ching-Jiunn Tseng, and Pei-Wen Cheng. "AKR1B1-Induced Epithelial–Mesenchymal Transition Mediated by RAGE-Oxidative Stress in Diabetic Cataract Lens." Antioxidants 9, no. 4 (March 25, 2020): 273. http://dx.doi.org/10.3390/antiox9040273.

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Purpose: Cataracts are a major cause of visual acuity deterioration in diabetes mellitus (DM) in developed and developing countries. Studies have demonstrated that overproduction of AKR1B1 and receptor for advanced glycation end products (RAGE) plays a major role in the pathogenesis of diabetic cataracts, but it is unclear whether the prevalence of diabetic cataracts is related to epithelial–mesenchymal transition (EMT) in lens epithelial cells. This study aimed to analyze the role of EMT in cataract formation of DM patients. Methods: Immunofluorescence and immunohistochemistry assays were used to estimate AKR1B1, RAGE, AMPK, and EMT levels in epithelial human lens of DM or non-DM cataracts. Results: Immunohistochemical staining demonstrated that pathologic phases and N-cadherin expression levels were significantly higher in epithelial human lens of DM (+) compared to DM (−) cataracts. Immunofluorescent staining showed that AKR1B1 and RAGE were significantly higher in epithelial human lens of DM (+) compared to DM (−) cataracts. Interestingly, acetyl superoxide dismutase 2 (AcSOD2) levels were significantly higher in DM patients’ lens epithelial cells (LECs), whereas AMPKT172 phosphorylation was significantly increased in non-DM patients. This indicates that AMPKT172 might be related to superoxide reduction and diabetic cataract formation. Conclusions: Our results suggest that AKR1B1 overexpression can decrease AMPK activation, thereby increasing AcSOD2 and RAGE-induced EMT in epithelial human lens of DM cataracts. These novel findings suggest that AKR inhibitors may be candidates for the pharmacological prevention of cataracts in patients with DM.
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Spassov, A. A., L. V. Naumenko, and Yu A. Govorova. "Fundamentals of Diabetic Cataractogenesis and Promising Ways of its Pharmacological Correction." Acta Biomedica Scientifica 6, no. 2 (June 24, 2021): 114–25. http://dx.doi.org/10.29413/abs.2021-6.2.13.

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Cataracts in diabetes mellitus lead to decreased visual function and blindness. Cataract surgery for diabetes mellitus has limitations and complications. The search for effective means of conservative cataract therapy continues. The review presents the analysis of data from scientific sources, mainly for 2015–2020 using Internet resources (PubMed, Web of Science, Medline, eLibrary.Ru, Cyberleninka). In the work, diabetic cataractogenesis is presented as a sum of interrelated pathobiochemical processes. The main ones are the polyol pathway of glucose conversion, non-enzymatic glycation and oxidative modification of lens proteins, which are enhanced in diabetes mellitus. The lens has a high protein content. The formation of high molecular weight protein aggregates is of particular importance for the appearance of light scattering zones and a decrease in lens transparency. This review presents data on anti-cataract compounds that affect post-translational crystallin modification, prevent osmotic and oxidative stress in the lens, and exhibit antiglycation properties. This information shows that the search for means of pharmacological correction of cataractogenesis should be carried out among compounds with antioxidant and antiglycation activity.
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Tangvarasittichai, Orathai, and Surapon Tangvarasittichai. "Oxidative Stress, Ocular Disease and Diabetes Retinopathy." Current Pharmaceutical Design 24, no. 40 (March 15, 2019): 4726–41. http://dx.doi.org/10.2174/1381612825666190115121531.

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Background: Oxidative stress is caused by free radicals or oxidant productions, including lipid peroxidation, protein modification, DNA damage and apoptosis or cell death and results in cellular degeneration and neurodegeneration from damage to macromolecules. Results: Accumulation of the DNA damage (8HOdG) products and the end products of LPO (including aldehyde, diene, triene conjugates and Schiff’s bases) were noted in the research studies. Significantly higher levels of these products in comparison with the controls were observed. Oxidative stress induced changes to ocular cells and tissues. Typical changes include ECM accumulation, cell dysfunction, cell death, advanced senescence, disarrangement or rearrangement of the cytoskeleton and released inflammatory cytokines. It is involved in ocular diseases, including keratoconus, Fuchs endothelial corneal dystrophy, and granular corneal dystrophy type 2, cataract, age-related macular degeneration, primary open-angle glaucoma, retinal light damage, and retinopathy of prematurity. These ocular diseases are the cause of irreversible blindness worldwide. Conclusions: Oxidative stress, inflammation and autophagy are implicated in biochemical and morphological changes in these ocular tissues. The development of therapy is a major target for the management care of these ocular diseases.
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Liu, Fei, Ying Ma, and Yanli Xu. "Taxifolin Shows Anticataractogenesis and Attenuates Diabetic Retinopathy in STZ-Diabetic Rats via Suppression of Aldose Reductase, Oxidative Stress, and MAPK Signaling Pathway." Endocrine, Metabolic & Immune Disorders - Drug Targets 20, no. 4 (May 18, 2020): 599–608. http://dx.doi.org/10.2174/1871530319666191018122821.

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Background: Due to the increased prevalence of diabetes-associated complications of the eye like diabetic retinopathy and cataract, the need for a novel therapeutic agent is urgent. Due to the advantages that the polyphenolic compounds enjoy in diabetes and associated complications, we postulated that Taxifolin (TXF), a poly-phenolic flavanol, could show anti-retinopathic and anti-cataract effect in diabetes-induced rats. Methods: TXF at a dose of 10, 25, and 50 mg/kg was given by oral route to STZ mediated diabetic rats for a time period of 10 weeks. The opacity of lens was studied after every 7 days of treatment till 10 weeks; evaluation of the severity of cataract and changes in the histology of lens as well as retina was done. Tissue homogenates of lens isolated after the end of the study were evaluated for markers of oxidative stress, levels of aldose reductase, p38MAPK, VEGF, and ERK1/2. Results: Outcomes suggested that TXF improved retinopathy and cataract in diabetes-induced rats. The treatment of TXF also improved the status of oxidative stress and inhibited the levels of p38MAPK, VEGF, and ERK1/2. The treatment also improved the lens opacity in diabetic rats. The results suggest that the protective effect of TXF against cataract and retinopathy may be due to the anti-oxidative potential of TXF and its inhibiting effect on VEGF, ERK1/2, p38MAPK, and aldose reductase. Conclusion: The study confirms that TXF is a potential candidate showing a protective effect against diabetic induced retinopathy and cataract..
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Natania, Maria Winney, Monica Claudia, Refita Maharani, Muhammad Ali Faisal, and Triawanti Triawanti. "The Correlation of Hba1c Level With GSH-PX Enzyme Activity, AOPP, and MDA Levels in The Eye Lenses of Diabetic Cataract Patients." Berkala Kedokteran 16, no. 2 (September 25, 2020): 105. http://dx.doi.org/10.20527/jbk.v16i2.9223.

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Abstract: Diabetes Mellitus (DM) is known to accelerate cataractogenesis because it may cause hyperglycemia-induced stress oxidative in the eye lens. HbA1c test can be performed to monitor glycemic control. Glutathione peroxidase (GSH-Px) is an enzyme that scavenges and prevents the formation of free radical. Advanced Oxidation Protein Products (AOPP) is a marker to estimate the degree of oxidative protein modification. Malondialdehyde (MDA) can reflect cells damage. This study was an observational analytic study, conducted in September 2019-January 2020, and aimed to determine the correlation of HbA1c level with GSH-Px enzyme activity, AOPP, and MDA levels in the eye lenses of diabetic cataract patients. Data of HbA1c level and eye lenses sample was obtained from 29 cataract patients with DM who underwent phacoemulsification surgery in Ulin and Bhayangkara Hospital in Banjarmasin and fulfilled the inclusion criteria. Spearman’s correlation test showed that there was no significant correlation of HbA1c with GSH-Px activity (p=0,095), AOPP (p=0,084), and MDA (p=0,084) levels in the eye lens of diabetic cataract patients. Keywords: Diabetes mellitus, cataract, HbA1c, glutathione peroxidase, AOPP, MDA
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Dissertations / Theses on the topic "Diabetes Cataract Oxidative stress"

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Chan, Wai-ho. "Study on the role of osmotic stress, oxidative stress and poly(ADP-ribose) polymerase in the pathogenesis of diabetic cataract." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B36371725.

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Chan, Wai-ho, and 陳韋豪. "Study on the role of osmotic stress, oxidative stress and poly(ADP-ribose) polymerase in the pathogenesis of diabetic cataract." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B36371725.

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Vinayak, Anubhav. "Role of Oxidative Stress in Diabetes Mellitus." Youngstown State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ysu1526905602340959.

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Dewar, Mairead. "Oxidative stress and cardiovascular ageing in diabetes." Thesis, University of Leicester, 2004. http://hdl.handle.net/2381/29910.

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Oxidative stress is thought to be elevated in diabetes as a consequence of hyperglycaemia. This thesis investigates oxidative DNA damage in diabetes, which may contribute to accelerated vascular ageing. Telomeric and mitochondrial DNA are two areas of the genome that may be more susceptible to oxidative stress and were therefore investigated.;51 patients with diabetes (aged 31-78 years) and 101 healthy controls (aged 19-75 years) were recruited. 51 of the controls were age- and sex-matched to be patient group. For both populations physiological profiles were obtained and pulse wave velocity (PWV), an index of vascular stiffness, was measured. Oxidative DNA damage was also investigated in peripheral blood using the comet assay, and in more depth by measuring terminal restriction fragment (TRF) lengths and quantifying mitochondrial DNA (mtDNA) content. PWV increased with age in both study groups (p<0.001) and was significantly higher in the patient group (8.00 +/- 2.89 versus 7.29 +/- 1.64 m/s; p=0.006), suggesting accelerated vascular ageing in diabetes. This was accompanied by elevated levels of oxidative DNA damage; 25.81 +/- 1.18 versus 21.40 +/- 0.81% Tail DNA (p=0.003) in patients and controls respectively. TRF length inversely correlated with age in both groups (p<0.05), with similar rates of attrition, and although they were shorter in the patients with diabetes, this was not significant (p=0.10). Quantification of mtDNA revealed significantly lower levels in the patients with diabetes compared to the controls (0.014 versus 0.016; p=0.020). There is accelerated vascular ageing in diabetes, which is accompanied by elevated oxidative DNA damage, and a decrease in mtDNA, but no alteration in TRF length compared to a healthy control population. The mechanisms underlying these alterations are unknown with the lack of correlations with glycaemic control suggesting it is not the sole cause but it may still contribute.
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Lassen, Natalie. "Roles of aldehyde dehydrogenases (ALDHs) against oxidative stress /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2006.

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Thesis (Ph.D. in Toxicology) -- University of Colorado at Denver and Health Sciences Center, 2006.
Typescript. Includes bibliographical references (leaves 119-138). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
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Stephens, Jeffrey Wayne. "Genetic determinants of oxidative stress in diabetes mellitus." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1446841/.

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Increased oxidative stress has been implicated in the pathogenesis of atherosclerosis and coronary heart disease, and is a key feature of diabetes mellitus. Increased oxidative stress has numerous adverse effects on the vascular system, including the altered expression of cell adhesion molecules, induction of pro-inflammatory mediators and more specifically the oxidation of low density lipoprotein (LDL) to form oxidised LDL (Ox-LDL). As well as measuring the total degree of oxidative stress in plasma, specific measures may also be recorded, such as the degree of LDL-oxidation. This thesis focuses on the association between plasma markers of oxidative stress and LDL-oxidation with other biochemical intermediate risk factors and common gene variants, in subjects with diabetes mellitus. Analysis focused on three candidate genes: a cellular anti-oxidant, glutathione-s-transferase; a plasma lipoprotein, apolipoprotein E; and a mitochondrial protein, uncoupling protein-2 (UCP2). The effect of common variants in these genes was explored in relation to plasma markers of oxidative stress, along with gene-environment interaction in the pro-oxidant environment of cigarette smoking. Initially a cohort of approximately 1000 subjects with diabetes, were recruited from the diabetes clinic at University College London Hospitals. Routine biochemical and clinical data was gathered, as well as plasma and blood for DNA extraction. Further in vitro functional studies were performed in respect to the UCP2 gene, to further our understanding of the role of this gene in the generation of oxidative stress and in the pathogenesis of coronary heart disease.
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Han, Bing. "Mechanistic Consequences of Cardiac Oxidative Stress." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1203478009.

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Catherwood, Mark Alexander. "Glucose-induced oxidative stress in vascular smooth muscle cells." Thesis, Queen's University Belfast, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268225.

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Pitre, Deepali. "Oxidative mechanisms in diabetes related urinary bladder dysfunction." The Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=osu1060880772.

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Hammerman, Malin. "Oxidative Stress and Protein Acetylation in Adipocytes." Thesis, Linköpings universitet, Proteinkemi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-75785.

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Obesity is an increasing health problem which is causally associated with insulin resistance and type 2 diabetes. Oxidative stress, i.e. overproduction of reactive oxygen species, is associated with insulin resistance and obesity and may be a major risk factor in the onset and progression of diabetes. Bernlohr Lab at University of Minnesota have study oxidative stress in adipocytes by silencing the enzyme glutathione S-transferase A-4 (GSTA4), an enzyme detoxifying 4-hydroxynonenal formed during oxidative stress. Their results indicate that lysine acetylation, an important post-translational modification, may be involved during oxidative stress. In this study lysine acetylation has been investigated in condition of oxidative stress in 3T3-L1 adipocytes and subcutaneous adipose tissue from mice using SDS-PAGE gel electrophoresis and western blot. Lysine acetylation was analyzed in different compartments of the cell such as in cytoplasm, mitochondria as well as in whole cell extracts. Silencing of GSTA4 and stimulation by TNF-α in 3T3-L1 adipocytes resulted in an increase of lysine acetylation in cytoplasm. Furthermore, stimulation by IL-6 did not have any effect on lysine acetylation. Surprisingly, subcutaneous adipose tissue from mice fed on a high-fat diet showed a decrease of lysine acetylation in cytoplasm compare to mice fed on a chow diet. In conclusion, lysine acetylation seems to change during oxidative stress and may be an important factor during insulin resistance, type 2 diabetes and obesity. Therefore, studying lysine acetylation and enzymes modulating acetylation may potentially increase our understanding of insulin resistance, type 2 diabetes and obesity and could lead to new therapies.
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Books on the topic "Diabetes Cataract Oxidative stress"

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Carla, Costa, and SpringerLink (Online service), eds. Oxidative Stress, Inflammation and Angiogenesis in the Metabolic Syndrome. Dordrecht: Springer Netherlands, 2009.

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Preedy, Victor R. Diabetes: Oxidative Stress and Dietary Antioxidants. Elsevier Science & Technology, 2020.

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Diabetes: Oxidative Stress and Dietary Antioxidants. Elsevier Science & Technology Books, 2013.

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Preedy, Victor R. Diabetes: Oxidative Stress and Dietary Antioxidants. Elsevier Science & Technology Books, 2020.

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Preedy, Victor R. Diabetes: Oxidative Stress and Dietary Antioxidants. Elsevier Science & Technology Books, 2013.

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Diabetes: Oxidative Stress and Dietary Antioxidants. Elsevier, 2014. http://dx.doi.org/10.1016/c2012-0-02421-0.

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(Editor), Lester Packer, Peter Rosen (Editor), Hans J. Tritschler (Editor), George L. King (Editor), Glenn A. King (Editor), and Angelo Azzi (Editor), eds. Antioxidants in Diabetes Management (Oxidative Stress & Disease). CRC, 2000.

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Keaneyjr, John F. Oxidative Stress and Vascular Disease. Springer, 2012.

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(Editor), Lester Packer, and Helmut Sies (Editor), eds. Oxidative Stress and Inflammatory Mechanisms in Obesity, Diabetes, and the Metabolic Syndrome (Oxidative Stress and Disease). CRC, 2007.

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C, Opara Emmanuel, ed. Nutrition & diabetes: Pathophysiology & management. Boca Raton: Taylor and Francis, 2005.

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Book chapters on the topic "Diabetes Cataract Oxidative stress"

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Crespo, Iñigo Corcóstegui, and Elío Díez-Feijóo Varela. "Cataract and Diabetic Retinopathy." In Oxidative Stress in Applied Basic Research and Clinical Practice, 371–83. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1935-2_20.

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Stadler, Krisztian. "Oxidative Stress in Diabetes." In Advances in Experimental Medicine and Biology, 272–87. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5441-0_21.

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Rachana, Shruti Thakur, and Sujata Basu. "Oxidative Stress and Diabetes." In Free Radicals in Human Health and Disease, 241–57. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-2035-0_16.

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Pitocco, Dario, Francesca Martini, Giuseppe Scavone, Francesco Zaccardi, and Giovanni Ghirlanda. "Oxidative Stress and Diabetes." In Systems Biology of Free Radicals and Antioxidants, 3283–317. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-30018-9_151.

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Sen, Saikat, Raja Chakraborty, and Biplab De. "Oxidative Stress and Diabetes Mellitus." In Diabetes Mellitus in 21st Century, 55–67. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-1542-7_7.

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Comazzi, Stefano. "Oxidative Stress in Diabetes Mellitus." In Oxidative Stress in Applied Basic Research and Clinical Practice, 77–91. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-071-3_5.

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Abdul-Ghani, Muhammad A., and Ralph A. DeFronzo. "Oxidative Stress in Type 2 Diabetes Mellitus." In Oxidative Stress in Aging, 191–211. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-420-9_11.

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Giugliano, D. "Oxidative Stress and Cardiovascular Complications of Diabetes." In Frontiers in Diabetes, 78–90. Basel: KARGER, 1998. http://dx.doi.org/10.1159/000060894.

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Shah, Mehul, and Shreya Shah. "Traumatic Cataract: A Review." In Oxidative Stress in Applied Basic Research and Clinical Practice, 385–413. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1935-2_21.

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Liu, Chao, Clayton E. Mathews, and Jing Chen. "Oxidative stress and type 1 diabetes." In Oxidative Stress and Antioxidant Protection, 319–28. Hoboken, NJ, USA: John Wiley & Sons, Inc, 2016. http://dx.doi.org/10.1002/9781118832431.ch19.

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Conference papers on the topic "Diabetes Cataract Oxidative stress"

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Konada, Sudhakar, Dr D. SarvaMangala, Dr R. Satyanarayana, and Dr U. S. N. Murthy. "Phytochemical activity of Morinda citrifolia on oxidative stress induced cataract formation in chick lens epithelial cells." In Annual International Conference on Advances in Biotechnology. Global Science & Technology Forum (GSTF), 2015. http://dx.doi.org/10.5176/2251-2489_biotech15.06.

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Aprilia, Dinda, Sri Angraeni, Eva Decroli, Asman Manaf, and Syafril Syahbuddin. "Correlation between Uncontrolled Blood Glucose and Oxidative Stress with Urinary Nephrin Level in Type 2 Diabetes Mellitus." In Proceedings of the 1st EAI International Conference on Medical And Health Research, ICoMHER November 13-14th 2018, Padang, West Sumatera, Indonesia. EAI, 2019. http://dx.doi.org/10.4108/eai.13-11-2018.2283551.

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Elcin, Huseyn. "EARLY IDENTIFICATION OF THE NEUROLOGICAL COMPLICATIONS OF DIABETES MELLITUS." In International Trends in Science and Technology. RS Global Sp. z O.O., 2021. http://dx.doi.org/10.31435/rsglobal_conf/30032021/7474.

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Diabetes mellitus is still a very common disease in the world and affects the daily lives of patients negatively. Diabetes is also known to be associated with neurological diseases such as peripheral nerve diseases, stroke and dementia. Among these, the most common disease is a peripheral nerve disease, and it has been reported that poor diabetic control increases the risk of development and can be prevented by education of the patients. Vascular dementia is more common in patients with diabetes than Alzheimer's disease, and it is thought that cerebrovascular diseases may berelated to cognitive impairment in diabetes. Although the mechanisms by which diabetes affects the brain are not clearly revealed, it is thought that changes in vascular structure, insulin resistance, glucose toxicity, oxidative stress, accumulation of glycation end products, hypoglycemic episodes and amyloid metabolism are effective.The aim of this article is to describe the neurological complications of diabetes and to emphasize the importance of patient education, good diabetes control and early diagnosis in preventing these complications.
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Elshiekh, Duaa Ibnomer, Hadeel Hendawi, Aya Goul, Dina Awartan, Isra Marei, Christopher Triggle, and Haissam Abou Saleh. "Effect of Hyperglycemia on eNOS function in EPCs." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0215.

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Type 2 diabetes mullites (T2DM) results in different cardiovascular complications. The main cause of these complications is endothelial dysfunction, which affects the endothelium physiologically and pathologically. The chronic hyperglycemia introduced by T2DM impacts the pivotal enzyme endothelial nitric oxide synthase (eNOS) in terms of phosphorylation and dimerization, which initiates oxidative stress and reduces the bioavailability of the vasodilator nitric oxide. To overcome endothelial dysfunction, endothelial progenitor cells (EPCs) contribute to vascular repair due to their regenerative characteristics. The effects of hyperglycemia on EPCs are understudied. Thus, this study aims to investigate the effects of hyperglycemia on the eNOS/Akt signaling pathway and reactive oxygen species (ROS) formation. Cells were treated with normal glucose (NG, 5.5mM) and high glucose (HG, 25mM) media for 3 & 6 days, and the effect on eNOS and Akt phosphorylation were assessed using western blot. ROS was assessed using CellROX stain following 1 and 3 days of treatment. Results showed that both acute and chronic hyperglycemia showed a trend towards decrease in phosphorylation of eNOS and Akt. In addition, ROS formation was increased following 24hr compared to NG. Further investigations are needed to enhance the capability of BOECs to serve as therapeutic tools in T2DM.
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Caverina, Sarah Lorenza, Retno Yulianti, and Andri Pramesyanti. "Effectiveness of Soursop Leaf Extract to Decrease Malondialdehyde Level." In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.05.07.

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ABSTRACT Background: In diabetes mellitus, hyperglycemia causes oxidative stress that enhances the production of free radicals. The presence of higher levels of malondialdehyde (MDA) indicates the rise of free radicals. On the basis of its role as an antioxidant that binds free radicals and reduces the level of malondialdehyde (MDA). Soursop leaf can act as an antidiabetic agent. This study aimed to examine the efficacy of soursop leaf extract (Annona muricata L.) to decrease the level of MDA level in alloxan-induced diabetic rats (Rattus norvegicus). Subjects and Method: This was an experiment study using pre- and pro-test with control group design. Total of 30 rats were selected for this study and divided into five groups of treatment i.e. group I was given distilled water and standard feed (Negative Control/KI), group II was given vitamin E 150 IU/kgBW/day (Positive Control/KII), group III was given soursop leaf extract 75 mg/kgBW/day (KIII), group IV was given soursop leaf extract 150 mg/kgBW/day (KIV), and group V was given soursop leaf extract 300 mg/kgBW/day (KV). Each group consisted of 5 rats and was given soursop leaf extract for 21 days after being induced by alloxan and high-fat diet. The data were analyzed using Mann-Whitney test. Results: There was a significant difference in KI group compared to KII, KIII, KIV, and KV groups. Soursop leaf extract of 150 mg/kgBW/day was the most effective dose to reduce MDA level in pancreatic rat. Conclusion: Soursop leaf extract of 150 mg/kgBW/day is the most effective dose on pancreatic MDA level reduction. Keywords: diabetes mellitus, soursop leaf extract, MDA, free radical Correspondence: Retno Yulianti. Department of Anatomical Pathology, Faculty of Medicine Universitas Pembangunan Nasional “Veteran” Jakarta. Jl. Fatmawati Hospital, Pondok Labu, South Jakarta. Email: retno.yulianti@upnvj.ac.id DOI: https://doi.org/10.26911/the7thicph.05.07
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