Clinical variables and ethnicity may influenced by polymorphism of CAT −262C/T and MnSOD 47C/T antioxidant enzymes in Algerian type1 diabetes without complications

Eddaikra, Atika; Amroun, Habiba; Raache, Rachida; Galleze, Assia; Abdallah-Elhadj, N.; Azzouz, M.; Meçabih, Fethi; Mechti, B.; Abbadi, Mohamed Chérif; Touil-Boukoffa, Chafia; Attal, Nabila

doi:10.1016/j.gene.2018.05.105

Cited by 5 publications

(3 citation statements)

References 77 publications

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“…Several previous studies have shown that hyperglycemia is associated with a decrease in oxidative defense. This confirms the hypothesis that hyperglycemia is at the origin of the production of reactive species and the decline in antioxidant defense [53,54]. On the other hand, another study, carried out on endothelial cells of human origin, shows that high concentrations of glucose increase the activities of anti-oxidant enzymes (SOD, catalase, glutathione-peroxidase) as well as their cellular overexpression.…”

Section: Auto-immune Diseasessupporting

confidence: 77%

Endogenous Enzymatic Antioxidant Defense and Pathologies

Eddaikra¹,

Eddaikra²

2021

Antioxidants - Benefits, Sources, Mechanisms of Action

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Oxidative stress is an important component of various diseases. It manifests as an imbalance caused by an excessive production of reactive oxygen species (ROS) which are associated with a deficit of antioxidant activity. This deficit can be the consequence of genetic factors, environmental ones, metabolic imbalance, toxicity or direct attacks by the accumulation of free radicals. These can induce metabolic dysfunction affecting biological macromolecules in their structures or activities. From a physiological perspective, the neutralization of free radicals is ensured by enzymatic, antioxidant and non-enzymatic defense systems. In the present chapter, we will focus on the endogenous enzymatic antioxidant defense system such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPxs), thioredoxin (Trx) and paraxonase which play an important role in homeostatic redox balance. Also, we will review this set of antioxidants enzymes within different pathological states such as diabetes, cancer, autoimmune diseases, cardiovascular, Alzheimer’s, Parkinson’s or parasitic diseases such as Leishmaniasis and Malaria.

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Section: Auto-immune Diseasessupporting

confidence: 77%

Endogenous Enzymatic Antioxidant Defense and Pathologies

Eddaikra¹,

Eddaikra²

2021

Antioxidants - Benefits, Sources, Mechanisms of Action

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“…Our data also suggest that CAT rs1001179 A allele significantly lowers odds for developing the edema for more than two times. This SNP has been reported to increase gene’s expression [75]. The mechanism of this AE is still not fully understood.…”

Section: Discussionmentioning

confidence: 99%

Genetic variability of inflammation and oxidative stress genes does not play a major role in the occurrence of adverse events of dopaminergic treatment in Parkinson’s disease

Redenšek

Flisar

Kojović

et al. 2019

J Neuroinflammation

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Background Inflammation and oxidative stress are recognized as important contributors to Parkinson’s disease pathogenesis. As such, genetic variability in these pathways could have a role in susceptibility for the disease as well as in the treatment outcome. Dopaminergic treatment is effective in management of motor symptoms, but poses a risk for motor and non-motor adverse events. Our aim was to evaluate the impact of selected single-nucleotide polymorphisms in genes involved in inflammation and oxidative stress on Parkinson’s disease susceptibility and the occurrence of adverse events of dopaminergic treatment. Methods In total, 224 patients were enrolled, and their demographic and clinical data on the disease course were collected. Furthermore, a control group of 146 healthy Slovenian blood donors were included for Parkinson’s disease’ risk evaluation. Peripheral blood was obtained for DNA isolation. Genotyping was performed for NLRP3 rs35829419, CARD8 rs2043211, IL1β rs16944, IL1β rs1143623, IL6 rs1800795, CAT rs1001179, CAT rs10836235, SOD2 rs4880, NOS1 rs2293054, NOS1 rs2682826, TNF-α rs1800629, and GPX1 rs1050450. Logistic regression was used for analysis of possible associations. Results We observed a nominally significant association of the IL1β rs1143623 C allele with the risk for Parkinson’s disease ( OR = 0.59; 95%CI = 0.38–0.92, p = 0.021). CAT rs1001179 A allele was significantly associated with peripheral edema (OR = 0.32; 95%CI = 0.15–0.68; p = 0.003). Other associations observed were only nominally significant after adjustments: NOS1 rs2682826 A allele and excessive daytime sleepiness and sleep attacks (OR = 1.75; 95%CI = 1.00–3.06, p = 0.048), SOD2 rs4880 T allele and nausea/vomiting (OR = 0.49, 95%CI = 0.25–0.94; p = 0.031), IL1β rs1143623 C allele and orthostatic hypotension (OR = 0.57, 95%CI = 0.32–1.00, p = 0.050), and NOS1 rs2682826 A allele and impulse control disorders (OR = 2.59; 95%CI = 1.09–6.19; p = 0.032). We did not find any associations between selected polymorphisms and motor adverse events. Conclusions Apart from some nominally significant associations, one significant association between CAT genetic variability and peripheral edema was observed as well. Therefore, the results of our stud...

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“…It is a heterogeneous disorder with two major forms, type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM), both of which are exacerbated by free radicals produced via glucose autoxidation [120][121][122]. Emerging evidence has indicated that the CT genotype of the MnSOD 47C/T gene is a significant risk factor for T1DM susceptibility (OR = 2.37; CI 95% = 1.03 to 5.46; p = 0.040) [123]. Here, we summarize the different roles of MnSOD in regulating diabetes and its complications.…”

Section: Diabetesmentioning

confidence: 99%

Insights into Manganese Superoxide Dismutase and Human Diseases

Liu

Sun

Chen

et al. 2022

IJMS

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Redox equilibria and the modulation of redox signalling play crucial roles in physiological processes. Overproduction of reactive oxygen species (ROS) disrupts the body’s antioxidant defence, compromising redox homeostasis and increasing oxidative stress, leading to the development of several diseases. Manganese superoxide dismutase (MnSOD) is a principal antioxidant enzyme that protects cells from oxidative damage by converting superoxide anion radicals to hydrogen peroxide and oxygen in mitochondria. Systematic studies have demonstrated that MnSOD plays an indispensable role in multiple diseases. This review focuses on preclinical evidence that describes the mechanisms of MnSOD in diseases accompanied with an imbalanced redox status, including fibrotic diseases, inflammation, diabetes, vascular diseases, neurodegenerative diseases, and cancer. The potential therapeutic effects of MnSOD activators and MnSOD mimetics are also discussed. Targeting this specific superoxide anion radical scavenger may be a clinically beneficial strategy, and understanding the therapeutic role of MnSOD may provide a positive insight into preventing and treating related diseases.

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Clinical variables and ethnicity may influenced by polymorphism of CAT −262C/T and MnSOD 47C/T antioxidant enzymes in Algerian type1 diabetes without complications

Cited by 5 publications

References 77 publications

Endogenous Enzymatic Antioxidant Defense and Pathologies

Endogenous Enzymatic Antioxidant Defense and Pathologies

Genetic variability of inflammation and oxidative stress genes does not play a major role in the occurrence of adverse events of dopaminergic treatment in Parkinson’s disease

Insights into Manganese Superoxide Dismutase and Human Diseases

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