Nitric oxide synthase-2 (NOS2) gene polymorphism c.1832C&gt;T (Ser608Leu) associated with nitrosative stress in Fanconi anaemia

George, Merin; Solanki, Avani; Mohanty, Purvi; Dhangar, Somprakash; Rajendran, Aruna; Mohan, Sheila; Vundinti, Babu Rao

doi:10.1007/s11033-021-06293-1

Cited by 2 publications

(1 citation statement)

References 24 publications

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“…Measurement of nitrite by Griess reagent revealed that the amount of nitrite in FancC-/-cells was significantly higher than FANCC WT cells suggesting a possible role of NO in the pathophysiology of FA (Figure 1). Our data supports earlier studies that have demonstrated an increase in 3-nitrotyrosine levels in FA patients [14] and established the effect of NOS on genomic instability in FANCC-/-cells [9].…”

Section: Nitrite (No 2 -supporting

confidence: 93%

Nitric Oxide Increases Mitomycin-C Cytotoxicity by Generation of Reactive Oxygen Species and Induces Cell Death by Apoptosis in FancC-/- Cells

Biswas¹,

Patra²,

Rs³

2021

annhematoloncol

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Fanconi Anemia (FA) is a rare genetic disorder and patients of FA exhibit progressive bone marrow failure, developmental defects and cancer predisposition. Mitochondrial dysfunction due to oxidative stress and higher levels of Reactive Oxygen Species (ROS) has been well documented in FA. Increase in the levels of Reactive Nitrogen Species (RNS) and Nitric Oxide Synthase (NOS) activity is often correlated with OS- related disorders which have altered mitochondrial function. Biological effects of Nitric Oxide (NO) and nitrosative stress depend on the cell type, concentration of NO, the time of incubation and cellular homeostasis. NO is known to have both prooncogenic as well as tumour -suppressing effects which are a result of regulation of S- nitrosylation, genome wide epigenetic changes and posttranslational modification of protein. NO plays strategic roles in metabolic and signalling pathways, making NO metabolism a key mediator in pathways that are responsible for supporting tumorigenesis. NO is also known to have important regulatory roles in the process of autophagy, which is an important mediator in the cross-talk with ROS and RNS. In the present study, we examined the interaction between ROS and NO, induction of apoptosis by NO and the possible role of NO in the pathogenesis of FA. Investigating the involvement of NO and NS and their interactions with the known hallmarks of FA will give a more comprehensive understanding of pathogenesis of FA.

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Section: Nitrite (No 2 -supporting

confidence: 93%

Nitric Oxide Increases Mitomycin-C Cytotoxicity by Generation of Reactive Oxygen Species and Induces Cell Death by Apoptosis in FancC-/- Cells

Biswas¹,

Patra²,

Rs³

2021

annhematoloncol

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Variation of genes encoding nitric oxide synthases and antioxidant enzymes as potential risks of multiple sclerosis development: a preliminary study

Wigner

Dziedzic

Synowiec

et al. 2022

Sci Rep

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Multiple sclerosis (MS) is a neurodegenerative disease characterized by a variable clinical course and diverse pathophysiology, including nitrative and oxidative stresses as well as inflammation. We aimed to detect the potential association between five selected single-nucleotide polymorphisms (SNPs) in genes encoding nitric oxide synthetases as well as antioxidant enzymes and the development of MS in a Polish population. Genomic DNA was isolated from peripheral blood collected from 142 MS patients and 140 controls. Using Taq-Man® probes, we genotyped the following SNPs: rs1879417 in NOS1, and rs2297518 in NOS2 as well as rs4880 in SOD2, rs7943316 in CAT, rs713041 in GPX4. In the case of rs2297518, the C/C genotype and C allele SNP were associated with an enhanced occurrence of MS, while the C/T, T/T genotypes, and T allele of the same polymorphism reduced this risk. Moreover, the C/C homozygote and C allele of the rs4880 SNP reduced MS risk, while the T allele increased the risk. In addition, the A/T heterozygote of rs7943316 polymorphism was associated with an increased risk of MS occurrence. We also detected that the C/C genotype and C allele of rs713041 decreased the risk of MS, whereas the T/T genotype and T allele increased this risk. In conclusion, the results of our study suggest some links between polymorphic variability in the nitrative/oxidative stress-related genes and the risk of MS development in the Polish population.

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Nitric oxide synthase-2 (NOS2) gene polymorphism c.1832C>T (Ser608Leu) associated with nitrosative stress in Fanconi anaemia

Cited by 2 publications

References 24 publications

Nitric Oxide Increases Mitomycin-C Cytotoxicity by Generation of Reactive Oxygen Species and Induces Cell Death by Apoptosis in FancC-/- Cells

Nitric Oxide Increases Mitomycin-C Cytotoxicity by Generation of Reactive Oxygen Species and Induces Cell Death by Apoptosis in FancC-/- Cells

Variation of genes encoding nitric oxide synthases and antioxidant enzymes as potential risks of multiple sclerosis development: a preliminary study

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