scholarly journals Point Mutations That Reduce Erythrocyte Resistance to Oxidative Stress

10.5772/34198 ◽  
2012 ◽  
Author(s):  
Dmitriy Volosnikov ◽  
Elena Serebryakov
Keyword(s):  
Oxidative Stress ◽  
Point Mutations ◽  
Erythrocyte Resistance

scholarly journals Dual Negative Control of spx Transcription Initiation from the P3 Promoter by Repressors PerR and YodB in Bacillus subtilis

2006 ◽  
Vol 189 (5) ◽  
pp. 1736-1744 ◽  
Author(s):  
Montira Leelakriangsak ◽  
Kazuo Kobayashi ◽  
Peter Zuber
Keyword(s):  
Oxidative Stress ◽  
Bacillus Subtilis ◽  
Transcription Initiation ◽  
Transcriptional Start Site ◽  
Regulatory Region ◽  
Point Mutations ◽  
Negative Control ◽  
Response To Treatment ◽  
Additive Increase

ABSTRACT The spx gene encodes an RNA polymerase-binding protein that exerts negative and positive transcriptional control in response to oxidative stress in Bacillus subtilis. It resides in the yjbC-spx operon and is transcribed from at least five promoters located in the yjbC regulatory region or in the yjbC-spx intergenic region. Induction of spx transcription in response to treatment with the thiol-specific oxidant diamide is the result of transcription initiation at the P3 promoter located upstream of the spx coding sequence. Previous studies conducted elsewhere and analyses of transcription factor mutants using transformation array technology have uncovered two transcriptional repressors, PerR and YodB, that target the cis-acting negative control elements of the P3 promoter. Expression of an spx-bgaB fusion carrying the P3 promoter is elevated in a yodB or perR mutant, and an additive increase in expression was observed in a yodB perR double mutant. Primer extension analysis of spx RNA shows the same additive increase in P3 transcript levels in yodB perR mutant cells. Purified YodB and PerR repress spx transcription in vitro when wild-type spx P3 promoter DNA was used as a template. Point mutations at positions within the P3 promoter relieved YodB-dependent repression, while a point mutation at position +24 reduced PerR repression. DNase I footprinting analysis showed that YodB protects a region that includes the P3 −10 and −35 regions, while PerR binds to a region downstream of the P3 transcriptional start site. The binding of both repressors is impaired by the treatment of footprinting reactions with diamide or hydrogen peroxide. The study has uncovered a mechanism of dual negative control that relates to the oxidative stress response of gram-positive bacteria.

Influence of hypothyroidism on lipid peroxidation, erythrocyte resistance and antioxidant plasma properties in rabbits

2003 ◽  
Vol 51 (3) ◽  
pp. 343-351 ◽  
Author(s):  
Ewa Brzezińska-Ślebodzińska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Thiobarbituric Acid ◽  
Organic Radicals ◽  
Plasma Properties ◽  
Phospholipid Liposomes ◽  
Chain Breaking ◽  
Erythrocyte Resistance ◽  
Radical Damage

The effect of hypothyroidism on some oxidative stress parameters is reported. Moderate hypothyroid state was induced in two groups of female rabbits (3 and 12 months old) by giving 50 mg/kg body weight (BW) of propylthiouracil (PTU) per os for 6 days and 20 mg/kg BW of methimazole (MMI) for further 14 days. Serum T4 and T3 concentrations decreased by about 38-40 and 32-36%, respectively. The induced hypothyroidism resulted in a significant decrease in the serum concentration of the lipid peroxidation end-product malondialdehyde, as measured by the thiobarbituric-acid assay. Erythrocytes of hypothyroid animals exhibited higher resistance to oxidative stress, while submitted to free radicals generator 2,2'-azo-bis(2-amidinopropane) hydrochloride (AAPH) in vitro. Using two detector systems (phospholipid liposomes and deoxyribose), sensitive to either organic or inorganic oxygen radical damage, the ability of euthyroid and hypothyroid rabbit plasma to protect against oxygen radicals was evaluated. The plasma of hypothyroid animals showed about 20% higher ability to protect against iron-binding organic radicals, but about 50% lower chain-breaking antioxidant activity. The antioxidant capacity of plasma against inorganic radicals was not affected by hypothyroidism. In conclusion, the results show that thyroid hormones modulate the free-radical-induced oxidative damage of lipids and that hypothyroidism offers some protection against lipid peroxidation.

scholarly journals THE USE OF PLASMAPHERESIS IN TREATMENT OF PATIENTS WITH INFERTILITY, PERITONEAL ENDOMETRIOSIS AND NAT2 GENE POLYMORPHISM

2016 ◽  
Vol 2 ◽  
pp. 3-10 ◽  
Author(s):  
Ekaterina Dubinskaya ◽  
Natalia Lapteva ◽  
Yana Lukyanova
Keyword(s):  
Oxidative Stress ◽  
Point Mutations ◽  
Free Radical Oxidation ◽  
Blood Rheology ◽  
Comprehensive Treatment ◽  
Radical Oxidation ◽  
Treatment Techniques ◽  
Peritoneal Endometriosis ◽  
Nat2 Gene ◽  
And Oxidative Stress

It is known that 30–40 % of patients with peritoneal endometriosis suffer from infertility. Half of the patients with endometriosis are identified point mutation in NAT2 – gene, which plays an important role in the acetylation of aromatic and heterocyclic amines, in the accumulation of endotoxins, activation of free radical oxidation, impaired microcirculation. These factors involve the use of methods of gemapheresis which have detoxification, the blood rheology corrective and immune corrective effects. The purpose of this study was to evaluate the efficacy of therapeutic plasma exchange in treatment of patients with peritoneal form of endometriosis, infertility and point mutations in the gene NAT2. The study included 140 patients with infertility, peritoneal form of endometriosis and point mutations in the gene NAT2. All patients are performed laparoscopy, coagulation foci of endometriosis. In the following 93 (66.4 %) patients were treated with a the course of therapeutic plasmapheresis using the apparatus «PCS-2» with the removal of 20–25 % the volume of circulating plasma with replacement plasma of crystalloid and colloid solutions. Before treatment were shown the signs of endotoxemia, activation of oxidative stress. After treatment with the use of plasmapheresis was revealed the significant reduction of endogenous intoxication parameters and oxidative stress. Also is noted the increase in the pregnancy rate, both independently and in IVF programs, especially during the first 3 months after treatment. The findings suggest that the efficiency of the proposed comprehensive treatment techniques (laparoscopy and subsequent course of therapeutic plasmapheresis) of patients with peritoneal endometriosis and infertility and with point mutations in the gene NAT2. The use of plasmapheresis is pathogenetically justified in patients of the studied group.

scholarly journals The influence of inflammaging on oncogenesis

2019 ◽  
Vol 75 (01) ◽  
pp. 6164-2019
Author(s):  
JANUSZ A. MADEJ
Keyword(s):  
Oxidative Stress ◽  
Point Mutations ◽  
Endocrine System ◽  
Gonadotropin Releasing Hormone ◽  
Surrounding Tissue ◽  
Nuclear Factor ◽  
Kappa Light Chain ◽  
Dependent Processes ◽  
Light Chain Enhancer

There is a specific antagonism between an aging organism and neoplasia, in which the tumor is considered to influence the local tissue. It returns to some atavistic features, including the thermodynamic approach (2nd law of thermodynamics, Fig. 1), causing the rejuvenation of the surrounding tissue. The existence of various theories of oncogenesis entitles their supplementation with the theory of inflammaging: an entropic inflammation that can potentially have an indirect influence on the oncogenesis. This theory covers the effects of various causes of aging, including genetically programmed changes, telomere dependent processes and damage of genome, epigenome and proteome particles. The paper describes the patomechanism of inflammaging, including the role of mitochondria (point mutations and deletions especially in mtDNA), oxidative stress with overproduction and accumulation of free radicals and NFkB factor (nuclear factor kappa-light chain-enhancer of activated B cells) and the possibility of the influence of inflammaging on oncogenesis (Fig. 2). The inflamma-ging is programmed by hypothalamus using the immune-neuro-endocrine system, including gonadotropin releasing hormone (GnRH) that inhibits the NFkB factor with the inactivation of kinase IKK-beta. Regardless of that, the chronic inflammation, exceeding its defensive competence, lasts for years and can also be the beginning of neoplastic cells proliferation.

scholarly journals Base-excision repair deficiency alone or combined with increased oxidative stress does not increase mtDNA point mutations in mice

2018 ◽  
Vol 46 (13) ◽  
pp. 6642-6669 ◽  
Author(s):  
Johanna H K Kauppila ◽  
Nina A Bonekamp ◽  
Arnaud Mourier ◽  
Marita A Isokallio ◽  
Alexandra Just ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Base Excision Repair ◽  
Excision Repair ◽  
Point Mutations ◽  
Repair Deficiency ◽  
Base Excision

scholarly journals Yacon (Smallanthus sonchifolius (Poepp. & Endl.) H. Robinson) Improved Erythrocyte Resistance to Oxidative Stress in Streptozotocin-induced Diabetic Rats

2015 ◽  
Vol 3 (3) ◽  
pp. 17-25
Author(s):  
Mariia Khokhla ◽  
Olexandra Horbulinska ◽  
Halina Hachkova ◽  
Lidiya Mishchenko ◽  
Olexandr Shulga ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Rats ◽  
Smallanthus Sonchifolius ◽  
Erythrocyte Resistance

scholarly journals Melatonin diminishes oxidative stress in plasma, retains erythrocyte resistance and restores white blood cell count after low-dose lipopolysaccharide exposure in mice

2018 ◽  
Vol 37 (05) ◽  
pp. 571-580 ◽  
Author(s):  
N. Kurhaluk ◽  
O. V. Zaitseva ◽  
A. Sliuta ◽  
S. Kyriienko ◽  
P. J. Winklewski
Keyword(s):  
Oxidative Stress ◽  
Blood Cell ◽  
Cell Count ◽  
White Blood Cell Count ◽  
White Blood Cell ◽  
Low Dose ◽  
Blood Cell Count ◽  
Erythrocyte Resistance

Abstract 1473: Cardiac Targeted Transgenic Models of Mutations in TK2 or Pol γ Genes Result in Ultrastructural Changes in Mitochondria and Cardiac Hypertrophy

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
James J Kohler ◽  
Seyed Hosseini ◽  
Brian Day ◽  
Ann Saada ◽  
Orly Elpeleg ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Hypertrophy ◽  
Cardiac Function ◽  
Point Mutations ◽  
Ultrastructural Changes ◽  
Mitochondrial Oxidative Stress ◽  
Mtdna Depletion ◽  
Lv Mass ◽  
Mtdna Replication ◽  
The Impact

Background: Mitochondrial (mt) biogenesis and homeostasis of precursor pools are critical to normal cardiac performance. Two important enzymes are involved in mtDNA replication. DNA polymerase gamma (Pol γ) is responsible for replication of mtDNA. Thymidine kinase 2 (TK2) is responsible for intramitochondrial monophosphorylation of pyrimidines. Point mutations in Pol γ and TK2 identified in mitochondrial genetic diseases include human chronic progressive external opthalmoplegia (CPEO) associated with a Pol γ Y955C mutation, while His121Asn (HIS) and Ile212Asn (ILE) mutations in TK2 result in heritable mtDNA depletion syndromes with organ dysfunction. Because nucleoside reverse transcriptase inhibitors (NRTI) can also disrupt mtDNA replication, we examined the impact of cardiac-targeted transgenic overexpressors of Pol γ or TK2 mutants in combination with NRTI-based HAART on cardiac function. Methods: Targeted transgenic mice (TG) were generated that overexpress Y955C, HIS or ILE in cardiac tissues driven by the α-MyHC promoter. Changes in cardiac and mitochondrial structure and function were examined by echocardiography (ECHO), transmission electron microscopy (EM), mtDNA abundance, 8-OH2dG and SDH enzyme histochemistry quantitation. TGs and wild-type (WT) littermates were treated with vehicle or NRTI-based HAART (ziduvodine, lamivudine, and indinavir, 35 days). Results: Y955C TGs had decreased cardiac mtDNA abundance, increased mitochondrial oxidative stress (increased 8-OH2dG), and mitochondrial destruction together with increased LV mass. HIS TGs (both treated and untreated) demonstrated increased LV mass and a 2-fold increase in mtDNA abundance compared to WT. Untreated ILE TGs had no analogous impact, but the addition of HAART treatment resulted in increased LV mass and mtDNA abundance. Conclusions: Inefficient mtDNA replication and mitochondrial oxidative stress contribute to mtDNA depletion. Pol γ Y955C and TK2 HIS each alters mtDNA replication. ILE had minimal impact on mitochondrial ultrastructure or cardiac function, but together with HAART had an effect. These pathogenic point mutations in genes involved in mtDNA replication may increase risk for cardiac hypertrophy compounded by NRTI treatment.

scholarly journals The repression of nuclear factor I/CCAAT transcription factor (NFI/CTF) transactivating domain by oxidative stress is mediated by a critical cysteine (Cys-427)

2000 ◽  
Vol 348 (1) ◽  
pp. 235-240 ◽  
Author(s):  
Yannick MOREL ◽  
Robert BAROUKI
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Critical Role ◽  
Point Mutations ◽  
Dependent Manner ◽  
Nuclear Factor ◽  
Factor I ◽  
Nuclear Factor I

The activity of the nuclear factor I/CCAAT transcription factor (NFI/CTF) is negatively regulated by oxidative stress. The addition of relatively high (millimolar) H2O2 concentrations inactivates cellular NFI DNA-binding activity whereas lower concentrations can repress NFI/CTF transactivating function. We have investigated the mechanism of this regulation using Gal4 fusion proteins and transfection assays. We show that micromolar H2O2 concentrations repress the transactivating domain of NFI/CTF in a dose-dependent manner and are less or not active on other transcription factors' transactivating domains. Studies using deletions and point mutations pointed to the critical role of Cys-427. Indeed, when this cysteine is mutated into a serine, the repression by H2O2 is totally blunted. Mutation of other cysteine, serine and tyrosine residues within the transactivating domain had no clear effect on the repression by H2O2. Finally, treatment of cells with the thiol-alkylating reagent N-ethylmaleimide leads to a decrease in the transactivating function, which is dependent on Cys-427. This study shows that transactivating domains of transcription factors can constitute very sensitive targets of oxidative stress and highlights the critical role of these domains.

scholarly journals Moderate intake of n−3 fatty acids is associated with stable erythrocyte resistance to oxidative stress in hypertriglyceridemic subjects

2001 ◽  
Vol 74 (4) ◽  
pp. 449-456 ◽  
Author(s):  
Laurence Mabile ◽  
Alain Piolot ◽  
Lucie Boulet ◽  
Louis-Jacques Fortin ◽  
Nancy Doyle ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Erythrocyte Resistance
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