DNA damage and glutathione level in children with asthma bronchiale: Effect of antiasthmatic therapy

Hasbal, Canan; Aksu, Bağdagül; Himmetoglu, Solen; Dinçer, Yıldız; Koç, Eylem Efe; Hatipoğlu, Sami; Akçay, Tülay

doi:10.1111/j.1399-3038.2009.00959.x

Cited by 17 publications

(14 citation statements)

References 21 publications

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“…In our study, TAS levels were decreased compared with the control group, probably because of being used to balance oxidative stress. In another study, Hasbal et al [23 ]reported high DNA strand breaks and reduced glutathione levels in pediatric asthmatics compared with healthy controls. After the treatment, that contained ICS + LT receptor antagonist + systemic antihistaminic and inhaled β 2 -mimetic if necessary, the DNA strand breaks were found to have decreased.…”

Section: Discussionmentioning

confidence: 99%

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Effect of Montelukast Monotherapy on Oxidative Stress Parameters and DNA Damage in Children with Asthma

Dilek

Özkaya²,

Koçyiğit³

et al. 2015

Int Arch Allergy Immunol

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Background: There is ample knowledge reported in the literature about the role of oxidative stress in asthma pathogenesis. It is also known that the interaction of reactive oxygen species with DNA may result in DNA strand breaks. The aim of this study was to investigate if montelukast monotherapy affects oxidative stress and DNA damage parameters in a population of pediatric asthma patients. Methods: Group I consisted of 31 newly diagnosed asthmatic patients not taking any medication, and group II consisted of 32 patients who had been treated with montelukast for at least 6 months. Forty healthy control subjects were also enrolled in the study. Plasma total oxidant status (TOS) and total antioxidant status (TAS) were measured to assess oxidative stress. DNA damage was assessed by means of alkaline comet assay. Results: The patients in both group I and group II had statistically significant higher plasma TOS (13.1 ± 4 and 11.1 ± 4.1 μmol H₂O₂ equivalent/liter, respectively) and low TAS levels (1.4 ± 0.5 and 1.5 ± 0.5 mmol Trolox equivalent/liter, respectively) compared with the control group (TOS: 6.3 ± 3.5 μmol H₂O₂ equivalent/liter and TAS: 2.7 ± 0.6 mmol Trolox equivalent/liter; p < 0.05). DNA damage was 18.2 ± 1.0 arbitrary units (a.u.) in group I, 16.7 ± 8.2 a.u. in group II and 13.7 ± 3.4 a.u. in the control group. There were statistically significant differences only between group I and the control group (p < 0.05). Conclusions: According to the findings, montelukast therapy makes only minimal but not statistically significant improvement in all TOS, TAS and DNA damage parameters.

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Section: Discussionmentioning

confidence: 99%

“…Likewise, although there are some reports that show that allergic diseases can cause increased DNA damage, there are only a few reports assessing if treatment alters such damage [22,23,24]. Apart from 1 in vitro study, there is no information on whether montelukast monotherapy can overcome oxidative stress in asthma [25].…”

Section: Introductionmentioning

confidence: 99%

Effect of Montelukast Monotherapy on Oxidative Stress Parameters and DNA Damage in Children with Asthma

Dilek

Özkaya²,

Koçyiğit³

et al. 2015

Int Arch Allergy Immunol

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“…DNA binding inhibitors of NF-κB such as GCs do not significantly influence the cellular antioxidant enzyme levels (Hasbal et al, 2010;Rahman et al, 1999). Additionally, as revealed by Mattson et al (2000), not the classical p50:p65 dimers, but rather RelB:p52 dimers may be responsible for antioxidant enzyme induction (Perkins, 2007;Perkins and Gilmore, 2006).…”

Section: Nf-κb and Melatoninmentioning

confidence: 94%

Gene regulation by melatonin linked to epigenetic phenomena

Korkmaz

Rosales-Corral

Reíter

2012

Gene

109

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“…GSH levels were determined using the method by Beutler et al, as described before [17]. The activity of enzymes GPx and SOD were measured using spectrophotometric kits (Randox, UK).…”

Section: Methodsmentioning

confidence: 99%

Evaluation of Leukocyte DNA Damage and Antioxidant Defense in Graves’ Disease; Effect of Medical Treatment

Akçay¹,

Erdem²,

S³

2017

IJCPT

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IntroductionGraves' disease is the most common cause of hyperthyroidism [1]. It is characterized by palpitations, fatigue, heat intolerance, weight loss, and sometimes dermopathy and ophthalmopathy manifests through the progression of the disease [2]. Thyroid hormones increase oxidative metabolism by affecting basal metabolic rate and several mitochondrial enzymes [3,4], and hyperthyroidism causes changes in the antioxidant systems in various tissues by increasing the production of free radicals [5]. These radicals induce a variety of lesions in DNA, including DNA strand breaks, oxidized bases, and formation of cross-links between DNA and proteins [6]. DNA damage is constantly fixed by repair mechanisms in aerobic organisms; however, if cell division occurs before repairs are completed, the DNA damage becomes permanent [7]. A major site of radical attack is at the 8th position of guanine to yield 8-hydroxy-2-deoxyguanosine (8-OHdG). This modification might cause severe mutations [8], and sites within DNA which contain these alterations are more susceptible to strand breaks. These lesions can be detected by employing single cell gel electrophoresis, also known as comet assay. Furthermore, utilizing formamidopyrimidine DNA glycosylase (FPG), a damage specificrepair endonuclease, during this assay will cause additional strand breaks at sites with oxidized bases [9].Several antioxidant defense mechanisms exist in order to counter the harmful effects of free radicals. One of these defense agents is glutathione [10]. Glutathione, in its reduced form (GSH), is a physiological component of the intracellular antioxidant mechanisms. It acts against the effects of free radicals through serving as a cofactor for the enzyme glutathione peroxidase (GPx) [11]. Beside GPx, superoxide dismutase (SOD) is another enzyme deAbstract Background: Oxidative stress has been implicated in many pathological conditions, including hyperthyroidism. In this study, our aim was to investigate the effect of medical treatment on oxidative/antioxidative status and subsequent DNA damage in Graves' disease, in terms of reduced glutathione (GSH) levels, superoxide dismutase (SOD), glutathione peroxidase (GPx) activity and DNA strand breaks. Methods: Fifty female patients suffering from Graves' disease and thirty-seven healthy female controls were recruited in the study. Blood samples were taken from the patients before and after treatment. Free T3, free T4 and thyroid stimulating hormone (TSH) levels were determined using chemiluminescent particle assay, GSH, SOD and GPx activity using photometric techniques, and comet assay was utilized to analyze strand breaks with formamidopyrimidine DNA glycosylase (FPG) sensitive sites. Results: Free T3, free T4, GPx activity, DNA strand breaks and FPG sensitive sites were significantly higher, and TSH and GSH levels were significantly lower in patients prior to treatment compared to healthy controls. Following treatment, the levels of free T3, free T4 and TSH were restored to those of healthy controls, but the ...

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DNA damage and glutathione level in children with asthma bronchiale: Effect of antiasthmatic therapy

Cited by 17 publications

References 21 publications

Effect of Montelukast Monotherapy on Oxidative Stress Parameters and DNA Damage in Children with Asthma

Effect of Montelukast Monotherapy on Oxidative Stress Parameters and DNA Damage in Children with Asthma

Gene regulation by melatonin linked to epigenetic phenomena

Evaluation of Leukocyte DNA Damage and Antioxidant Defense in Graves’ Disease; Effect of Medical Treatment

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