کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9909143 | 1548436 | 2005 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Interaction of hyperbaric oxygen, nitric oxide, and heme oxygenase on DNA strand breaks in vivo
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Interaction of hyperbaric oxygen, nitric oxide, and heme oxygenase on DNA strand breaks in vivo Interaction of hyperbaric oxygen, nitric oxide, and heme oxygenase on DNA strand breaks in vivo](/preview/png/9909143.png)
چکیده انگلیسی
Hyperbaric oxygen (HBO), e.g. pure oxygen breathing at supra-atmospheric pressures, represents a well-suited model for investigating oxidative stress-induced DNA damage as well as protective mechanisms. While the induction of heme oxygenase-1 (HO-1) seems to be crucial for this protection against this DNA damage, the role of nitric oxide (NO) remains unclear. HO-1 expression is a major regulator of the inducible NO synthase (iNOS), and therefore we investigated the effect of the interaction between HBO, NO, and HO-1 on DNA damage. Prior to exposure to HBO (3 h at 3 bar ambient pressure) rats randomly received vehicle (HBO alone, 1 mL 0.9% saline, n = 8), the NO donor molsidomine (SIN-10, 40 mg/kg, n = 8) or the HO-1 blocker tin-mesopophyrin (Sn-MP, 50 μmol/kg, n = 8). Additional groups received SIN-10 without epxosure to HBO, i.e. breathing air under normobaric conditions for 3 h (SIN-10 alone, 40 mg/kg, n = 6), vehicle without HBO (negative controls, n = 6), and ethylmethanesulfonate without HBO (EMS, 200 mg/kg) (positive controls n = 4). Immediately after the 3 h HBO or air breathing period blood was analysed for DNA strand breaks (tail moment in the alkaline comet assay) and nitrite + nitrate (chemoluminescence). Whereas the tail moment was ten-fold higher after EMS than in the negative controls, there was no effect of HBO nor SIN-10 alone. Together with HBO, pretreatment with SIN-10 doubled the tail moment, and Sn-MP increased it by 50%. In contrast to Sn-MP or HBO alone, SIN-10 resulted in a five-fold increase of nitrite + nitrate concentrations. We conclude that both HO-1 blockade and excess NO release promote DNA damage during HBO exposure in vivo. The effect of HO-1 inhibition is probably independent of the regulatory function of HO-1 for iNOS.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 572, Issues 1â2, 2 May 2005, Pages 167-172
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 572, Issues 1â2, 2 May 2005, Pages 167-172
نویسندگان
Michael Gröger, Günter Speit, Peter Radermacher, Claus-Martin Muth,