| 1. |
- Cooke, Marcus S, et al.
(author)
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Interlaboratory comparison of methodologies for the measurement of urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine.
- 2009
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In: Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals. - : Informa UK Limited. - 1366-5804. ; 14:2, s. 103-10
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Journal article (peer-reviewed)abstract
- Urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) is widely used as a marker of oxidative stress. Here we report the comparison of two, distinct chromatographic assays with an enzyme-linked immunosorbent assay (ELISA). The chromatographic assays displayed good agreement (r =:0.89, p < 0.0001), whereas there was markedly worse, albeit still significant, agreement with the ELISA (high-pressure liquid chromatography followed by gas chromatography (HPLC-GC/MS), r = 0.43; HPLC with electrochemical detection (HPLC-EC), r = 0.56; p < 0.0001). Mean values differed significantly between the chromatographic assays and the ELISA (HPLC-GC/MS 3.86, HPLC-EC 4.20, ELISA 18.70 ng mg(-1) creatinine; p < 0.0001). While it is reassuring to note good agreement between chromatographic assays, this study reveals significant short-comings in the ELISA, which brings into question its continued use in its present form.
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| 2. |
- Danielsen, Pernille Hogh, et al.
(author)
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Oxidatively damaged DNA and its repair after experimental exposure to wood smoke in healthy humans.
- 2008
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In: Mutation research. - : Elsevier BV. - 0027-5107. ; 642:1-2, s. 37-42
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Journal article (peer-reviewed)abstract
- Particulate matter from wood smoke may cause health effects through generation of oxidative stress with resulting damage to DNA. We investigated oxidatively damaged DNA and related repair capacity in peripheral blood mononuclear cells (PBMC) and measured the urinary excretion of repair products after controlled short-term exposure of human volunteers to wood smoke. Thirteen healthy adults were exposed first to clean air and then to wood smoke in a chamber during 4h sessions, 1 week apart. Blood samples were taken 3h after exposure and on the following morning, and urine was collected after exposure, from bedtime until the next morning. We measured the levels of DNA strand breaks (SB), oxidized purines as formamidopyrimidine-DNA-glycosylase (FPG) sites and activity of oxoguanine glycosylase 1 (hOGG1) in PBMC by the comet assay, whereas mRNA levels of hOGG1, nucleoside diphosphate linked moiety X-type motif 1 (hNUDT1) and heme oxygenase 1 (hHO1) were determined by real-time RT-PCR. The excretion of 8-oxo-7,8-dihydro-oxoguanine (8-oxoGua) and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in urine was measured by high performance liquid chromatography purification followed by gas chromatography with mass spectrometry. The morning following exposure to wood smoke the PBMC levels of SB were significantly decreased and the mRNA levels of hOGG1 significantly increased. FPG sites, hOGG1 activity, expression of hNUDT1 and hHO1, urinary excretion of 8-oxodG and 8-oxoGua did not change significantly. Our findings support that exposure to wood smoke causes systemic effects, although we could not demonstrate genotoxic effects, possibly explained by enhanced repair and timing of sampling.
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| 3. |
- Skonieczna, Magdalena, et al.
(author)
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The impact of DIDS-induced inhibition of voltage-dependent anion channels (VDAC) on cellular response of lymphoblastoid cells to ionizing radiation.
- 2017
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In: Medicinal chemistry. - : Bentham Science Publishers Ltd.. - 1573-4064. ; 13:5, s. 477-483
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Journal article (peer-reviewed)abstract
- Background: The voltage-dependent ion channels (VDAC) play an essential role in the cross talk between mitochondria and the rest of the cell. Their implication in cell life and cell death has been studied extensively in recent years. In this work we studied the impact of mitochondrial membrane voltage-dependent anion channels (VDACs) on cell survival and response to X-ionizing radiation (IR) of human lymphoblastoid K562 cells. Methods: The inhibition of VDACs was achieved by 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS) inhibitor and in vitro experiments including clonogenity assay, UV-visible spectrophotometry, comet assay and FACS analysis were implemented. Results: Inhibition of VDAC led to augmentation of IR-induced apoptosis and ROS production. Additionally, DIDS affected repair of IR-induced DNA strand breaks and was in line with both induction of apoptosis and caspase activity. The IR-induced NO production was potently reduced by inhibition of VDAC. Conclusion: Our results suggest that VDAC control cellular response to ionizing radiation through modulation of the ROS- and NO-dependent signaling pathways. Inhibition of VDAC with DIDS induced apoptosis in irradiated K562 lymphoblastoid cells points at DIDS, as a promising agent to enhance the effectiveness of radiotherapy.
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