Oxidative DNA damage and repair in skeletal muscle of humans exposed to high-altitude hypoxia.

Research output: Contribution to journalJournal articlepeer-review

Standard

Oxidative DNA damage and repair in skeletal muscle of humans exposed to high-altitude hypoxia. / Lundby, Carsten; Pilegaard, Henriette; van Hall, Gerrit; Sander, Mikael; Calbet, Jose; Loft, Steffen; Møller, Peter.

In: Toxicology, Vol. 192, No. 2-3, 2003, p. 229-36.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Lundby, C, Pilegaard, H, van Hall, G, Sander, M, Calbet, J, Loft, S & Møller, P 2003, 'Oxidative DNA damage and repair in skeletal muscle of humans exposed to high-altitude hypoxia.', Toxicology, vol. 192, no. 2-3, pp. 229-36.

APA

Lundby, C., Pilegaard, H., van Hall, G., Sander, M., Calbet, J., Loft, S., & Møller, P. (2003). Oxidative DNA damage and repair in skeletal muscle of humans exposed to high-altitude hypoxia. Toxicology, 192(2-3), 229-36.

Vancouver

Lundby C, Pilegaard H, van Hall G, Sander M, Calbet J, Loft S et al. Oxidative DNA damage and repair in skeletal muscle of humans exposed to high-altitude hypoxia. Toxicology. 2003;192(2-3):229-36.

Author

Lundby, Carsten ; Pilegaard, Henriette ; van Hall, Gerrit ; Sander, Mikael ; Calbet, Jose ; Loft, Steffen ; Møller, Peter. / Oxidative DNA damage and repair in skeletal muscle of humans exposed to high-altitude hypoxia. In: Toxicology. 2003 ; Vol. 192, No. 2-3. pp. 229-36.

Bibtex

@article{ca865950ac0111ddb5e9000ea68e967b,
title = "Oxidative DNA damage and repair in skeletal muscle of humans exposed to high-altitude hypoxia.",
abstract = "Recent research suggests that high-altitude hypoxia may serve as a model for prolonged oxidative stress in healthy humans. In this study, we investigated the consequences of prolonged high-altitude hypoxia on the basal level of oxidative damage to nuclear DNA in muscle cells, a major oxygen-consuming tissue. Muscle biopsies from seven healthy humans were obtained at sea level and after 2 and 8 weeks of hypoxia at 4100 m.a.s.l. We found increased levels of strand breaks and endonuclease III-sensitive sites after 2 weeks of hypoxia, whereas oxidative DNA damage detected by formamidopyrimidine DNA glycosylase (FPG) protein was unaltered. The expression of 8-oxoguanine DNA glycosylase 1 (OGG1), determined by quantitative RT-PCR of mRNA levels did not significantly change during high-altitude hypoxia, although the data could not exclude a minor upregulation. The expression of heme oxygenase-1 (HO-1) was unaltered by prolonged hypoxia, in accordance with the notion that HO-1 is an acute stress response protein. In conclusion, our data indicate high-altitude hypoxia may serve as a good model for oxidative stress and that antioxidant genes are not upregulated in muscle tissue by prolonged hypoxia despite increased generation of oxidative DNA damage.",
author = "Carsten Lundby and Henriette Pilegaard and {van Hall}, Gerrit and Mikael Sander and Jose Calbet and Steffen Loft and Peter M{\o}ller",
note = "Keywords: Adaptation, Physiological; Adult; Altitude Sickness; DNA Damage; DNA Repair; Female; Humans; Male; Muscle, Skeletal; Oxidative Stress; Time Factors",
year = "2003",
language = "English",
volume = "192",
pages = "229--36",
journal = "Toxicology",
issn = "0300-483X",
publisher = "Elsevier Ireland Ltd",
number = "2-3",

}

RIS

TY - JOUR

T1 - Oxidative DNA damage and repair in skeletal muscle of humans exposed to high-altitude hypoxia.

AU - Lundby, Carsten

AU - Pilegaard, Henriette

AU - van Hall, Gerrit

AU - Sander, Mikael

AU - Calbet, Jose

AU - Loft, Steffen

AU - Møller, Peter

N1 - Keywords: Adaptation, Physiological; Adult; Altitude Sickness; DNA Damage; DNA Repair; Female; Humans; Male; Muscle, Skeletal; Oxidative Stress; Time Factors

PY - 2003

Y1 - 2003

N2 - Recent research suggests that high-altitude hypoxia may serve as a model for prolonged oxidative stress in healthy humans. In this study, we investigated the consequences of prolonged high-altitude hypoxia on the basal level of oxidative damage to nuclear DNA in muscle cells, a major oxygen-consuming tissue. Muscle biopsies from seven healthy humans were obtained at sea level and after 2 and 8 weeks of hypoxia at 4100 m.a.s.l. We found increased levels of strand breaks and endonuclease III-sensitive sites after 2 weeks of hypoxia, whereas oxidative DNA damage detected by formamidopyrimidine DNA glycosylase (FPG) protein was unaltered. The expression of 8-oxoguanine DNA glycosylase 1 (OGG1), determined by quantitative RT-PCR of mRNA levels did not significantly change during high-altitude hypoxia, although the data could not exclude a minor upregulation. The expression of heme oxygenase-1 (HO-1) was unaltered by prolonged hypoxia, in accordance with the notion that HO-1 is an acute stress response protein. In conclusion, our data indicate high-altitude hypoxia may serve as a good model for oxidative stress and that antioxidant genes are not upregulated in muscle tissue by prolonged hypoxia despite increased generation of oxidative DNA damage.

AB - Recent research suggests that high-altitude hypoxia may serve as a model for prolonged oxidative stress in healthy humans. In this study, we investigated the consequences of prolonged high-altitude hypoxia on the basal level of oxidative damage to nuclear DNA in muscle cells, a major oxygen-consuming tissue. Muscle biopsies from seven healthy humans were obtained at sea level and after 2 and 8 weeks of hypoxia at 4100 m.a.s.l. We found increased levels of strand breaks and endonuclease III-sensitive sites after 2 weeks of hypoxia, whereas oxidative DNA damage detected by formamidopyrimidine DNA glycosylase (FPG) protein was unaltered. The expression of 8-oxoguanine DNA glycosylase 1 (OGG1), determined by quantitative RT-PCR of mRNA levels did not significantly change during high-altitude hypoxia, although the data could not exclude a minor upregulation. The expression of heme oxygenase-1 (HO-1) was unaltered by prolonged hypoxia, in accordance with the notion that HO-1 is an acute stress response protein. In conclusion, our data indicate high-altitude hypoxia may serve as a good model for oxidative stress and that antioxidant genes are not upregulated in muscle tissue by prolonged hypoxia despite increased generation of oxidative DNA damage.

M3 - Journal article

C2 - 14580789

VL - 192

SP - 229

EP - 236

JO - Toxicology

JF - Toxicology

SN - 0300-483X

IS - 2-3

ER -

ID: 8442619