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

Carsten Lundby; Henriette Pilegaard; Gerrit van Hall; Mikael Sander; Jose Calbet; Steffen Loft; Peter Møller

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

Carsten Lundby, Henriette Pilegaard, Gerrit van Hall, Mikael Sander, Jose Calbet, Steffen Loft, Peter Møller

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

40 Citationer (Scopus)

Abstract

Udgivelsesdato: 2003-Nov-5

Originalsprog	Engelsk
Tidsskrift	Toxicology
Vol/bind	192
Udgave nummer	2-3
Sider (fra-til)	229-36
Antal sider	7
ISSN	0300-483X
Status	Udgivet - 2003

Bibliografisk note

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

Citationsformater

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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",

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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 -