X-Message-Number: 25554
Date: Sat, 15 Jan 2005 12:06:46 -0800 (PST)
From: Doug Skrecky <>
Subject: oxidative stress and telomeres

[Telomere length as well as other signs of aging are very slow to
deteriorate in young adults. These signs of aging greatly accelerate in
the elderly, and increased inflamation and oxidation has been targeted
as a possible cause for this acceleration.]

J Gerontol A Biol Sci Med Sci. 2004 Apr;59(4):324-37
Effects of oxidative damage and telomerase activity on human articular
cartilage chondrocyte senescence.
  Senescence compromises the ability of chondrocytes to maintain and
repair articular cartilage. We hypothesized that oxidative stress and
telomere loss contribute to chondrocyte senescence. To test this
hypothesis, we compared the growth of human articular cartilage
chondrocytes incubated in 5% O2 and 21% O2. Cells grown in 5% O2 reached
60 population doublings (PD) before senescing, but growth in 21% O2
induced DNA damage and premature senescence at less than 40 PD. Human
telomerase reverse transcriptase (hTERT)-transduction failed to prevent
chondrocyte senescence in 21% O2, but allowed 1 of 3 chondrocyte strains
to exceed 90 PD in 5% O2. These results show that oxidative stress causes
premature chondrocyte senescence. They may help explain the increased
risk of osteoarthritis with age and after joint trauma and inflammation,
and suggest that minimizing oxidative damage will help produce optimal
results for chondrocyte transplantation.

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