X-Message-Number: 22289
Date: Sat, 2 Aug 2003 21:21:02 -0700 (PDT)
From: Doug Skrecky <>
Subject: Mouse and human cells versus oxygen.

Sci Aging Knowl Environ. 2003 Jul 30;2003(30):PE21
Mouse and human cells versus oxygen.

	Mice and humans are at opposite ends of the mammalian spectrum of
longevity. A major question in biology is whether this difference can be
accounted for by differences in the properties of cells from these two
species. A new publication from Judith Campisi's lab reports that human
cells in culture are more resistant than mouse cells to the damaging
effects of 20% oxygen. The greater burden of DNA damage sustained by
mouse cells causes them to rapidly enter a phase of culture in which most
cells enter permanent growth arrest (replicative senescence). However,
some mouse cells usually escape from senescence and then grow into an
immortal cell line. This never happens in human fibroblast cell cultures.
	Human cells also eventually enter replicative senescence in culture,
but this phenomenon is caused by shortening of telomeres and not by DNA
damage of the type responsible for mouse cell senescence. Human
fibroblasts never spontaneously escape from senescence. This Perspective
reviews differences between mouse and human cells that could account for
these differences in behavior. Some evidence indicates that human cells
are generally more resistant than mouse cells to oxidative damage to DNA,
but more needs to be done to confirm this finding and to understand the
underlying mechanisms. Whether or not there are differences in the amount
of DNA damage caused by oxygen or in the early phase of repair, there may
be important differences in the later consequences of DNA damage. Mouse
cells appear to be able to continue to divide with DNA damage that has
not been repaired or has been misrepaired, and becomes fixed in the form
of chromosomal abnormalities. The checkpoints that cause cells to stop
dividing when chromosomes develop abnormalities (aberrations or shortened
telomeres) appear to operate more efficiently in human cells. Much more
work is needed to understand the basis for these differences and the
implications for aging and cancer.

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