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Vol. 9, Issue 5, 1037-1051, May 1998
Department of Anatomy and Cellular Biology, Tufts University
Medical School, Boston, Massachusetts 02111
Previously, we identified the heavy chain of ferritin as a
developmentally regulated nuclear protein of embryonic chicken corneal
epithelial cells. The nuclear ferritin is assembled into a
supramolecular form indistinguishable from the cytoplasmic form of
ferritin found in other cell types and thus most likely has iron-sequestering capabilities. Free iron, via the Fenton reaction, is
known to exacerbate UV-induced and other oxidative damage to cellular
components, including DNA. Since corneal epithelial cells are
constantly exposed to UV light, we hypothesized that the nuclear ferritin might protect the DNA of these cells from free radical damage.
To test this possibility, primary cultures of cells from corneal
epithelium and stroma, and from skin epithelium and stroma, were UV
irradiated, and DNA strand breaks were detected by an in situ 3'-end
labeling method. Corneal epithelial cells without nuclear ferritin were
also examined. We observed that the corneal epithelial cells with
nuclear ferritin had significantly less DNA breakage than other cell
types examined. Furthermore, increasing the iron concentration of the
culture medium exacerbated the generation of UV-induced DNA strand
breaks in corneal and skin fibroblasts, but not in the corneal
epithelial cells. Most convincingly, corneal epithelial cells in which
the expression of nuclear ferritin was inhibited became much more
susceptible to UV-induced DNA damage. Therefore, it seems that corneal
epithelial cells have evolved a novel, nuclear ferritin-based mechanism
for protecting their DNA against UV damage.
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