Hepatic oxidative DNA damage correlates with iron overload in chronic
hepatitis C patients.
Fujita N, Horiike S, Sugimoto R, Tanaka H, Iwasa M, Kobayashi Y,
Hasegawa K, Ma N, Kawanishi S, Adachi Y, Kaito M
Free Radic Biol Med. 2007 Feb 1; 42(3): 353-362

Hepatic oxidative stress occurs in chronic hepatitis C (CH-C), but
little is known about its producing mechanisms and precise role in the
pathogenesis of the disease. To determine the relevance of hepatic
oxidatively generated DNA damage in CH-C, 8-hydroxy-2'-deoxyguanosine
(8-OHdG) adducts were quantified in liver biopsy specimens by
immunohistochemical staining, and its relationship with clinical,
biochemical, and histological parameters, and treatment response was
assessed in 40 CH-C patients. Hepatic 8-OHdG counts were significantly
correlated with serum transaminase levels (r = 0.560, p = 0.0005) and
histological grading activity (p = 0.0013). Remarkably, 8-OHdG levels
were also significantly related to body and hepatic iron storage
markers (vs serum ferritin, r = 0.565, p = 0.0004; vs hepatic total
iron score, r = 0.403, p = 0.0119; vs hepatic hepcidin messenger RNA, r
= 0.516, p = 0.0013). Baseline hepatic oxidative stress was more
prominent in nonsustained virological responder (non-SVR) than in SVR
to interferon (IFN)/ribavirin treatment (50.8 vs 32.7 cells/10(5)
mum(2), p = 0.0086). After phlebotomy, hepatic 8-OHdG levels were
significantly reduced from 53.4 to 21.1 cells/10(5) mum(2) (p = 0.0125)
with concomitant reductions of serum transaminase and iron-related
markers in CH-C patients. In conclusion, this study showed that hepatic
oxidatively generated DNA damage frequently occurs and is strongly
associated with increased iron deposition and hepatic inflammation in
CH-C patients, suggesting that iron overload is an important mediator
of hepatic oxidative stress and disease progression in chronic HCV
infection.

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