Effect of vitamin E on serum aminotransferase and thioredoxin levels in patients with viral hepatitis C.
OBJECTIVE
Oxidative stress induces cellular responses such as cell death, gene activation and cell proliferation, in the liver. Vitamin E (Vit. E) has been found to protect the liver against oxidative stress in animal experiments. Thioredoxin (TRX) is a stress inducible, multifunctional protein, secreted during oxidative stress. This study evaluated effects of Vit. E on serum TRX and aminotransferase levels in hepatitis C virus (HCV) patients, partly non-responsive to initial interferon (IFN), with higher than average level of serum alanine aminotransferase (ALT) after receiving anti-inflammatory drug treatment.


METHODS
Seventeen HCV patients (male = 3; female = 14) of age 62 +/- 7.65 years receiving anti-inflammatory drug therapy, at least 6 months prior to Vit. E administration, were given d-alpha-tocopherol 500 mg/day, orally, for a period of 3 months. ALT, aspartate aminotransferase (AST), TRX and Vit. E were measured at 0, 1, 2 and 3 months and 1 month after end of treatment. As controls, the same patients biochemical data, 3 months from the start of therapy were used. Patients were divided into three categories: total patients "T", low ALT group "L" (ALT < 70 IU/l) and high ALT group "H" (ALT > 70 IU/l), respectively.


RESULTS
The ALT level was lowered, significantly in group H, in the 1st, 2nd, 3rd and 1-month post therapy, compared to the initial value. But group L showed little or no change in ALT. Post Vit. E therapy, in groups T and H, the TRX level was elevated but remained below initial levels, whereas in group L, TRX level remained significantly lower than the pretreatment value. Groups T and L, showed significant reduction (p < 0.05) in serum TRX levels in the 2nd and 3rd month. Group H showed a tendency towards TRX reduction, but not significantly. Serum Vit. E levels increased significantly (p < 0.0001) from the 1st to 3rd month in all three T, H and L groups.


CONCLUSIONS
Oxidative stress induced liver damage is reduced by Vit. E in patients with viral hepatitis C, particularly those with initial ALT levels > 70 IU/l. Vit. E treatment causes reduction of oxidative stress markers as TRX and ALT in sera. Therefore, Vit. E can act as a supportive therapy to combat liver damage caused by oxidative stress, in such patients with continuously high levels of ALT even after anti-viral and anti-inflammatory drug therapy.
Mahmood
Sabina
S
Department of Internal Medicine, Center for Liver Diseases, Kawasaki Hospital, Kawasaki Medical School, Okayama, Japan.
Yamada
Gotaro
G
Niiyama
Gouichi
G
Kawanaka
Miwa
M
Togawa
Kazumi
K
Sho
Miho
M
Ito
Toshio
T
Sasagawa
Takayo
T
Okita
Misako
M
Nakamura
Hajime
H
Yodoi
Junji
J
D000368:Aged; D000410:Alanine Transaminase / Q000097:blood*; D005260:Female; D006526:Hepatitis C / Q000097:blood* / Q000201:enzymology; D006801:Humans; D007372:Interferons / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D013879:Thioredoxins / Q000097:blood*; D013997:Time Factors; D014810:Vitamin E / Q000378:metabolism / Q000494:pharmacology*; D024502:alpha-Tocopherol / Q000494:pharmacology
D014810:Vitamin E; D013879:Thioredoxins; D007372:Interferons; D000410:Alanine Transaminase; D024502:alpha-Tocopherol