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Vitamin B‐6 supplementation might mediate antioxidant capacity by reducing plasma homocysteine concentration in patients with hepatocellular carcinoma after tumor resection
Author(s) -
Huang YiChia,
Cheng ShaoBin,
Liu HsiaoTien
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1159.2
Subject(s) - homocysteine , hepatocellular carcinoma , antioxidant , medicine , oxidative stress , trolox equivalent antioxidant capacity , glutathione , endocrinology , gastroenterology , chemistry , antioxidant capacity , biochemistry , enzyme
Deficient vitamin B‐6 status might be a causative factor for hepatocellular carcinoma (HCC) development, it would be useful to determine whether vitamin B‐6 supplementation would have a preventive effect in reducing plasma homocysteine, or indirectly increasing glutathione and its dependent antioxidant enzyme capacities in patients with HCC. The purpose of this study was to investigate whether vitamin B‐6 supplementation had a significant effect on plasma homocysteine, oxidative stress, and antioxidant capacities in HCC patients following tumor resection. Thirty‐three HCC patients were included in the study. Patients were randomly assigned to either the placebo (n = 16) group or the vitamin B‐6 50 mg/d (n = 17) group for 12 weeks. Plasma homocysteine in the vitamin B‐6 group was significantly decreased at week 12, while the level of trolox equivalent antioxidant capacity (TEAC) was significantly increased at the end of the intervention period. Vitamin B‐6 supplementation had significant reducing effect on the change of plasma homocysteine (β = −2.4, p = 0.02) but not on the change of TEAC level after adjusting for potential confounders. The change of plasma homocysteine was significantly associated with the change of TEAC after adjusting for potential confounders (β = −162.0, p = 0.03). Vitamin B‐6 supplementation seemed to mediate antioxidant capacity via by reducing plasma homocysteine rather than having a direct anti‐oxidative effect in HCC patients who had recently undergone tumor resection. Support or Funding Information This study was supported by the Ministry of Science and Technology, Taiwan (MOST 104‐2320‐B‐040‐009‐MY3).