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BioMed Research International
Volume 2016, Article ID 7658981, 7 pages
http://dx.doi.org/10.1155/2016/7658981
Clinical Study

Vitamin B-6 Supplementation Could Mediate Antioxidant Capacity by Reducing Plasma Homocysteine Concentration in Patients with Hepatocellular Carcinoma after Tumor Resection

1Division of General Surgery, Department of Surgery, Taichung Veterans General Hospital, Taichung 40705, Taiwan
2School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan
3School of Nutrition, Chung Shan Medical University, Taichung 40201, Taiwan
4Department of Nutrition, Chung Shan Medical University Hospital, Taichung 40201, Taiwan

Received 30 December 2015; Accepted 17 February 2016

Academic Editor: Gang Liu

Copyright © 2016 Shao-Bin Cheng et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Vitamin B-6 has a strong antioxidative effect. It would be useful to determine whether vitamin B-6 supplementation had effects on antioxidant capacities in patients with hepatocellular carcinoma (HCC) who had recently undergone tumor resection. Thirty-three HCC patients were randomly assigned to either the placebo group or the vitamin B-6 50 mg/d group for 12 weeks. Plasma pyridoxal 5′-phosphate, homocysteine, indicators of oxidative stress, and antioxidant capacities were measured. 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 a significant reducing effect on the change of plasma homocysteine (, ) 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 (, ). Vitamin B-6 supplementation seemed to mediate antioxidant capacity via reducing plasma homocysteine rather than having a direct antioxidative effect in HCC patients who had recently undergone tumor resection. The clinical trial number is NCT01964001, ClinicalTrials.gov.