4.5 Article

B vitamins deficiency and decreased anti-oxidative state in patients with liver cancer

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EUROPEAN JOURNAL OF NUTRITION
卷 46, 期 5, 页码 293-299

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DR DIETRICH STEINKOPFF VERLAG
DOI: 10.1007/s00394-007-0665-8

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hepatocellular carcinoma; oxidative stress; B vitamins; glutathione; ghrelin

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Background This study examined the status of oxidative stress and B vitamins in hepatocellular carcinoma (HCC) patients in different tumor-node-metastasis stages. Patients were divided into two groups as I + II (n = 21) and III + IV (n = 19). Methods Plasma levels of lipid oxidation, alpha-tocopherol, beta-carotene, vitamin C, glutathione and the activity of antioxidant enzymes (glutathione peroxidase, superoxide dismutase, catalase, and xanthine oxidase) were determined for evaluating oxidative status. Blood B vitamins (B-1, B-2, B-6, B-12, and folate) and serum ghrelin were analyzed, and the relationship between serum ghrelin and vitamins B-2 (or B-6) was evaluated. Results HCC patients at III + IV stage showed significantly lower ghrelin, higher cholesterol, triglyceride, and uric acid than patients at I + II stage and healthy subjects (P < 0.05). Plasma lipid oxidation level in HCC patients was significantly greater than healthy subjects (P < 0.05). The activity of glutathione peroxidase, superoxide dismutase or catalase was significantly decreased, but xanthine oxidase activity was significantly elevated in HCC patients (P < 0.05). Plasma level of glutathione and vitamin C, not alpha-tocopherol and beta-carotene, in HCC patients was significantly lower (P < 0.05). Vitamins B-2 and B-6 levels in red blood cells from these HCC patients were significantly lower (P < 0.05). Conclusion This study provided novel clinical findings regarding the status of oxidative stress and B vitamins in HCC patients. Plasma glutathione level may be a proper biomarker for evaluating oxidative status for HCC patients. Our data indicate that HCC patients might need B vitamins supplementation. The increased serum level of triglyceride and cholesterol might be a consequence of an impaired hepatic fat metabolism, and might be improved by a lower fat administration to these patients.

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