| Summary: | 碩士 === 國立臺灣大學 === 微生物與生化學研究所 === 97 === Abstract
2, 5, 7,8-tetramethyl-2-(2’-carboxyethyl)-6-hydroxychroman (α-CEHC) has been demonstrated to be the urinary metabolite of α-tocopherol. It has been reported that α-CEHC could be detected in the human urine while the plasma α-tocopherol concentration of the subject was higher than a threshold value (Shultz et al., 1995),implying that the urinary α-CEHC excretion might be related to the nutritional status of vitamin E.
To characterizing the quantitative relationship between α-CEHC level and dietary α-tocopherol intake, rats were fed diets of which the vitamin E level ranged from 0 to 75 mg/kg diet. The response of α-CEHC in urine and plasma to increasing intake of vitamin E were compared to other biomarkers of vitamin E status.
Forty-eight weanling Wistar rats were fed vitamin E-deficient diet for 1 week. They were then randomly assigned to eight groups and respectively fed diets containing 0 (E0), 5 (E5), 10 (E10), 15 (E15), 25 (E25), 35 (E35) or 75 (E75) mg/kg diet of RRR-α-tocopheryl acetate or 102mg/kg diet of all-rac-α-tocopheryl acetate(EA) for 13.5 weeks. Twenty-four hour urine was collected and daily water intake recorded on week 8, 10 and 13.5. After an overnight fasting, rats were sacrificed on day 94.
Among the 8 groups, only E0 showed significantly higher plasma pyruvate kinase activity as well as the in vitro RBC hemolysis.(p < 0.05) The plasma α-tocopherol concentration of the E0,E5,E10, E25,E35 and E75 group were respectively 0.09, 0.3, 0.63,1.01, 1.38, 1.61and 1.74 fold that of the E15 group. The liver α-tocopherol content of the E0, E5, E10, E25, E35 and E75 group were 0.09, 0.34, 0.68, 1.21, 1.78 and 3.31 fold that of the E15 group. The EWAT α-tocopherol content of the E0,E5,E10, E25,E35 and E75 group were 1.14, 0.72, 1.3, 2.83, 1.46 and 2.43 fold that of the E15 group. The linear relationship between plasma α-tocopherol and dietary vitamin E level was sharper in the range of 0-15 mg/kg diet than in the range of 25-75 mg/kg diet. The correlation coefficient between α-tocopherol level and vitamin E intake in the range of 0 to 75 mg/kg diet was highest with the liver.
The urinary α-CEHC excretion of the 8 groups were not significant different in week 0. After 8 weeks , the urinary α-CEHC excretion markedly increased with the increase of the dietary vitamin E level. The excretion (μg/day) of free α-CEHC of E0,E5,E10, E25,E35 and E75 group were 1.14, 0.88, 1.03, 1.2, 1.32 and 2.66 (p＜0.05)fold that of the E15 group, respectively. The excretion of conjugated α-CEHC of E0,E5,E10, E25,E35 and E75 group were 0.17, 0.42, 0.67,1.78, 3.78 and 9.95 fold that of E15 group, respectively. The excretion of total α-CEHC of E0,E5,E10, E25,E35 and E75 group were0.14, 0.43, 0.68, 1.77, 3.73 and 8.91 fold that of the E15 group, respectively. EA showed significant difference with E75 after 13.5 weeks. The plasma α-CEHC concentration also increased markedly with the increase of dietary vitamin E level. The plasma concentration (μM) of free α-CEHC of E0,E5,E10, E25,E35 and E75 group were 0.17, 0.27, 0.82, 0.86, 1.26 and 1.53 fold that of the E15 group, respectively. The concentration(μM) of conjugated α-CEHC of E0,E5,E10, E25,E35 and E75 group were 0.44, 0.79, 0.98, 2.61, 3.24 and 4.6 fold that of the E15 group, respectively. The concentration (μM) of total α-CEHC of E0,E5,E10, E25,E35 and E75 group were0.35, 0.61, 0.93, 2.01, 2.57 and 3.55 fold that of the E15 group, respectively. EA also showed no significant difference with E75.
The correlation of various responder to dietary vitamin intake were found to be highest with the liver α-tocopherol content (r = 0.96, p＜0.000), and the plasma conjugated α-CEHC(r = 0.9, p＜0.000) and total α-CEHC(r = 0.88, p＜0.000) were next to it.
In conclusion, the plasma and liverα--tocopherol responded more sharply to dietary vitamin E level in the range between 0-15 mg/kg diet of RRR-α-tocopheryl acetate while plasma and urinary α-CEHC responded more sharply to dietary vitamin E intake in the range between 0-25 and 25-75 mg/kg diet.
The results implied the potential of using the plasma α-CEHC as an indicator of dietary vitamin E intake beyond the adequate level.
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