Liu Chun, Russell Robert M, Wang Xiang-Dong
Nutrition and Cancer Biology Laboratory, Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.
J Nutr. 2004 Feb;134(2):426-30. doi: 10.1093/jn/134.2.426.
Previously, we found that exposing ferrets to cigarette smoke enhanced oxidative excentric cleavage of beta-carotene. In the present study, we examined whether alpha-tocopherol, ascorbic acid, or the two combined can prevent smoke-altered beta-carotene metabolism. In vitro incubation of beta-carotene (10 micro mol/L) with lung postnuclear fractions from ferrets exposed to cigarette smoke was carried out in the absence or presence of alpha-tocopherol (50 micro mol/L), ascorbic acid (10 or 50 micro mol/L), or both vitamins to evaluate their effects on the production of beta-apo-carotenals and retinoids from beta-carotene. The oxidative cleavage metabolites of beta-carotene, beta-apo-carotenals (beta-apo-14', beta-apo-12', beta-apo-10', and beta-apo-8'), retinoic acid (RA), and retinal were analyzed by HPLC. We found that the smoke-enhanced production of individual beta-apo-carotenals was significantly decreased by 36-77% when alpha-tocopherol (50 micro mol/L) and ascorbic acid (50 micro mol/L) were added together to the incubation mixture. alpha-Tocopherol alone had a modest effect. Ascorbic acid in the presence of alpha-tocopherol inhibited the production of beta-apo-carotenals in a dose-dependent manner, although ascorbic acid alone had no effect. In contrast, the production of RA and retinal among smoke-exposed ferrets was substantially increased ( approximately 3-fold, P < 0.05) when both alpha-tocopherol and ascorbic acid were added to the incubation mixtures. However, when ascorbic acid or alpha-tocopherol alone was added, the production of RA among smoke-exposed ferrets increased only modestly (80%, P < 0.05) and did not differ from the RA levels in control ferrets. In conclusion, these data indicate that alpha-tocopherol and ascorbic acid may act synergistically in preventing the enhanced oxidative excentric cleavage of beta-carotene induced by smoking exposure, thereby facilitating the conversion of beta-carotene into RA and retinal.
此前，我们发现将雪貂暴露于香烟烟雾中会增强β-胡萝卜素的氧化偏心裂解。在本研究中，我们研究了α-生育酚、抗坏血酸或两者联合使用是否可以预防烟雾改变的β-胡萝卜素代谢。在存在或不存在α-生育酚（50μmol/L）、抗坏血酸（10或50μmol/L）或两种维生素的情况下，将β-胡萝卜素（10μmol/L）与暴露于香烟烟雾的雪貂的肺核后组分进行体外孵育，以评估它们对β-胡萝卜素产生β-阿朴-胡萝卜醛和类视黄醇的影响。通过HPLC分析β-胡萝卜素的氧化裂解代谢产物β-阿朴-胡萝卜醛（β-阿朴-14'、β-阿朴-12'、β-阿朴-10'和β-阿朴-8'）、视黄酸（RA）和视黄醛。我们发现，当将α-生育酚（50μmol/L）和抗坏血酸（50μmol/L）一起添加到孵育混合物中时，烟雾增强的单个β-阿朴-胡萝卜醛的产生显著降低了36-77%。单独的α-生育酚有适度的作用。在α-生育酚存在下，抗坏血酸以剂量依赖性方式抑制β-阿朴-胡萝卜醛的产生，尽管单独的抗坏血酸没有作用。相反，当将α-生育酚和抗坏血酸都添加到孵育混合物中时，暴露于烟雾的雪貂中RA和视黄醛的产生显著增加（约3倍，P<0.05）。然而，当单独添加抗坏血酸或α-生育酚时，暴露于烟雾的雪貂中RA的产生仅适度增加（80%，P<0.05），并且与对照雪貂中的RA水平没有差异。总之，这些数据表明，α-生育酚和抗坏血酸可能协同作用，预防吸烟暴露诱导的β-胡萝卜素氧化偏心裂解增强，从而促进β-胡萝卜素向RA和视黄醛的转化。
