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首页> 外文期刊>Drug Metabolism and Disposition: The Biological Fate of Chemicals >Biotransformation of fucoxanthinol into amarouciaxanthin a in mice and hepg2 cells: formation and cytotoxicity of fucoxanthin metabolites.
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Biotransformation of fucoxanthinol into amarouciaxanthin a in mice and hepg2 cells: formation and cytotoxicity of fucoxanthin metabolites.

机译：在小鼠和hepg2细胞中将岩藻黄质生物转化为金刚烷黄质a：岩藻黄质代谢产物的形成和细胞毒性。

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Fucoxanthin, a major carotenoid in edible brown algae, potentially inhibits the proliferation of human prostate cancer cells via apoptosis induction. However, it has been postulated that dietary fucoxanthin is hydrolyzed into fucoxanthinol in the gastrointestinal tract before absorption in the intestine. In the present study, we investigated the further biotransformation of orally administered fucoxanthin and estimated the cytotoxicity of fucoxanthin metabolites on PC-3 human prostate cancer cells. After the oral administration of fucoxanthin in mice, two metabolites, fucoxanthinol and an unknown metabolite, were found in the plasma and liver. The unknown metabolite was isolated from the incubation mixture of fucoxanthinol and mouse liver preparation (10,000gsupernatant of homogenates), and a series of instrumental analyses identified it as amarouciaxanthin A [(3S,5R,6'S)-3,5,6'-trihydroxy-6,7-didehydro-5,6,7',8'-tetrahydro-beta,eps ilon-carotene-3',8'-dione]. The conversion of fucoxanthinol into amarouciaxanthin A was predominantly shown in liver microsomes. This dehydrogenation/isomerization of the 5,6-epoxy-3-hydroxy-5,6-dihydro-betaend group of fucoxanthinol into the 6'-hydroxy-3'-oxo-epsilonend group of amarouciaxanthin A required NAD(P)(+) as a cofactor, and the optimal pH for the conversion was 9.5 to 10.0. Fucoxanthinol supplemented to culture medium via HepG2 cells was also converted into amarouciaxanthin A. The 50% inhibitory concentrations on the proliferation of PC-3 human prostate cancer cells were 3.0, 2.0, and 4.6 microM for fucoxanthin, fucoxanthinol, and amarouciaxanthin A, respectively. To our knowledge, this is the first report on the enzymatic dehydrogenation of a 3-hydroxyl end group of xanthophylls in mammals.
机译：岩藻黄质，可食用的褐藻中的主要类胡萝卜素，可能通过凋亡诱导而抑制人前列腺癌细胞的增殖。然而，据推测，日粮岩藻黄质在肠中被吸收之前在胃肠道中被水解为岩藻黄质。在本研究中，我们研究了口服施用的岩藻黄质的进一步生物转化，并评估岩藻黄质代谢产物对PC-3人前列腺癌细胞的细胞毒性。在小鼠中口服岩藻黄质后，在血浆和肝脏中发现了两种代谢物，岩藻黄质和一种未知的代谢物。从岩藻黄酮和小鼠肝脏制剂（10,000g匀浆的上清液）的孵育混合物中分离出未知的代谢物，并通过一系列仪器分析将其鉴定为金刚烷黄嘌呤A [（3S，5R，6'S）-3,5,6'-三羟基-6,7-didehydro-5,6,7'，8'-tetrahydro-beta，eps ilon-carotene-3'，8'-dione]。在肝微粒体中主要显示出岩藻黄质醇向金刚烷黄质A的转化。将岩藻黄质的5,6-环氧-3-羟基-5,6-二氢-β末端基团脱氢/异构化为金刚烷黄质A的6'-羟基-3'-氧-ε末端基团需要NAD（P）（+ ）作为辅助因子，转化的最佳pH为9.5至10.0。通过HepG2细胞补充到培养基中的岩藻黄质也被转化为金刚烷黄质A。对PC-3人前列腺癌细胞增殖的50％抑制浓度分别为：岩藻黄质，岩藻黄质和amarouciaxanthin A 3.0、2.0和4.6 microM。据我们所知，这是关于哺乳动物叶黄素3-羟基端基酶促脱氢的第一个报道。

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