Stahl W, Sies H
Institut für Physiologische Chemie I, Heinrich-Heine-Universität Düsseldorf, Germany.
Int J Vitam Nutr Res. 1998;68(6):354-9.
Induction of gap junctional communication (GJC) is discussed as one possible mechanism underlying the cancer-preventive properties of carotenoids. Structurally different carotenoids have different effects on this GJC pathway. Beta-carotene, echinenone, canthaxanthin, cryptoxanthin and 4-hydroxy-beta-carotene efficiently induce GJC in murine fibroblasts. Decomposition products of canthaxanthin (e.g. 4-oxo-retinoic acid) enhance both GJC and expression of connexin 43 mRNA. Thus, the biological activity of canthaxanthin is due at least in part to formation of active decomposition products such as 4-oxo-retinoic acid. A number of other small molecules such as 1,25-dihydroxycholecalciferol or thyroid hormones serve as nuclear receptor ligands. Cholecalciferol, 3,3',5-triiodo-L-thyronine and L-thyroxine induce GJC to a similar extent as carotenoids or retinoic acid. Interactions between these signalling pathways may be involved in GJC regulation.
间隙连接通讯(GJC)的诱导被认为是类胡萝卜素防癌特性的一种可能机制。结构不同的类胡萝卜素对这条GJC途径有不同影响。β-胡萝卜素、海胆酮、角黄素、隐黄质和4-羟基-β-胡萝卜素能有效诱导小鼠成纤维细胞中的GJC。角黄素的分解产物(如4-氧代视黄酸)可增强GJC和连接蛋白43 mRNA的表达。因此,角黄素的生物活性至少部分归因于活性分解产物如4-氧代视黄酸的形成。许多其他小分子如1,25-二羟基胆钙化醇或甲状腺激素作为核受体配体。胆钙化醇、3,3',5-三碘-L-甲状腺原氨酸和L-甲状腺素诱导GJC的程度与类胡萝卜素或视黄酸相似。这些信号通路之间的相互作用可能参与GJC的调节。