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首頁(yè)> 美國(guó)衛(wèi)生研究院文獻(xiàn)>ISRN Toxicology >Cadmium Transport in a Model of Neonatal Intestinal Cells Correlates to MRP1 and Not DMT1 or FPN1
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Cadmium Transport in a Model of Neonatal Intestinal Cells Correlates to MRP1 and Not DMT1 or FPN1

機(jī)譯：新生兒腸道細(xì)胞模型中的鎘轉(zhuǎn)運(yùn)與MRP1相關(guān)而不與DMT1或FPN1相關(guān)。

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Newborns have a higher gastrointestinal uptake of cadmium than adults. In adults, the iron transporters DMT1 and FPN1 are involved in the intestinal absorption of cadmium, while in neonates, the mechanisms for cadmium absorption are unknown. We have investigated possible cadmium transporters in the neonatal intestine by applying a model of immature human intestinal epithelial Caco-2 cells. To mimic the continuous cadmium exposure via diet in neonates, cells were allowed to differentiate for 7 days in medium containing 1 μM CdCl2. A dramatic upregulation of the MT1 gene expression followed cadmium pretreatment, indicating a high sensitivity of the immature cells to cadmium. Cadmium pretreatment increased the basolateral efflux of 109Cd, without causing any effects on the passive diffusion of mannitol or the transepithelial electrical resistance. The augmented transport of cadmium was correlated to an upregulation of MRP1 gene expression and increased activity of the efflux protein MRP1. No effects were observed on gene expression of the efflux proteins MRP2 and P-gp or the iron transporters DMT1, DMT1-IRE and FPN1. In conclusion, our data indicate that continuous cadmium exposure increases the absorption of the metal in immature intestinal cells and that MRP1 is involved in the intestinal cadmium absorption in newborns.
機(jī)譯：新生兒比成年人有更高的胃腸道對(duì)鎘的吸收。在成年人中，鐵轉(zhuǎn)運(yùn)體DMT1和FPN1與鎘的腸吸收有關(guān)，而在新生兒中，鎘吸收的機(jī)制尚不清楚。我們已經(jīng)通過(guò)應(yīng)用未成熟的人類腸道上皮Caco-2細(xì)胞模型研究了新生兒腸道中可能的鎘轉(zhuǎn)運(yùn)蛋白。為了模擬新生兒飲食中鎘的連續(xù)暴露，允許細(xì)胞在含有1μMCdCl2的培養(yǎng)基中分化7天。鎘預(yù)處理后，MT1基因表達(dá)急劇上調(diào)，這表明未成熟細(xì)胞對(duì)鎘具有很高的敏感性。鎘預(yù)處理增加了 109 Cd的基底外側(cè)流出，而對(duì)甘露醇的被動(dòng)擴(kuò)散或跨上皮電阻沒(méi)有任何影響。鎘的運(yùn)輸增加與MRP1基因表達(dá)的上調(diào)和外排蛋白MRP1的活性增加有關(guān)。沒(méi)有觀察到外排蛋白MRP2和P-gp或鐵轉(zhuǎn)運(yùn)蛋白DMT1，DMT1-IRE和FPN1的基因表達(dá)的影響?？傊覀兊臄?shù)據(jù)表明，持續(xù)的鎘暴露會(huì)增加未成熟腸細(xì)胞中金屬的吸收，并且MRP1參與了新生兒腸道鎘的吸收。

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