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首頁> 美國衛(wèi)生研究院文獻>International Journal of Molecular Sciences >Myelin Disturbances Produced by Sub-Toxic Concentration of Heavy Metals: The Role of Oligodendrocyte Dysfunction
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Myelin Disturbances Produced by Sub-Toxic Concentration of Heavy Metals: The Role of Oligodendrocyte Dysfunction

機譯：重金屬的亞毒性濃度產生的髓磷脂紊亂：少突膠質細胞功能障礙的作用。

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Evidence has been accumulated demonstrating that heavy metals may accumulate in various organs, leading to tissue damage and toxic effects in mammals. In particular, the Central Nervous System (CNS) seems to be particularly vulnerable to cumulative concentrations of heavy metals, though the pathophysiological mechanisms is still to be clarified. In particular, the potential role of oligodendrocyte dysfunction and myelin production after exposure to subtoxic concentration I confirmed. It is ok of heavy metals is to be better assessed. Here we investigated on the effect of sub-toxic concentration of several essential (Cu2 +, Cr3 +, Ni2 +, Co2+) and non-essential (Pb2 +, Cd2+, Al3+) heavy metals on human oligodendrocyte MO3.13 and human neuronal SHSY5Y cell lines (grown individually or in co-culture). MO3.13 cells are an immortal human–human hybrid cell line with the phenotypic characteristics of primary oligodendrocytes but following the differentiation assume the morphological and biochemical features of mature oligodendrocytes. For this reason, we decided to use differentiated MO3.13 cell line. In particular, exposure of both cell lines to heavy metals produced a reduced cell viability of co-cultured cell lines compared to cells grown separately. This effect was more pronounced in neurons that were more sensitive to metals than oligodendrocytes when the cells were grown in co-culture. On the other hand, a significant reduction of lipid component in cells occurred after their exposure to heavy metals, an effect accompanied by substantial reduction of the main protein that makes up myelin (MBP) in co-cultured cells. Finally, the effect of heavy metals in oligodendrocytes were associated to imbalanced intracellular calcium ion concentration as measured through the fluorescent Rhod-2 probe, thus confirming that heavy metals, even used at subtoxic concentrations, lead to dysfunctional oligodendrocytes. In conclusion, our data show, for the first time, that sub-toxic concentrations of several heavy metals lead to dysfunctional oligodendrocytes, an effect highlighted when these cells are co-cultured with neurons. The pathophysiological mechanism(s) underlying this effect is to be better clarified. However, imbalanced intracellular calcium ion regulation, altered lipid formation and, finally, imbalanced myelin formation seem to play a major role in early stages of heavy metal-related oligodendrocyte dysfunction.
機譯：已經積累了證據，表明重金屬可能在各種器官中積累，從而導致哺乳動物的組織損傷和毒性作用。特別是，中樞神經系統(tǒng)（CNS）似乎特別容易受到重金屬累積濃度的影響，盡管其病理生理機制仍有待闡明。特別是，我證實了暴露于亞毒性濃度后少突膠質細胞功能障礙和髓磷脂產生的潛在作用?？梢詫χ亟饘龠M行更好的評估。在這里，我們研究了幾種必需的（Cu 2 + ，Cr 3 + ，Ni 2 + ，Co < sup> 2 + ）和非必需（Pb 2 + ，Cd 2 + ，Al 3 + ）重金屬人少突膠質細胞MO3.13和人神經元SHSY5Y細胞系（單獨或共培養(yǎng)）。 MO3.13細胞是具有永久性少突膠質細胞表型特征的永生人-人雜交細胞系，但隨著分化，它們呈現(xiàn)出成熟的少突膠質細胞的形態(tài)和生化特征。因此，我們決定使用分化的MO3.13細胞系。特別地，與單獨生長的細胞相比，兩種細胞系都暴露于重金屬導致共培養(yǎng)的細胞系細胞活力降低。當細胞在共培養(yǎng)物中生長時，在對金屬比少突膠質細胞更敏感的神經元中，這種作用更為明顯。另一方面，暴露于重金屬后，細胞中的脂質成分顯著減少，這種作用伴隨著共同培養(yǎng)的細胞中構成髓磷脂（MBP）的主要蛋白質的大量減少。最后，通過熒光Rhod-2探針測量，重金屬在少突膠質細胞中的作用與細胞內鈣離子濃度失衡有關，從而證實即使在亞毒性濃度下使用的重金屬也會導致功能不全的少突膠質細胞。總而言之，我們的數據首次顯示了幾種重金屬的亞毒性濃度會導致少突膠質細胞功能失調，當這些細胞與神經元共培養(yǎng)時，這種作用就更加突出。更好地闡明了這種作用的病理生理機制。但是，細胞內鈣離子調節(jié)失衡，脂質形成改變以及髓磷脂形成失衡似乎在重金屬相關少突膠質細胞功能障礙的早期階段起著重要作用。

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