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甲基汞诱导的星形胶质细胞肿胀与钠/氢反向转运体的激活有关,并且可被氨氯吡咪完全逆转。

Methylmercury-induced astrocytic swelling is associated with activation of the Na+/H+ antiporter, and is fully reversed by amiloride.

作者信息

Aschner M, Vitarella D, Allen J W, Conklin D R, Cowan K S

机构信息

Departments of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC, USA.

出版信息

Brain Res. 1998 Jul 20;799(2):207-14. doi: 10.1016/s0006-8993(98)00399-0.

DOI:10.1016/s0006-8993(98)00399-0
PMID:9675283
Abstract

Astrocytes are a known 'sink' for brain methylmercury (MeHg) deposition. Yet, the significance of the preferential accumulation of MeHg within these cells is imprecisely defined. To determine whether MeHg in isotonic buffer has the potential to interfere with homeostatic functions, we measured its effect on astrocytic volume using an electrical impedance method [E.R. O'Connor, H.K. Kimelberg, C.R. Keese, I. Giaever, Electrical impedance method for measuring volume changes in astrocytes, Am. J. Physiol. 264 (1993) C471-C478.]. In addition, we have characterized the alterations in astrocytic ion permeability associated with exposure to this organometal. The results show that MeHg rapidly induces astrocytic swelling, and that this effect is secondary to increased astrocytic Na+ uptake. Furthermore, the effect of MeHg on astrocytic swelling is completely inhibited by amiloride, but not by SITS (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid), furosemide, or bumetanide. Accordingly, increased cellular permeability to Na+ via the Na+/H+ antiporter is invoked as the primary mechanism of MeHg-induced astrocytic swelling.

摘要

星形胶质细胞是脑内甲基汞(MeHg)沉积的一个已知“库”。然而,MeHg在这些细胞内优先蓄积的意义尚未明确界定。为了确定等渗缓冲液中的MeHg是否有可能干扰稳态功能,我们使用电阻抗法[E.R.奥康纳、H.K.金梅尔伯格、C.R.基斯、I.贾埃弗,《测量星形胶质细胞体积变化的电阻抗法》,《美国生理学杂志》264卷(1993年)C471 - C478页]测量了其对星形胶质细胞体积的影响。此外,我们还描述了与暴露于这种有机金属相关的星形胶质细胞离子通透性的变化。结果表明,MeHg迅速诱导星形胶质细胞肿胀,且这种效应继发于星形胶质细胞Na⁺摄取增加。此外,MeHg对星形胶质细胞肿胀的影响完全被氨氯地平抑制,但不受4 - 乙酰氨基 - 4'-异硫氰酸基芪 - 2,2'-二磺酸(SITS)、呋塞米或布美他尼抑制。因此,通过Na⁺/H⁺反向转运体导致细胞对Na⁺通透性增加被认为是MeHg诱导星形胶质细胞肿胀的主要机制。

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