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Role of Calcium Channels in Heavy Metal Toxicity

機譯：鈣通道在重金屬毒性中的作用

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The role of voltage-dependent Ca channels (VDCC) in the membrane permeation of two toxic metals, lead (Pb) and cadmium (Cd), was studied in mammalian cells. Both metals interact with Ca-binding sites, but, while Cd influx appears to occur mainly through the same pathways as Ca, Pb is also rapidly taken up by different passive transport systems. Furthermore, I compared the effect of Cd in two Chinese hamster ovary (CHO) cell lines, a wild-type and a modified cell line, which were permanently transfected with an L-type VDCC. When cultures were subjected to a brief (30–60 min) exposure to 50–100 μM Cd, apoptotic features, metal accumulation, and death were comparable in both cell lines although, in transfected cells, the effect of Cd treatment was partially prevented by nimodipine (VDCC antagonist) and enhanced by BayK8644 (VDCC agonist). Thus, expression of L-type Ca channels is not sufficient to modify Cd accumulation and sensitivity to a toxicological significant extent and while both Cd and Pb can take advantage of VDCC to permeate the membrane, these transport proteins are not the only, and frequently not the most important, pathways of permeation.
機譯：在哺乳動物細胞中研究了電壓依賴性Ca通道（VDCC）在兩種有毒金屬（鉛（Pb）和鎘（Cd））的膜滲透中的作用。兩種金屬都與Ca結合位點相互作用，但是Cd流入似乎主要通過與Ca相同的途徑發(fā)生，而Pb也會被不同的被動傳輸系統(tǒng)迅速吸收。此外，我比較了鎘對兩種中國倉鼠卵巢（CHO）細胞系（野生型和修飾的細胞系）的作用，這些細胞系均被L型VDCC永久轉染。當將培養(yǎng)物短暫（30-60分鐘）暴露于50-100μMCd時，兩種細胞系的凋亡特征，金屬積累和死亡情況相當，盡管在轉染的細胞中，Cd處理的效果可通過尼莫地平（VDCC拮抗劑），并被BayK8644（VDCC激動劑）增強。因此，L型Ca通道的表達不足以在毒理學上顯著改變Cd的積累和敏感性，盡管Cd和Pb都可以利用VDCC滲透膜，但這些轉運蛋白并不是唯一的，而且經常不是最重要的是滲透途徑。

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