Modulation of levels of free calcium within synaptosomes by organochlorine insecticides.
Modulation of levels of free calcium within synaptosomes by organochlorine insecticides.
复制标题
有机氯杀虫剂调节突触体内游离钙的水平。
DOI：
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发表时间：
1987
影响因子：
3.5
通讯作者：
S. Bondy
中科院分区：
文献类型：
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作者：
H. Komulainen;S. Bondy
有机氯杀虫剂十氯酮、灭蚁灵、1-(2-氯苯基)-1-(4-氯苯基)-2,2,2-三氯乙烷和1,1-双(4-氯苯基)-2,2,2-三氯乙烷对体外游离突触体内Ca2+ [( Ca++]i)、突触体45Ca摄取以及突触体血浆和线粒体膜电位的影响被研究了。十氯酮 (10-50 µM) 以剂量和时间依赖性方式将 [Ca++]i 从静息水平 370 nM 增加至 1.5 µM 以上。这是在存在 1 mM 突触体外 Ca++ 的情况下发生的，但不是在名义上不含 Ca++ 的培养基中发生的。 Verapamil 是一种电压敏感的 Ca++ 通道阻滞剂，可抑制十氯酮引起的 [Ca++]i 初始增加 40%。十氯酮还能升高突触体中的 [Ca++]i，其中线粒体 Ca++ 摄取已被缬氨霉素消除。十氯酮部分去极化突触体质膜，并在较小程度上去极化突触体内线粒体的电位。然而，十氯酮似乎能抑制突触体 K+ 刺激和未刺激的 45Ca++ 摄取 20% 至 30%。由于十氯酮还刺激预载突触体释放 45Ca++ 和荧光染料 fura-2，因此明显的摄取抑制可能是由于十氯酮裂解了一些突触体。当培养中的组织总量增加时，十氯酮对[Ca++]i 的影响降低。在相同浓度范围内，灭蚁灵仅略微升高[Ca++]i。结果表明，十氯酮主要通过增加突触外 Ca++ 的流入来增加游离突触体内 Ca++。主要机制似乎是 Ca++ 通过质膜的非特异性泄漏，但由于十氯酮诱导的膜去极化，一些 Ca++ 可能会通过电压敏感的 Ca++ 通道。
Effects of the organochlorine insecticides chlordecone, mirex, 1-(2-chlorophenyl)-1-(4-chlorophenyl)-2,2,2-trichloroethane and 1,1-bis(4-chlorophenyl)-2,2,2-trichloroethane on free intrasynaptosomal Ca2+ [( Ca++]i), synaptosomal 45Ca uptake and synaptosomal plasma and mitochondrial membrane potentials in vitro were studied. Chlordecone (10-50 microM) increased [Ca++]i from the resting level of 370 nM in a dose- and time-dependent manner to above 1.5 microM. This took place in the presence of 1 mM extrasynaptosomal Ca++ but not in nominally Ca++-free medium. Verapamil, a voltage sensitive Ca++ channel blocker, inhibited the initial increase of [Ca++]i caused by chlordecone, by 40%. Chlordecone also elevated [Ca++]i in synaptosomes in which mitochondrial Ca++ uptake had been abolished by valinomycin. Chlordecone depolarized partially the synaptosomal plasma membrane and, to a lesser extent, the potential of mitochondria within synaptosomes. However, chlordecone appeared to inhibit synaptosomal K+-stimulated and unstimulated 45Ca++ uptake by 20 to 30%. Inasmuch as chlordecone also stimulated release of 45Ca++ and the fluorescent dye fura-2 from preloaded synaptosomes, the apparent inhibition of uptake might be due to lysis of some synaptosomes by chlordecone. The effect of chlordecone on [Ca++]i decreased when the total amount of tissue in incubations was increased. [Ca++]i was only elevated marginally by mirex at the same concentration range. The results suggest that chlordecone increases free intrasynaptosomal Ca++ mainly by increasing influx of extrasynaptosomal Ca++. The principal mechanism appears to be a nonspecific leakage of Ca++ through the plasma membrane but some Ca++ may pass through voltage-sensitive Ca++ channels due to chlordecone-induced membrane depolarization.
十氯酮神经毒性的神经化学相关性。
DOI：
10.1080/15287398109530107
发表时间：
1981
期刊：
Journal of toxicology and environmental health
影响因子：
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作者：
End,DW;Carchman,RA;Dewey,WL
通讯作者：
Dewey,WL