Sorensen E M
College of Pharmacy, Department of Pharmacology/Toxicology, University of Texas, Austin 78712.
Toxicol Lett. 1988 Apr;41(1):39-48. doi: 10.1016/0378-4274(88)90006-9.
Primary cultures of rat hepatocytes were exposed to 3 or 30 microM stable cadmium (Cd) in the presence or absence of 1.8 or 3.6 mM calcium (Ca). The presence of Ca significantly reduced the efflux of lactate dehydrogenase (LDH) from cells regardless of Cd concentration or exposure time. During a 3-h time interval, the influx of Cd into hepatocytes increased from about 5 to 14% of the total extracellular Cd present. The presence of Ca during 30 microM Cd exposures resulted in an 18% reduction (P less than 0.01 or 0.001) in Cd influx during a 3-h exposure. About 11% more Cd was bound to those cells exposed in the absence of Ca following 2-h, but not 0.5-h, exposures. Therefore, binding of Cd to hepatocytes was not related directly to Cd uptake since Cd uptake (but not binding) was elevated at the 0.5-h time interval. Although the presence of Cd did not affect the influx of Ca, the presence of Cd increased the binding of Ca by 557% (P less than 0.001). Interaction between these cations at the same binding and/or entry sites on (or adjacent to) phospholipid head groups could account for the modulatory effect of Ca on Cd-challenged hepatocytes.
将大鼠肝细胞原代培养物置于含有或不含1.8或3.6 mM钙（Ca）的环境中，使其暴露于3或30 microM稳定镉（Cd）中。无论Cd浓度或暴露时间如何，Ca的存在均显著降低了乳酸脱氢酶（LDH）从细胞中的流出。在3小时的时间间隔内，Cd进入肝细胞的内流从细胞外总Cd的约5%增加到14%。在30 microM Cd暴露期间，Ca的存在导致3小时暴露期间Cd内流减少了18%（P小于0.01或0.001）。在2小时而非0.5小时暴露后，与在无Ca环境中暴露的细胞相比，有Ca环境中暴露的细胞结合的Cd多约11%。因此，Cd与肝细胞的结合与Cd摄取没有直接关系，因为在0.5小时时间间隔时Cd摄取（而非结合）增加了。尽管Cd的存在不影响Ca的内流，但Cd的存在使Ca的结合增加了557%（P小于0.001）。这些阳离子在磷脂头部基团上（或其附近）相同的结合和/或进入位点的相互作用可能解释了Ca对受Cd攻击的肝细胞的调节作用。
