Kodavanti P R, Ward T R, McKinney J D, Waller C L, Tilson H A
Cellular and Molecular Toxicology Branch, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA.
Toxicol Appl Pharmacol. 1996 Jun;138(2):251-61. doi: 10.1006/taap.1996.0123.
Our previous reports indicate that ortho-substituted non-coplanar polychlorinated biphenyl (PCB) congeners perturbed neuronal Ca2+-homeostasis in vitro, altered agonist-stimulated inositol phosphate accumulation, and caused protein kinase C (PKC) translocation. The structure-activity relationship (SAR) with 24 PCB congeners was consistent with a chlorination pattern that favored non-coplanarity while those with chlorination that favored coplanarity were less active. To test the hypothesis that coplanarity (or lack thereof) is a significant factor in the activity of PCBs, studies with related classes of chemicals such as the polychlorinated diphenyl ethers (PCDEs), in which coplanarity is more difficult to achieve regardless of degree and pattern of chlorination, were initiated. The selected PCDEs and their analogs are predicted to be active, since they are non-coplanar in nature. The effects of these chemicals were studied using the same measures for which PCBs had differential effects based on structural configuration. These measures include PKC translocation as determined by [3H]-phorbol ester ([3H]PDBu) binding in cerebellar granule cells and 45Ca2+ sequestration as determined by 45Ca2+ uptake by microsomes and mitochondria isolated from adult rat cerebellum. All the PCDE congeners studied, increased [3H]PDBu binding in a concentration-dependent manner. The order of potency was 2,4,4'-trichlorodiphenyl ether > 4,4'-dichlorodiphenyl ether > diphenyl ether, 3,3',4,4'-tetrachlorodiphenyl ether and, 2,2',4,4',5- and 2,3',4,4',5-pentachlorodiphenyl ethers. The structurally related diphenyl ether nitrofen and diphenyl ethanes o,p'-1,1,1-trichloro-2,2-bis[p-chlorophenyl]ethane (DDT) and p,p'-DDT increased [3H]PDBu binding to a similar extent (28-35% stimulation at 100 microM). All PCDE congeners and their analogs inhibited 45Ca2+ sequestration by microsomes and mitochondria. Of all the chemicals, unchlorinated diphenyl ether was the least active. These results are in agreement with previous SAR findings in which non-coplanar PCBs are active and support our hypothesis that the extent of coplanarity determined by a pattern of chlorination on certain aromatic hydrocarbons can weaken their potency in vitro, although the extent of chlorination is also important.
我们之前的报告表明,邻位取代的非共平面多氯联苯(PCB)同系物在体外会扰乱神经元的Ca2+稳态,改变激动剂刺激的肌醇磷酸积累,并导致蛋白激酶C(PKC)易位。与24种PCB同系物的构效关系(SAR)与有利于非共平面性的氯化模式一致,而那些具有有利于共平面性的氯化模式的同系物活性较低。为了验证共平面性(或缺乏共平面性)是多氯联苯活性的一个重要因素这一假设,我们开展了对相关化学类别如多氯二苯醚(PCDE)的研究,在多氯二苯醚中,无论氯化程度和模式如何,都更难实现共平面性。所选的多氯二苯醚及其类似物预计具有活性,因为它们本质上是非共平面的。使用与多氯联苯基于结构构型产生不同影响的相同测量方法来研究这些化学物质的影响。这些测量方法包括通过[3H]-佛波酯([3H]PDBu)结合来测定小脑颗粒细胞中的PKC易位,以及通过从成年大鼠小脑中分离的微粒体和线粒体摄取45Ca2+来测定45Ca2+螯合。所有研究的多氯二苯醚同系物均以浓度依赖性方式增加[3H]PDBu结合。效力顺序为2,4,4'-三氯二苯醚>4,4'-二氯二苯醚>二苯醚、3,3',4,4'-四氯二苯醚以及2,2',4,4',5-和2,3',4,4',5-五氯二苯醚。结构相关的二苯醚除草醚以及二苯乙烷邻,对'-1,1,1-三氯-2,2-双[对氯苯基]乙烷(滴滴涕)和对,对'-滴滴涕在相似程度上增加[3H]PDBu结合(在100 microM时刺激28 - 35%)。所有多氯二苯醚同系物及其类似物均抑制微粒体和线粒体的45Ca2+螯合。在所有化学物质中,未氯化的二苯醚活性最低。这些结果与之前的构效关系研究结果一致,即非共平面的多氯联苯具有活性,并支持我们的假设:由某些芳烃上的氯化模式决定的共平面程度会削弱它们在体外的效力,尽管氯化程度也很重要。