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失调的差距交界细胞间通信(GJIC)与不同的疾病,包括癌症;然而,分子机制调节GJIC并不完全理解。有丝分裂原激活蛋白激酶(MAPK)端依赖GJIC-dysregulation机制完善,然而最近的发现涉及phosphatidylcholine-specific磷脂酶C (PC-PLC) GJIC的监管。不知道是如何流行这两个信号机制在毒物/ toxin-induced GJIC的失调,和毒物/毒素通过信号机制或工作,或通过其他信号机制。也许不同的化学毒物被用来评估是否通过MEK GJIC或PC-PLC或MEK和PC-PLC,或通过其他信号通路,使用多功能鼠肝上皮oval-cell线,WB-F344。表皮生长因子、12-O-tetradecanoylphorbol-13-acetate凝血酶受体激活peptide-6和林丹监管GJIC PC-PLC通过MEK1/2-dependent机制,是独立的;而多环芳烃,滴滴涕,PCB 153 dicumylperoxide perfluorodecanoic酸抑制GJIC通过PC-PLC Mek独立的。失调并GJIC的酸和R59022需要MEK1/2 PC-PLC;花生四烯酸,benzoylperoxide 18β-glycyrrhetinic酸,perfluorooctane磺酸、1-monolaurin、五氯苯酚、无论是MEK1/2还是PC-PLC所需草不绿。白藜芦醇阻止失调GJIC的毒物,通过MEK1/2或PC-PLC行事。 Except for alachlor, resveratrol did not prevent dysregulation of GJIC by toxicants that worked through PC-PLC-independent and MEK1/2-independent pathways, which indicated at least two other, yet unidentified, pathways that are involved in the regulation of GJIC. In conclusion: the dysregulation of GJIC is a contributing factor to the cancer process; however the underlying mechanisms by which gap junction channels are closed by toxicants vary. Thus, accurate assessments of risk posed by toxic agents, and the role of dietary phytochemicals play in preventing or reversing the effects of these agents must take into account the specific mechanisms involved in the cancer process.