汞盐诱导烟草悬浮细胞产生细胞编程死亡

 【目的】阐明氯化汞处理烟草悬浮细胞产生的细胞死亡具有细胞编程死亡（programmed cell death，PCD）的特征和分子机制。【方法】采用形态和生物化学方法观察氯化汞处理细胞后的变化，并采用药理学方法，通过添加抑制剂和抗氧化剂阐明氯化汞引发的信号转导途径。【结果】氯化汞诱导产生的细胞死亡具有PCD特征，包括染色质浓缩、细胞核的TUNEL检测呈阳性和DNA ladder的形成。氯化汞诱导烟草悬浮细胞过氧化氢积累，过氧化氢酶和抗坏血酸等抗氧化剂能降低细胞死亡率。蛋白激酶抑制剂、磷脂酶C和磷脂酶D的抑制剂能显著地降低氯化汞引起的细胞死亡和过氧化氢积累。【结论】氯化汞引起的细胞死亡是一种PCD，蛋白激酶和磷脂信号介导的过氧化氢积累参与细胞死亡过程。

HgCl2-Induced Programmed Cell Death in Tobacco Cells

【Objective】 The objective of this study is to investigate the characteristics of cell death and molecular mechanisms induced by HgCl2. 【Method】 HgCl2-induced cell death was studied in suspension-cultured tobacco cells via neutral red staining, a set of cellular morphological and biochemical characteristics was elucidated in the occurrence of cell death, and pharmacological method was used to explore the mechanisms activated by HgCl2. 【Result】 Within 24 and 48 h, HgCl2 treatment induced cell death in a concentration-dependent manner. Tobacco cells treated with HgCl2 showed typical features of PCD such as chromatin condensation, TUNEL-positive nuclei and DNA ladder formation. HgCl2-induced cell death was accompanied by an increasing production of H2O2. Consistently, the addition of the antioxidants greatly reduced cell death. Pretreatment with protein kinase inhibitor staurosporin, phospholipase C (PLC) inhibitors U73122 and neomycin, and phospholipase D (PLD) inhibitor 1-butanol significantly diminished HgCl2-induced cell death and H2O2 accumulation. 【Conclusion】 HgCl2 induces PCD exhibiting apoptotic-like features. The cell death process requires increased H2O2 production regulated by activation of protein phosphorylation and phospholipid signaling pathways.