Abstract: Ce⁴⁺ at 1 mmol·L^-1 induces apoptosis of suspension cultures of Taxus cuspidata cells;however，the underlying signal regulation of superoxide anions (O^-₂·) and extracellularly-responsive kinase (ERK)-like MAP kinase is unknown. It was shown that an approximately 46×103 ERK-like MAP kinase appeared to be activated in 5 min，and a significant activity increase was detected in 60 min，reaching 2.1-fold higher than that of the control cells. ERK-like activity remained at this high level until 120 min，and started to diminish within 240 min. By the 240th minute the activity reached about 43% of control value，and in 48 h declined to 25%. Ce⁴⁺-induced O^-₂·transient burst，and the first peak appeared in about 3.7—4 h，the second peak appeared in about 7 h.The burst of O^-₂· was effectively suppressed by the application of diphenyl iodonium (DPI) at 5 μmol·L^-1 or 10 μmol·L^-1.The inhibition of O^-₂· production increased and prolonged ERK-like activity. ERK-like activity increased by about 7.3 and 18.8-fold of control value in 60 min，and reached about 9.6 and 10.5-fold in 240 min. These results suggested that it was possible that ERK-like activation and O^-₂· burst were separate signal events in early times. O^-₂· burst formed signal negative regulation to ERK-like activity. Down-regulation of ERK-like partly participated in mediating apoptotic signal transduction.

摘要： 对1 mmol·L^-1Ce⁴⁺诱导东北红豆杉细胞凋亡中ERK-like和O^-₂·的变化规律及其信号调控进行了分析和研究.结果表明，一相对分子质量约为46×10³的ERK-like激酶在诱导5 min时被快速激活，60 min时达到对照水平的2.1倍，并在120 min内持续激活，诱导240 min后ERK-like下调到对照水平的43%，到48 h下调到对照的25%.Ce⁴⁺诱导O^-₂·迅速产生，并有两次迸发峰分别出现在3.7～4 h和7 h.在Ce⁴⁺诱导前2 h分别加入5 μmol·L^-1和10 μmol·L^-1DPI有效抑制了O^-₂·迸发， 并且显著提高和延长了ERK-like磷酸化水平， 诱导60 min时ERK-like达到对照水平的7.3和18.8倍， 240 min时达到对照的9.6和10.5倍.这些结果揭示ERK-like的激活和O^-₂·迸发在诱导早期应是相互独立的信号事件，诱导约4 h后O^-₂·大量迸发对ERK-like的激活有明显信号负调控作用，并通过ERK-like的下调介导了凋亡信号传递.