In this mini review we summarize recent studies from our laboratory, which show the involvement of 4-hydroxynonenal (4-HNE) in cell cycle signaling. We demonstrate 4-HNE induced apoptosis in various cell lines is accompanied with c-Jun-N-terminal kinase and caspase-3 activation. Cells exposed to mild, transient, heat or oxidative stress acquire capacity to exclude intracellular 4-HNE at a faster rate by inducing hGST5.8 which conjugate 4-HNE to GSH, and RLIP76 which mediates the ATP-dependent transport of the GSH-conjugate of 4-HNE. The cells preconditioned with mild transient stress acquire resistance to H(2)O(2) and 4-HNE induced apoptosis by excluding intracellular 4-HNE at an accelerated pace. Furthermore, a decrease in intracellular concentration of 4-HNE achieved by transfecting cells with mGSTA4-4 or hGSTA4-4 results in a faster growth rate. These studies strongly suggest a role of 4-HNE in stress mediated signaling.

中文翻译：

---

4-羟基壬烯醛在应激介导的细胞凋亡信号传导中的作用。

在本微型综述中，我们总结了来自实验室的最新研究，这些研究表明4-羟基壬烯醛（4-HNE）参与细胞周期信号传导。我们证明4-HNE诱导的各种细胞系中的凋亡伴随着c-Jun-N-末端激酶和caspase-3激活。暴露于轻度，短暂，热或氧化应激的细胞通过诱导将4-HNE与GSH结合的hGST5.8和介导GSH-结合物的ATP依赖性转运的RLIP76，从而具有更快地排除细胞内4-HNE的能力。 4-HNE。通过轻度瞬态应力进行预处理的细胞通过快速排除细胞内4-HNE，获得了对H（2）O（2）和4-HNE诱导的凋亡的抵抗力。此外，通过用mGSTA4-4或hGSTA4-4转染细胞实现的4-HNE细胞内浓度的降低导致更快的生长速率。