Premature senescence, which share common features with replicative senescence such as morphology, senescence-associated galactosidase (SA-β-gal) activity, cell cycle regulation, and gene expression, can be triggered by the exposure of various xenobiotics including environmental pollutant, peroxides, and anticancer drugs. The exact mechanisms underlying the senescence onset and stabilization are still obscure. In this review, we summarized the possible cellular and molecular mechanisms of xenobiotics-induced premature senescence, including induction of reactive oxygen species (ROS), tumor suppressors, and DNA damage; disequilibrium of calcium homeostasis; activation of transforming growth factor-β (TGF-β); and blockage of aryl hydrocarbon receptor (AHR) pathway. The deeper understanding of the molecular mechanisms underlying xenobiotics-induced senescence may shed light on new therapeutic strategies for age-related pathologies and extend healthy lifespan.

中文翻译：

---

异生素诱导早衰的细胞和分子机制

过早衰老与复制衰老具有共同的特征，例如形态学、衰老相关的半乳糖苷酶 (SA-β-gal) 活性、细胞周期调节和基因表达，可以由暴露于各种异生物质（包括环境污染物、过氧化物、和抗癌药物。衰老开始和稳定的确切机制仍不清楚。在这篇综述中，我们总结了异生素诱导的过早衰老可能的细胞和分子机制，包括活性氧 (ROS)、肿瘤抑制因子和 DNA 损伤的诱导；钙稳态失衡；转化生长因子-β (TGF-β) 的激活；和阻断芳烃受体 (AHR) 通路。