Soil salinization, an overwhelming problem exacerbated by climate change and anthropogenic activities, poses a significant threat to global food security by impairing plant growth, development, and crop productivity. Salinity stress induces osmotic, ionic, and oxidative stresses, disrupting physiological and biochemical processes in plants. Anthocyanins, a class of flavonoids, have emerged as key players in mitigating salt stress through their antioxidant properties, ROS scavenging, and regulation of stress-responsive pathways. During salt stress, ROS act as damaging agents and signaling molecules, upregulating anthocyanin-related genes to mitigate oxidative stress and maintain cellular homeostasis. Anthocyanins mitigate salt stress by regulating osmotic balance, ion homeostasis, and antioxidant defenses. Their biosynthesis is regulated by a network of structural and regulatory genes, including MYB, bHLH, and WD40 transcription factors, influenced by epigenetic modifications and hormonal signaling pathways such as ABA, JA, and SA. Advances in genetic engineering, including CRISPR/Cas9-mediated gene editing, have enabled the development of anthocyanin-rich transgenic plants with enhanced salt tolerance. For instance, transgenic plants overexpressing anthocyanin biosynthesis genes like DFR and ANS have demonstrated enhanced salt tolerance in crops such as tomatoes and rice. However, challenges such as variability in anthocyanin accumulation and stability under environmental stressors remain. This review highlights the translational potential of anthocyanins in crop improvement, emphasizing the need for integrated multi-omics approaches and field trials to validate their efficacy. By elucidating the molecular mechanisms of salt stress and anthocyanin-mediated stress alleviation, this work provides a foundation for developing resilient crops to address the growing challenges of soil salinization.

Chlorothalonil (CTL) is widely used in agricultural production and antifoulant additive globally due to its broad spectrum and non-systemic properties, resulting in its widespread existence in foods, soil and water. Extensive evidence demonstrated that exposure to CTL induced adverse effects on organisms and in particular its reproductive toxicity has been attracted public concern. However, the influences of CTL on oocyte maturation is mysterious so far. In this study, we documented the toxic effects of CTL on oocyte in vitro maturation and the related underlying mechanisms. Exposure to CTL caused continuous activation of spindle assembly checkpoints (SAC) which in turn compromised meiotic maturation in mouse oocyte, featured by the attenuation of polar body extrusion (PBE). Detection of cytoskeletal dynamics demonstrated that CTL exposure weakened the acetylation level of alpha-tubulin and impaired meiotic spindle apparatus, which was responsible for the aberrant state of SAC. Meanwhile, exposure to CTL damaged the function of mitochondria, inducing the decline of ATP content and the elevation of reactive oxygen species (ROS), which thereby induced early apoptosis and DNA damage in mouse oocytes. In addition, exposure to CTL caused the alteration of the level of histone H3 methylation, indicative of the harmful effects of CTL on epigenetic modifications in oocytes. Further, the CTL-induced oxidative stress activated mitogen-activated protein kinase (MAPK) pathway and injured the maturation of oocytes. In summary, exposure to CTL damaged mouse oocyte in vitro maturation via destroying spindle assembly, inducing oxidative stress and triggering MAPK pathway activation.