As the global population continues to grow, achieving ecological sustainability and ensuring food production have become urgent challenges. Among various environmental stresses, heavy metals, particularly cadmium (Cd), pose a significant threat to plant growth and development. Breeding cadmium-resistant crop varieties that minimize Cd accumulation is therefore crucial for promoting sustainable agriculture. In response to Cd stress, plants undergo a series of regulatory mechanisms, including DNA methylation, chromatin remodeling, and histone acetylation, to mitigate cellular damage. Understanding the epigenetic responses of plants to cadmium stress is a key research area that holds substantial significance for both agriculture and environmental biology. This article reviews the current research on plant responses to cadmium stress and the underlying mechanisms of their epigenetic responses, aiming to provide theoretical insights for analyzing the epigenetic mechanisms of heavy metal stress in major crops. We can leverage genomics, single-cell sequencing, stereo-seq, and other advanced technologies in conjunction with epigenomics, plant genetics and molecular biology techniques to conduct comprehensive and in-depth studies on the epigenetic changes that occur in plants following Cd exposure. Systematically elucidating the molecular mechanisms by which plants perceive and respond to Cd stress will aid in the development of more effective bioremediation strategies for heavy metal-contaminated soils and facilitate.

This study explored morphological, physiological, molecular, and epigenetic responses of tomatoes (Solanum lycopersicum) to soil contamination with polyethylene nanoplastics (PENP; 0.01, 0.1, and 1 gkg-1 soil). The PENP pollution led to severe changes in plant morphogenesis. The PENP treatments were associated with decreased plant biomass, reduced internode length, delayed flowering, and prolonged fruit ripening. Abnormal inflorescences, flowers, and fruits observed in the PENP-exposed seedlings support genetic changes and meristem dysfunction. Exposure of seedlings to PENP increased H2O2 accumulation and damaged membranes, implying oxidative stress. The PENP treatments induced activities of catalase (EC1.11.1.6), peroxidase (EC1.11.1.7), and phenylalanine ammonia-lyase (EC4.3.1.24) enzymes. Soil contamination with PENP also decreased the net photosynthesis, maximum photosystem efficiency, stomatal conductance, and transpiration rate. The nanopollutant upregulated the expression of the histone deacetylase (HDA3) gene and R2R3MYB transcription factor. However, the AP2a gene was down-regulated in response to the PENP treatment. Besides, EPNP epigenetically contributed to changes in DNA methylation. The concentrations of proline, soluble phenols, and flavonoids also displayed an upward trend in response to the applied PENP treatments. The long-term exposure of seedlings to PENP influenced fruit biomass, firmness, ascorbate, lycopene, and flavonoid content. These findings raise concerns about the hazardous aspects of PENP to agricultural ecosystems and food security.

Genotoxic agents are substances that can induce DNA damage; this damage can be caused by chemical, biological, and physical agents. The dose, time and route of exposure, and the genetic constitution of the individual influence the capacity of these agents to induce damage and may also be related to lifestyle habits and place of residency. Directly associated with genotoxicity is epigenetics, which is the study of hereditary changes in the function of hereditary genes not attributed to alterations in the DNA sequence. These processes regulate the expression of genes through the modulation of chromatin structure. The interaction of genetic and non-genetic factors in the control of hereditary patterns of this expression may cause diseases or disorders such as cancer, infertility, inflammatory processes, degenerative diseases, and endocrine disruption that could be transmitted to the offspring. Several epidemiological studies have shown that changes in lifestyle and eating habits could prevent or reduce cancer incidence; particularly by increasing the level of antioxidants and reducing the formation of free radicals with intracellular effects. At the Biotechnology Research Center of the Technological Institute of Costa Rica, various genotoxic agents to which the population in Costa Rica is exposed are investigated, including bacteria such as Helicobacter pylori, micro plastics in marine species for human consumption, and heavy metals in drinking water and in soils. These investigations are relevant to determine the presence of these genotoxic agents in the country, to evaluate the risk of exposure of the population, and thus generate strategies for prevention and mitigation of the damage.

Atrazine (ATR) is a widely used agricultural herbicide, and its accumulation in soil and water can cause various environmental health problems. ATR has neurotoxic effects on dopaminergic neurons, which can lead to a Parkinson's disease (PD)-like syndrome. Epigenetics regulates gene expression dynamically through DNA methylation, histone post-translational modification, microRNA (miRNA) interaction, and RNA methylation. MicroRNA (miRNA), representing one of the primary epigenetic mechanisms responsible for regulating gene expression, plays a crucial role in maintaining normal cellular function, while dysregulation of miRNA expression has been observed in PD. This study aims to investigate the regulatory mechanisms of miRNA in ATR exposure. The results show that ATR-exposure significantly upregulates the expression level of miR-217-5p. Both miR-217-5p overexpression and ATR exposure is able to trigger the autophagy process and apoptosis. Conversely, inhibiting the expression of miR-217-5p can reverse the levels of ATR-induced autophagy and apoptosis. Moreover, ATR causes damage to dopaminergic neurons, as indicated by the altered expression of tyrosine hydroxylase and alpha-synuclein. Taken together, these results suggest that ATR-induced autophagy can accelerate the progression of neurodegenerative diseases and that miR-217-5p is probably an important target involved in ATR-induced dopaminergic damage, shedding important light on the development of a novel strategy for treating neurodegenerative diseases.