This text discusses the toxic effects of Rare Earth Elements (REEs) on various cellular processes. Here is a summary of the main points:
Cellular toxicity
- REEs can induce apoptosis, cell death, and mitochondrial dysfunction in various cell types.
- The elements can interact with DNA, RNA, and proteins, leading to damage and disruption of cellular functions.
Apoptosis mechanisms
- Mitochondrial-mediated pathways are involved in CECl3-induced apoptosis in mouse hippocampus.
- Gd exposure impairs the oxidative state, leads to mitochondrial apoptosis, and induces autophagy.
Autophagy
- Autophagy is activated by REEs, which can induce this process as a survival mechanism.
- The elements can modulate autophagy through various signaling pathways, such as ROS-AMPK-mTOR.
DNA damage
- Lanides (Ln) are effective catalysts for hydrolytic cleavage of phosphate ester bonds in DNA.
- Exposure to La metal-organic frameworks alters DNA methylation and demethylation enzymes.
- Single-evaluation analysis shows that Y, La, and Tb can increase mitochondrial DNA copy number.
Protein interactions
- REEs interact with proteins, influencing their stability and function.
- Satapathy et al. (2019) demonstrated that low concentrations of LREEs stabilize G-quadruplex structures in human telomere sequences.
Inflammation and oxidative stress
- CeO2 stimulates mast cell activation, leading to inflammation and oxidative stress.
- REEs can induce pulmonary inflammation through long-term exposure.
Epigenetic modifications
- LaCl3 exposure alters DNA methylation and demethylation enzymes, potentially influencing epigenetic regulation.
Biological significance
- Understanding the mechanisms of REE toxicity is crucial for developing strategies to mitigate its environmental and health impacts.
- The findings suggest that REEs can modulate various cellular processes, including apoptosis, autophagy, and epigenetic regulation.
This summary highlights the main points discussed in the text regarding the toxic effects of REEs on various cellular processes.