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Mitophagy is a selective cellular process critical for the removal of damaged mitochondria. It is essential in regulating mitochondrial number, ensuring mitochondrial functionality, and maintaining cellular equilibrium, ultimately influencing cell destiny. Numerous pathologies, such as neurodegenerative diseases, cardiovascular disorders, cancers, and various other conditions, are associated with mitochondrial dysfunctions. Thus, a detailed exploration of the regulatory mechanisms of mitophagy is pivotal for enhancing our understanding and for the discovery of novel preventive and therapeutic options for these diseases. Nanomaterials have become integral in biomedicine and various other sectors, offering advanced solutions for medical uses including biological imaging, drug delivery, and disease diagnostics and therapy. Mitophagy is vital in managing the cellular effects elicited by nanomaterials. This review provides a comprehensive analysis of the molecular mechanisms underpinning mitophagy, underscoring its significant influence on the biological responses of cells to nanomaterials. Nanoparticles can initiate mitophagy via various pathways, among which the PINK1‐Parkin pathway is critical for cellular defense against nanomaterial‐induced damage by promoting mitophagy. The role of mitophagy in biological effects was induced by nanomaterials, which are associated with alterations in Ca2+ levels, the production of reactive oxygen species, endoplasmic reticulum stress, and lysosomal damage. Mitophagy, a form of selective autophagy that maintains mitochondrial homeostasis and protects cells, is closely associated with the pathogenesis of numerous diseases. Given the widespread use and increasing exposure of nanomaterials to the human body, it is crucial to comprehend their biological effects. Therefore, we conducted a comprehensive review of the regulatory mechanisms of mitophagy and its impact on cellular responses to nanomaterials, in order to provide intervention strategies for diagnosing and treating mitochondria‐related disorders. [ABSTRACT FROM AUTHOR]

Silver nanoparticles (AgNPs) are widely used in many commercial and medical products. Serious concerns are paid on their adverse potentials to the environment and human health. In this study, toxic effects and oxidative stress induced by AgNPs with different sizes and coatings (20 nm AgNPs, 20 nm polyvinylpyrrolidone (PVP) -AgNPs and 50 nm AgNPs) in Caenorhabditis elegans (C. elegans) were investigated. The toxic effects including the shortened lifespan and decreased frequency of head thrashes and body bends of C. elegans were induced in a dose-dependent manner by AgNPs. The reactive oxygen species (ROS) production and the oxidative stress-related indicators including malondialdehyde (MDA) and glutathione (GSH) in nematodes were changed after exposure to three kinds of AgNPs. These effects were the most obvious in a 20 nm PVP-AgNPs exposure group. AgNPs could also induce the expression of genes related to oxidative stress in nematodes. In addition, the up-regulation of mtl-1 and mtl-2 in nematodes might reduce the oxidative damage caused by AgNPs, by using transgenic strains CF2222 and CL2120 nematodes. Metallothionein (MT), an antioxidant, could relieve the oxidative damage caused by AgNPs. These results suggested that 20 nm PVP-AgNPs with a smaller particle size and better dispersion have stronger toxic effects and the oxidative damage to nematodes. Mtl-1 and mtl-2 might be involved in alleviating the oxidative damage caused by AgNPs. Our findings provide clues for the safety evaluation and mechanism information of metal nanoparticles. Graphical Abstract [ABSTRACT FROM AUTHOR]

Recombinant human metallothionein III (rh‐MT‐III) is a genetically engineered product produced by Escherichia coli fermentation technology. Its molecules contain abundant reducing sulfhydryl groups, which possess the ability to bind heavy metal ions. The present study was to evaluate the binding effects of rh‐MT‐III against copper and cadmium in vitro and to investigate the antioxidant activity of rh‐MT‐III using Caenorhabditis elegans in vivo. For in vitro experiments, the binding rates of copper and cadmium were 91.4% and 97.3% for rh‐MT‐III at a dosage of 200 μg/mL at 10 h, respectively. For in vivo assays, the oxidative stress induced by copper (CuSO4, 10 μg/mL) and cadmium (CdCl2, 10 μg/mL) was significantly reduced after 72 h of exposure to different doses of rh‐MT‐III (5–500 μg/mL), indicated by restoring locomotion behavior and growth, and reducing malondialdehyde and reactive oxygen species levels in C. elegans. Moreover, rh‐MT‐III decreased the deposition of lipofuscin and fat content, which could delay the progression of aging. In addition, rh‐MT‐III (500 μg/mL) promoted the up‐regulation of Mtl‐1 and Mtl‐2 gene expression in C. elegans, which could enhance the resistance to oxidative stress by increasing the enzymatic activity of antioxidant defense system and scavenging free radicals. The results indicated that supplemental rh‐MT‐III could effectively protect C. elegans from heavy metal stress, providing an experimental basis for the future application and development of rh‐MT‐III. Rh‐MT‐III is a genetically engineered product fermented by Escherichia coli. This study evaluated the binding effects of rh‐MT‐III against copper and cadmium and the antioxidant activity of rh‐MT‐III in Caenorhabditis elegans. The data showed that rh‐MT‐III had high affinity for copper and cadmium and enhanced the stress resistance of nematodes by increasing the enzymatic activity of antioxidant defense system and scavenging free radicals. The results indicated that rh‐MT‐III could be used as an antioxidant to protect organisms from oxidative damage. [ABSTRACT FROM AUTHOR]