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Cell organelles as targets of mammalian cadmium toxicity
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This review examines how cadmium — an industrial heavy metal increasingly present in soil, water, and food — damages cell organelles including mitochondria, lysosomes, the nucleus, and the endoplasmic reticulum, with connections to microplastics as a delivery vector for cadmium exposure.
Ever increasing environmental presence of cadmium as a consequence of industrial activities is considered a health hazard and is closely linked to deteriorating global health status. General animal and human cadmium exposure ranges from ingestion of foodstuffs sourced from heavily polluted hotspots and cigarette smoke to widespread contamination of air and water, including cadmium-containing microplastics found in household water. Cadmium is promiscuous in its effects and exerts numerous cellular perturbations based on direct interactions with macromolecules and its capacity to mimic or displace essential physiological ions, such as iron and zinc. Cell organelles use lipid membranes to form complex tightly-regulated, compartmentalized networks with specialized functions, which are fundamental to life. Interorganellar communication is crucial for orchestrating correct cell behavior, such as adaptive stress responses, and can be mediated by the release of signaling molecules, exchange of organelle contents, mechanical force generated through organelle shape changes or direct membrane contact sites. In this review, cadmium effects on organellar structure and function will be critically discussed with particular consideration to disruption of organelle physiology in vertebrates.
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Polystyrene exacerbates cadmium‐induced mitochondrial damage to lung by blocking autophagy in mice
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Researchers found that polystyrene microplastics exacerbated cadmium-induced mitochondrial damage in mouse lungs by blocking autophagy, revealing a synergistic toxicity mechanism when these two common environmental contaminants co-occur.
Micro- and nanoplastic-induced mitochondrial dysfunction and organelle miscommunication: A toxicological perspective
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This review examined how micro- and nanoplastics disrupt mitochondrial function and inter-organelle communication in cells. The evidence indicates that these particles cause oxidative stress, calcium dysregulation, impaired energy production, and activation of stress responses including autophagy and cell death, with cascading effects on lysosomes, the endoplasmic reticulum, and nuclear function.
Mitochondria as a target of micro- and nanoplastic toxicity
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This review examines how micro- and nanoplastics damage mitochondria, the energy-producing structures inside cells. Studies show that plastic particles can disrupt energy production, cause harmful oxidative stress, and interfere with the cell's ability to repair or recycle damaged mitochondria. Since mitochondrial damage is linked to many chronic diseases including heart disease, neurodegeneration, and diabetes, this helps explain why microplastic exposure may have widespread health effects.
Redefining the synergistic toxicity of nano-plastics and cadmium in earthworm coelomocytes: the mechanism of α-amylase molecular docking orientation and energy crisis
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Researchers exposed earthworm immune cells (coelomocytes) to polystyrene nanoplastics combined with the heavy metal cadmium, finding that nanoplastics act as carriers that amplify cadmium uptake and worsen oxidative stress, energy metabolism disruption, and enzyme damage beyond what cadmium causes alone.
Mitochondria as a target of micro- and nanoplastic toxicity
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This review examines how micro- and nanoplastics damage mitochondria, the energy-producing structures inside our cells. Research shows these tiny plastic particles can cross biological barriers, enter cells, and disrupt mitochondrial function by triggering oxidative stress and altering energy production. Since mitochondrial damage is linked to diseases like cancer, diabetes, and neurodegeneration, this represents a key concern for human health.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.