Journal of Hazardous Materials, Journal Year: 2024, Volume and Issue: 484, P. 136691 - 136691
Published: Nov. 30, 2024
Language: Английский
Journal of Hazardous Materials, Journal Year: 2024, Volume and Issue: 484, P. 136691 - 136691
Published: Nov. 30, 2024
Language: Английский
The Science of The Total Environment, Journal Year: 2025, Volume and Issue: 963, P. 178534 - 178534
Published: Jan. 17, 2025
Language: Английский
Citations
0Journal of Hazardous Materials, Journal Year: 2025, Volume and Issue: unknown, P. 138210 - 138210
Published: April 1, 2025
Language: Английский
Citations
0Journal of Toxicology and Environmental Health Part B, Journal Year: 2025, Volume and Issue: unknown, P. 1 - 4
Published: April 19, 2025
Language: Английский
Citations
0Environment International, Journal Year: 2024, Volume and Issue: 195, P. 109193 - 109193
Published: Dec. 13, 2024
Fine particulate matter (PM2.5) is increasingly recognized for its detrimental effects on human health, with substantial evidence linking exposure to various forms of cell death and dysfunction across multiple organ systems. This review examines key mechanisms triggered by PM2.5, including PANoptosis, necroptosis, autophagy, ferroptosis, while other such as oncosis, paraptosis, cuprotosis remain unreported in relation PM2.5 exposure. Mitochondria, endoplasmic reticulum, lysosomes emerge pivotal organelles the disruption cellular homeostasis, mitochondrial particularly implicated metabolic dysregulation activation pro-apoptotic pathways. Although primarily affects nucleus, cytoskeleton, mitochondria, lysosomes, like ribosomes, Golgi apparatus, peroxisomes have received limited attention. Interactions between these organelles, reticulum-associated membranes, lysosome-associated mitophagy, mitochondria-nuclei retro-signaling may significantly contribute cytotoxic PM2.5. The toxicity, encompassing oxidative stress, inflammatory responses, imbalances, are described detail. Notably, activates NLRP3 inflammasome, amplifying responses contributing chronic diseases. Furthermore, disrupts genetic epigenetic regulation, often resulting cycle arrest exacerbating damage. composition, concentration, seasonal variability modulate effects, underscoring complexity PM2.5-induced dysfunction. Despite significant advances understanding pathways, further research required elucidate long-term exposure, role potential strategies mitigate harmful impact health.
Language: Английский
Citations
2International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(23), P. 12646 - 12646
Published: Nov. 25, 2024
The widespread use of polyvinyl chloride (PVC) and its entry into humans livestock is serious concern. In our study, we investigated the impact PVC treatments on physiological, pathological, hormonal, microbiota changes in female rabbits. Trend-like alterations weight were observed spleen, liver, kidney both low (P1) high dose (P2) treatment groups. Histopathological examination revealed exfoliation intestinal mucosa treated groups compared to control, microplastic particles penetrated embedded spleen. Furthermore, P1 P2 showed increased 17-beta-estradiol (E2) hormone levels, indicating early sexual maturation. Moreover, elevated tumor necrosis factor alpha (TNF-α) levels suggest inflammatory reactions associated with treatment. Genus-level analyses gut group several genera or decreased abundance. conclusion, significant trend-like correlations demonstrated between content feed parameters. To knowledge, this first study investigate broad-spectrum effects exposure These results highlight potential health risks exposure, warranting further investigations animals humans.
Language: Английский
Citations
0Journal of Hazardous Materials, Journal Year: 2024, Volume and Issue: 484, P. 136691 - 136691
Published: Nov. 30, 2024
Language: Английский
Citations
0