Impact of Microplastics on Human Health: Risks, Diseases, and Affected Body Systems

Microplastics, Journal Year: 2025, Volume and Issue: 4(2), P. 23 - 23

Published: May 7, 2025

This review article aims to highlight the potential harm caused by microplastics (MPs) in different organs and systems underscore need for further investigation into their action mechanisms. MPs, such as polystyrene, polypropylene, polyethylene, significantly impact human health, causing inflammation respiratory gastrointestinal systems, compromising immune function, increasing risk of cardiovascular diseases neurotoxicity. These effects are largely attributed role MPs disrupting hormonal regulation, which can lead reproductive disorders an elevated cancer. microscopic particles (less than 5 mm size) now ubiquitous air, water, food. However, much existing research on focuses mechanisms association with health disease, limited emphasis direct humans or long-term consequences. To effectively address plastic toxicity, it is crucial understand policy implications relevance disease development. Recent has highlighted more stringent regulatory oversight these materials better mitigate health.

Language: Английский

MoS₂ Nanosheets at Low Doses Induced Cardiotoxicity in Developing Zebrafish via Ferroptosis: Influence of Lateral Size and Surface Modification

Environmental Science & Technology, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 26, 2024

The widespread applications of molybdenum disulfide (MoS2) nanosheets inevitably result in their release into aquatic environments, necessitating an exploration potential toxic effects on organisms. This study analyzes the cardiac responses zebrafish larvae exposed to MoS2, with a focus influence size and surface modifications. At higher concentrations (1 5 mg/L), MoS2 hampered larval growth without influencing cardiomyogenesis. lower doses (0.5–100 μg/L), small-sized (ssMoS2, 187.2 nm) significantly impaired development, as proved by morphology abnormality, decreased heartbeat, stroke volume, output, whereas these undesirable changes were not observed cysteine-modified form. Large-sized (1.638 μm) did localize heart, barely showing disorder. Transcriptomics, biochemical analysis, computational simulation validated that ssMoS2 aggravated Fe2+ overload through excessive ferritinophagy ferroportin-1 inhibition, accompanied down-regulation glutathione peroxidase 4 activation PUFAs esterification, leading ferroptosis. Significant associations between ferroptosis signals indices, along ferrostatin-1 inhibition test, confirmed ferroptosis-mediated cardiotoxicity ssMoS2. Our provides key understanding molecular events underlying MoS2-induced highlights importance characteristics, which are significant for risk assessment safe design nanoproducts.

Language: Английский