Microplastics reach the brain and interfere with honey bee cognition

Pasquini, Elisa; Ferrante, Federico; Passaponti, Leonardo; Pavone, Francesco Saverio; Costantini, Irene; Baracchi, David

doi:10.1016/j.scitotenv.2023.169362

Cited by 8 publications

(1 citation statement)

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“…The inhalation of NPs/MPs could exacerbate the toxicity of the lung, while the oral exposure of NPs/MPs could localize in the gut and bioaccumulate in multifarious organs such as the brain, liver, kidney, and reproductive organ, thereby eliciting corresponding detrimental effects. In recent years, growing literature has revealed that NPs/MPs exposure could bring about a series of unfavorable health outcomes, such as the damage of central nervous system and cerebral function [12], pulmonary injury [13], gut microbiota dysbiosis [14], hepatocellular apoptosis and necroptosis [15], kidney lesion [16], as well as reproductive impairment [17]. Mounting epidemiological evidence has indicated that human fertility displays a gradually declining trend in recent decades and approximately 8%-12% couples of childbearing ages worldwide are affected by infertility [18].…”

Section: Introductionmentioning

confidence: 99%

Threats of nano/microplastics to reproduction and offspring: Potential mechanisms and perspectives

Ha,

Tang,

Huang

et al. 2024

J. Toxicol. Stud.

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Due to the ubiquitous occurrence in the aquatic environment and terrestrial ecosystem and underlying eco-environmental risks, nano/microplastics (NPs/MPs) have sparked great public concerns. The purpose of this work is aimed to summarize the harmful influence of NPs/MPs on reproduction and offspring health and further explore the potential mechanisms of action, thereby facilitating the more comprehensive understanding of NPs/MPs features. Literature search databases included EMBASE, Web of Science, and PubMed. The study selection and data extraction were implemented according to the inclusion criteria. NPs/MPs could accumulate and trigger reproductive toxic responses and thereafter generate deleterious effects on the offspring health. Accordingly, the reproductive toxicity of NPs/MPs was characterized as the sperm deformity, decline in sperm count and motility, follicular growth tardiness, ovarian fibrosis, granulosa cell death, disorder of reproductive hormone secretion, as well as the fetal growth restriction, glycolipid metabolism disorder, and inflammatory responses of the next generation. Additionally, mechanism research revealed that NPs/MPs exposure brought about inflammatory responses and oxidative stress and thereafter, destroyed the blood-testis barrier (BTB) integrity, motivated spermatogenic cell apoptosis by activating the JNK and p38/MAPK-Nrf2/NF-κB pathways, and induced ovarian granulosa cell pyroptosis and apoptosis and subsequent ovarian fibrosis via the Wnt/β-Catenin and NLRP3/Caspase-1 pathways. Nevertheless, this work also highlighted the imperative requirements for scientific and systematic risk assessments of NPs/MPs, so as to identify the feasible risk mitigation strategies.

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