微(纳米)塑料(MNPs)已在各种生态环境中被检测到,并由于其稳定的性能而被广泛使用,引起人们对其潜在的人类生殖毒性的广泛关注。目前,不孕症影响全球约10-30%的育龄夫妇。MNPs,作为环境污染物,已被证明通过内在机制或作为其他有害物质的载体表现出生殖毒性。许多研究已经确定,不同大小和类型的MNPs可以穿透生物屏障,并通过四种主要途径进入生物体的组织甚至细胞器:饮食摄入,吸入,皮肤接触,和医疗干预。然而,关于MNPs对生殖的毒性作用的历史研究主要集中在下层和水生物种上。我们对涉及陆地哺乳动物的研究进行了包容性审查,揭示了MNPs可以通过各种机制诱导生殖毒性,如氧化应激,炎症,纤维化,凋亡,自噬,肠道菌群的破坏,内分泌干扰,内质网应激,和DNA损伤。在陆地哺乳动物中,生殖毒性主要表现为血睾丸屏障(BTB)的破坏,精子发生受损,精子畸形,精子DNA损伤,精子受精能力降低,卵母细胞成熟受损,卵泡生长受损,颗粒细胞凋亡,卵巢储备功能减少,子宫和卵巢纤维化,和内分泌干扰,在其他影响中。此外,MNPs可以穿越母胎界面,可能影响后代的生殖健康。为了全面了解不同大小MNPs的潜在生殖毒性和潜在机制,聚合物类型,形状,携带毒素,以及探索减轻生殖损害的有效保护性干预措施,进一步深入的动物研究,临床试验,迫切需要大规模的流行病学研究。
Micro(nano)plastics (MNPs) have been detected in various ecological environments and are widely used due to their stable properties, raising widespread concern about their potential human reproductive toxicity. Currently, infertility affects approximately 10-30% of couples of reproductive age globally. MNPs, as environmental pollutants, have been shown to exhibit reproductive toxicity through intrinsic mechanisms or as carriers of other hazardous substances. Numerous studies have established that MNPs of varying sizes and types can penetrate biological barriers, and enter tissues and even organelles of organisms through four main routes: dietary ingestion, inhalation, dermal contact, and medical interventions. However, historical research on the toxic effects of MNPs on reproduction mainly focused on lower and aquatic species. We conducted an inclusive review of studies involving terrestrial mammals, revealing that MNPs can induce reproductive toxicity via various mechanisms such as oxidative stress, inflammation, fibrosis, apoptosis, autophagy, disruption of intestinal flora, endocrine disruption, endoplasmic reticulum stress, and DNA damage. In terrestrial mammals, reproductive toxicity predominantly manifests as disruption in the blood-testis barrier (BTB), impaired spermatogenesis, sperm malformation, sperm DNA damage, reduced sperm fertilizing capacity, compromised oocyte maturation, impaired follicular growth, granulosa cell apoptosis, diminished ovarian reserve function, uterine and ovarian fibrosis, and endocrine disruption, among other effects. Furthermore, MNPs can traverse the maternal-fetal interface, potentially impacting offspring reproductive health. To gain a comprehensive understanding of the potential reproductive toxicity and underlying mechanisms of MNPs with different sizes, polymer types, shapes, and carried toxins, as well as to explore effective protective interventions for mitigating reproductive damage, further in-depth animal studies, clinical trials, and large-scale epidemiological studies are urgently required.