Plastics are extensively used in our daily life. However, a significant amount of plastic waste is discharged to the environment directly or via improper reuse or recycling. Degradation of plastic waste generates micro-or nanosized plastic particles that are defined as micro-or nanoplastics (MNPs). Microplastics (MPs) are plastic particles with a diameter less than 5 mm, while nanoplastics (NPs) range in diameter from 1 to 100 or 1000 nm. In the current review, we first briefly summarized the environmental contamination of MNPs and then discussed their health impacts based on existing MNP research. Our review indicates that MNPs can be detected in both marine and terrestrial ecosystems worldwide and be ingested and accumulated by animals along the food chain. Evidence has suggested the harmful health impacts of MNPs on marine and freshwater animals. Recent studies found MPs in human stool samples, suggesting that humans are exposed to MPs through food and/or drinking water. However, the effect of MNPs on human health is scarcely researched. In addition to the MNPs themselves, these tiny plastic particles can release plastic additives and/or adsorb other environmental chemicals, many of which have been shown to exhibit endocrine disrupting and other toxic effects. In summary, we conclude that more studies are necessary to provide a comprehensive understanding of MNP pollution hazards and also provide a basis for the subsequent pollution management and control.

BackgroundInfertility and gonadal dysfunction can result from gonadotoxic therapies, environmental exposures, aging, or genetic conditions. In men, non‐obstructive azoospermia (NOA) results from defects in the spermatogenic process that can be attributed to spermatogonial stem cells (SSC) or their niche, or both. While assisted reproductive technologies and sperm banking can enable fertility preservation (FP) in men of reproductive age who are at risk for infertility, FP for pre‐pubertal patients remains experimental. Therapeutic options for NOA are limited. The rapid advance of stem cell research and of gene editing technologies could enable new FP options for these patients. Induced pluripotent stem cells (iPSC), SSC, and testicular niche cells, as well as mesenchymal stromal cells (aka medicinal signaling cells, MSCs), have been investigated for their potential use in male FP strategies.ObjectiveHere, we review the benefits and challenges for three types of stem cell‐based approaches under investigation for male FP, focusing on the role that promising sources of MSC derived from human umbilical cord, specifically human umbilical cord perivascular cells (HUCPVC), could fulfill. These approaches are as follows: 1. isolation and ex vivo expansion of autologous SSC for in vivo transplantation or in vitro spermatogenesis; 2. in vitro differentiation toward germ cell and testicular somatic cell lineages using autologous SSC, or stem cells such iPSC or MSC; and 3. protection or regeneration of the spermatogenic niche after gonadotoxic insults in vivo.ConclusionOur studies suggest that HUCPVC are promising sources of cells that could be utilized in multiple aspects of male FP strategies.

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Ovarian toxicity (ovotoxicity) is one of the major side effects of pharmaceutical compounds for women at or before reproductive age. The current gold standard for screening of compounds’ ovotoxicity largely relies on preclinical investigations using whole animals. However, in vivo models are time-consuming, costly, and harmful to animals. Here, we developed a three-tiered ovotoxicity screening approach starting from encapsulated in vitro follicle growth (eIVFG) and screened for the potential ovotoxicity of 8 preclinical compounds from AstraZeneca (AZ). Results from Tier 1 and 2 screenings using eIVFG showed that the first 7 tested AZ compounds, AZ-A, -B, -C, -D, -E, -F, and -G, had no effect on examined mouse follicle and oocyte reproductive outcomes, including follicle survival and development, 17β-estradiol (E2) secretion, ovulation, and oocyte meiotic maturation. However, AZ-H, a preclinical compound targeting the checkpoint kinase 1 (Chk1) inhibitor to potentiate the anticancer effects of DNA-damaging agents, significantly promoted granulosa cell apoptosis and the entire growing follicle atresia at clinically-relevant concentrations of 1 and 10 μM. The more targeted explorations in Tier 2 revealed that the ovotoxic effect of AZ-H primarily resulted from Chk1 inhibition in granulosa cells. Using in vivo mouse model, the Tier 3 screening confirmed the in vitro ovotoxicities of AZ-H discovered in Tiers 1 and 2. Also, although AZ-H at 0.1 μM alone was not ovotoxic, it significantly exacerbated gemcitabine-induced ovotoxicities on growing follicles. Taken together, our study demonstrates that the tiered ovotoxicity screening approach starting from eIVFG identifies and prioritize pharmaceutical compounds of high ovotoxicity concern.