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The impact of micro/nano plastics (MPs/NPs) on human health is a significant area of research. Studies on the effects of maternal exposure to microplastics (MPs) on the fertility in offspring have been conducted, but the damage caused by nanoplastics (NPs) remains ambiguous. In this study, pregnant Kunming mice were exposed to 30 mg/kg/day PS-NPs from 0.5 gestation day (GD) to 21 days postpartum (dpp). Increased rates of miscarriage and premature delivery were observed, as well as reduced litter size, indicating potential permanent reproductive injury in mice of PS-NPs group. Maternal exposure to PS-NPs impaired fertility of the female offsprings. Decreased primordial and increased growing follicles were observed in the ovaries of offspring at 1 dpp and 7 dpp in PS-NPs group, indicating premature activation of primordial follicles. This premature activation is likely due to the PS-NPs'induction of the AKT-FOXO3a signaling pathway by downregulating AMPK phosphorylation level and enhancing mTOR activity. Furthermore, a significant reduction in transzonal projections (TZPs) was noted in the ovaries of adult offspring mice in PS-NPs group. RNA sequencing of the ovaries from adult offspring female mice revealed that the TZPs related genes may be linked to CAMKIIβ, with a corresponding downregulation in expression levels. Overall, maternal exposure to PS-NPs induced profound and enduring effects on the reproductive functions of female offspring, raising critical alarms regarding the multigenerational reproductive toxicity risks associated with nanoplastic exposure in mammals.

In recent years, nanoplastics (NPs) and triclosan (TCS, a pharmaceutical and personal care product) have emerged as environmental pollution issues, and their combined presence has raised widespread concern regarding potential risks to organisms. However, the combined toxicity and mechanisms of NPs and TCS remain unclear. In this study, we investigated the toxic effects of polystyrene NPs and TCS and their mechanisms on KGN cells, a human ovarian granulosa cell line. We exposed KGN cells to NPs (150 μg/mL) and TCS (15 μM) alone or together for 24 hours. Co-exposure significantly reduced cell viability. Compared with exposure to NPs or TCS alone, co-exposure increased reactive oxygen species (ROS) production. Interestingly, co-exposure to NPs and TCS produced synergistic effects. We examined the activity of superoxide dismutase (SOD) and catalase (CAT), two antioxidant enzymes; it was significantly decreased after co-exposure. We also noted an increase in the lipid oxidation product malondialdehyde (MDA) after co-exposure. Furthermore, co-exposure to NPs and TCS had a more detrimental effect on mitochondrial function than the individual treatments. Co-exposure activated the NRF2–KEAP1–HO-1 antioxidant stress pathway. Surprisingly, the expression of SESTRIN2, an antioxidant protein, was inhibited by co-exposure treatments. Co-exposure to NPs and TCS significantly increased the autophagy-related proteins LC3B-II and LC3B-Ⅰ and decreased P62. Moreover, co-exposure enhanced CASPASE-3 expression and inhibited the BCL-2/BAX ratio. In summary, our study revealed the synergistic toxic effects of NPs and TCS in vitro exposure. Our findings provide insight into the toxic mechanisms associated with co-exposure to NPs and TCS to KGN cells by inducing oxidative stress, activations of the NRF2-KEAP1-HO-1 pathway, autophagy, and apoptosis.

Nanoplastics (NPs) have recently emerged in the context of global plastic pollution. They may be more toxic than macroplastics litter and microplastic fragments due to its abundances, tiny sizes, and cellular accessibility. The female reproductive toxicity of NPs has been widely documented for aquatic animals, but their effects and underlying mechanisms remain poorly understood in mammals. This study aimed to explore the effects of NPs on female reproduction using human ovarian granulosa cells (GCs) and female mice. The accumulation of polystyrene NPs (PS-NPs) in human granulosa-like tumor cells (KGN cells) and the ovaries of female Balb/c mice were evaluated by exposure to fluorescent PS-NPs. Proliferation and apoptosis, reactive oxygen species (ROS), and Hippo signaling pathway-related factors were analyzed in KGN cells. In addition, fertility rate, litter size, ovarian weight and microstructure, follicle development, serum level of anti-Mullerian hormone, and apoptosis in ovaries were examined in female mice. Here, the PS-NPs can penetrate the KGN cells and accumulate in the ovaries. In vitro, 100 μg/ml PS-NPs inhibited proliferation, induced apoptosis, accumulated ROS, activated three key regulators of the Hippo signaling pathway (MST1, LATS1, and YAP1), and downregulated the mRNA levels of CTGF and Cyr61 in KGN cells. Furthermore, salidroside, an antioxidative compound extracted from Rhodiola rosea, alleviated the damage of PS-NPs to KGN and inhibited the activation of the Hippo signal pathway. In vivo, exposure to 1 mg/day PS-NPs resulted in decreased fertility, abnormal ovarian function, and increased ovarian apoptosis in female mice. Overall, our data suggest that PS-NPs cause granulosa cell apoptosis and affect ovarian functions, leading to reduced fertility in female mice, by inducing oxidative stress and dysregulating the Hippo pathway.

This article presents a miniature ultrawideband active magnetic probe which is composed of a passive structure and an active amplification circuit structure. The active circuit mainly contains two chips, specifically an amplification chip (HMC797APM5E) and a power management chip (HMC980LP4E). The maximum size of the probe is no more than 64 × 41.5 mm2. Compared with the passive probe with the same-sized loop, the sensitivity of the proposed probe is enhanced by 25 dB through the active circuit design. The working frequency bandwidth of the proposed probe can cover 9 kHz to 18 GHz. Additionally, the flatness is about ±4 dB in terms of |S21| in the stable working bandwidth. It is efficient for high-frequency near-field scanning.

The radiation emission from high-speed digital circuit may result in radio-frequency interference (RFI) problems in modern electronic devices. In this paper, an improved equivalent dipole source based on a new transfer model and a new regularization method is proposed. The equivalent source is obtained by solving an inverse equation with near-field data. The tangential component of electric field used in conventional equivalent source extraction is replaced by the normal component, which can reduce the test difficulty and enhance the measurement efficiency. The new regularization method based on Tikhonov and truncated singular value decomposition (TSVD) can enhance the stability and accuracy of the dipole solution. In addition, the new transfer model and regularization method are verified by simulations and measurements.