Plastics have caused serious environmental pollution. In recent years, microplastics (MPs) have caused widespread concern about their potential toxicity on animals and humans, especially on organ and tissue deposition. However, there is little known about the reproductive toxic effects of MPs in female mammals. In this study, the reproductive toxicity of polystyrene MPs (PS-MPs) in female mice was evaluated after continued exposure for 35 days. Results showed that PS-MPs could accumulate in heart, liver, spleen, lung, kidney, brain, large intestine, small intestine, uterus, ovary and blood of exposed mice. Moreover, PS-MPs exposure increased the IL-6 level and decreased malondialdehyde (MDA) level in mouse ovaries. The results also showed that PS-MPs exposure decreased the first polar body extrusion rate and the survival rate of superovulated oocytes. Meanwhile, PS-MPs reduced the level of glutathione (GSH), mitochondrial membrane potential (MMP), endoplasmic reticulum calcium ([Ca²⁺]_ER) and increased reactive oxygen species (ROS) in oocytes. In conclusion, our study illustrated that PS-MPs exposure induced the inflammation of ovaries and reduced the quality of oocytes in mice, which provided a basis for studying the reproductive toxic mechanism of PS-MPs in female mammals.

Maternal obesity alters oocytes and subsequent fetal metabolism. An increasing number of studies have shown that the endoplasmic reticulums (ER) or mitochondria have important effects on oocyte quality, but there has been no study of the effect of mitochondria-associated ER membranes (MAMs) on oocyte quality. The present study was designed to assess whether the level of MAM and MAM-related proteins were different in oocytes from obese and control mice. First, oocytes from mice with high-fat-diet (HFD)-induced obesity had higher levels (either greater numbers or a higher proportion for the same numbers) of MAM than oocytes from control mice. The abundance of MAM-related proteins in oocytes from obese mice was significantly greater at both the messenger RNA and protein levels, including inositol 1,4,5-trisphosphate receptor, type 1 (IP3R1), inositol 1,4,5-trisphosphate receptor, type 2 (IP3R2) and phosphofurin acidic cluster sorting protein 2 (PACS-2). Further, there was an increase in mitochondrial Ca2+ ([Ca2+]m) which was associated with increased apoptosis and compromised cytoplasmic maturation in oocytes from obese mice. Down-regulation of MAM-related protein IP3R1 in oocytes from obese mice decreased [Ca2+]m and apoptosis and improved cytoplasmic maturation but did not reduce the overall MAM level. However, down-regulating MAM-related protein PACS-2 in oocytes from obese mice did reduce the level of MAM and [Ca2+]m, which decreased the rate of apoptosis and improved cytoplasmic maturation of oocytes from obese mice. It is possible that enriched MAM could increase [Ca2+]m, and this increase has been found to be associated with increased apoptosis and compromised cytoplasmic maturation in oocytes from obese mice. This finding suggests a novel therapeutic target for obesity-induced oocyte defects.