Abstract
Bisphenol A (BPA) is one of the ubiquitous environmental endocrine disruptors (EEDs). Previous studies have shown that the reproduction toxicity of BPA could cause severe effects on the mammal oocytes and disturb the quality of mature oocytes. However, the toxic effects of BPA on the organelles of mouse oocytes have not been reported. In this study, to investigate whether BPA can be toxic to the organelles, we used different concentrations of BPA (50, 100, and 200 μM) to culture mouse oocytes in vitro. The results showed that 100 μM BPA exposure could significantly decrease the developmental capacity of oocytes. Then, we used the immunofluorescence staining, confocal microscopy, and western blotting to investigate the toxic effects of BPA on the organelles. The results revealed that mitochondrial dysfunction is manifested by abnormal distribution and decreased mitochondrial membrane potential. Moreover, the endoplasmic reticulum (ER) is abnormally distributed which is accompanied by ER stress showing increased expression of GRP78. For the Golgi apparatus, BPA-exposed dose not disorder the Golgi apparatus distribution but caused abnormal structure of Golgi apparatus, which is manifested by the decrease of GM130 protein expression. Moreover, we also found that BPA-exposed led to the damage of lysosome, which were shown by the increase of LAMP2 protein expression. Collectively, our findings demonstrated that the exposure of BPA could damage the normal function of the organelles, which may explain the reduced maturation quality of oocytes.
Highlights
In recent years, with the continuous development of human society, the contradiction between rapidly rising pollution levels and human health has become increasingly prominent
We observed polar body extrusion, and the results showed that most oocytes could extrude first polar body in the control group and 50 μM Bisphenol A (BPA) treatment group; in the 100 and 200 μM treatment groups, most oocytes had developmental block (Figure 1A)
Rate of first polar body extrusion: Control group: 82.56 ± 2.1984%, n = 134, 50 μM: 71.29 ± 8.807%, n = 165, P > 0.05, 100 μM: 44.29 ± 5.053%, n = 145, P < 0.001, 200 μM: 15.62 ± 4.07%, n = 94, P < 0.0001, Figure 1C). These results suggested that BPA exposure could reduce the developmental competence of mouse oocytes in the dose-dependent manner
Summary
With the continuous development of human society, the contradiction between rapidly rising pollution levels and human health has become increasingly prominent. Excessive exposure to environmental pollutants can induce severe health problems, including reproductive health problems, which have attracted increased attention in recent years. This situation is being followed closely by scholars at home and worldwide (Vandenberg et al, 2007; Kabir et al, 2015). The United States Environmental Protection Agency defines EED as “a substance that disrupts the synthesis, secretion, transport, binding, or attenuation of natural hormones needed to maintain homeostasis, reproduction, development, and normal behavior” (Kavlock et al, 1996). EEDs have attracted the attention of various research institutions because they may contribute to the development of endocrine system disorders in mammals and interfere with normal reproductive functions (Lucaccioni et al, 2020; Shi et al, 2021)
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