Abstract
Testosterone plays an important prenatal role in male testis development. Bisphenol A (BPA) exposure during pregnancy affects testosterone levels and germ cell apoptosis of male pups, but little information is available for the mechanism. The aim of the present study was to investigate the mechanism by which BPA alters testosterone levels and germ cell apoptosis. Pregnant female C57BL/6J mice, throughout gestation, had access to drinking water containing BPA at 5 and 50 μg/mL. Male pups were euthanized on postnatal days (PNDs) 1, 14, and 35. Relative to control, BPA exposure at 5 and 50 μg/ml decreased testosterone level, as measured by chemiluminescent immunoassay, on PND14. Real-time PCR indicated mRNA levels for steroidogenic acute regulatory protein (StAR), cholesterol side-chain cleavage enzyme (CYP11A1), and 3-β-hydroxysteroid dehydrogenase/△-5-4 isomerase (3β-HSD) were significantly lower in the BPA pups compared to control. Additionally, BPA increased the percentage of TUNEL-positive seminiferous tubules, decreased the mRNA level of Bcl-2, and increased Bax expression, indicative of increased apoptosis. These results suggest that BPA exposure in utero decreases the testosterone concentration by decreasing steroidogenic enzymes (StAR, CYP11A1, and 3β-HSD). Furthermore, BPA exposure increases the apoptosis of germ cells, which is associated with proapoptotic changes in the levels of Bcl-2 and Bax.
Highlights
Bisphenol A (BPA) is widely used in a variety of consumer products, such as plastic bottles, food containers, and beverage cans, which can be ingested by humans because BPA is released from those products [1]
Mean body weights of pups exposed to BPA at 5 and 50 μg/mL were 6.97±0.73 and 6.84±0.50 g, respectively, which were lower than the control (7.43±0.69 g) on PND14
Our results show that the mRNA levels of steroidogenic acute regulatory protein (StAR), CYP11A1, and 3βHSD are lower after the BPA exposure in utero on postnatal days (PNDs) 1 and 14 (Figure 1), indicating that the ability of the testis to produce testosterone is weaker in mice prenatally exposed to BPA, which explains the decreased serum testosterone concentration after BPA exposure
Summary
Bisphenol A (BPA) is widely used in a variety of consumer products, such as plastic bottles, food containers, and beverage cans, which can be ingested by humans because BPA is released from those products [1]. We studied the male pups from maternal mice exposed to BPA during pregnancy. Exposure to high doses of BPA during pregnancy has been shown to decrease plasma testosterone at birth [9]. Perinatal exposure from gestational day (GD) 6 to postnatal day (PND) 20 to BPA at 4 mg/kg body weight (bw) increases plasma testosterone concentrations in adulthood [10]. Adult male rats perinatally exposed to BPA (1.2 and 2.4 μg/kg bw) possess increased serum testosterone levels [11]. Exposure of male rats to BPA at 2.5 μg/kg/day (GD12 to PND21) did not affect serum testosterone, but it decreased intratesticular testosterone concentrations in adult animals [12]. Early life exposure to BPA results in aberrant testicular
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