Kabakci, Ruhi, et al. Environmental Pollution 338 (2023): 122698.
Perfluorooctanoic acid (PFOA) is a persistent environmental pollutant. Due to its widespread presence in the environment, PFOA exposure affects not only human reproductive health but may also impact livestock reproductive health.
This study focuses on determining the effects of PFOA on the physiological functions of bovine granulosa cells in vitro. Primary bovine granulosa cells were exposed to 0, 4, and 40 μM PFOA for 48 and 96 hours, and then granulosa cell functions, including cell viability, steroidogenesis, and mitochondrial activity, were analyzed. The results indicated that PFOA inhibited steroid hormone secretion and altered the expression of key enzymes required for steroidogenesis. Gene expression analysis showed that exposure to PFOA decreased mRNA transcripts of CYP11A1, HSD3B, and CYP19A1, while STAR expression increased. Similarly, PFOA reduced the protein levels of CYP11A1 and CYP19A1. PFOA did not affect cell viability, alter the cell cycle, or induce apoptosis, although it did reduce metabolic activity, suggesting mitochondrial dysfunction. We observed that PFOA treatment led to a loss of mitochondrial membrane potential and an increase in PINK protein expression, indicating mitochondrial autophagy and mitochondrial damage. Further analysis revealed that these changes were associated with elevated levels of reactive oxygen species (ROS). After exposure to PFOA, the expression of autophagy-related proteins phospho-ULK1 and LAMP2 increased, along with enhanced lysosomal abundance, which is characteristic of increased autophagy. In conclusion, these findings suggest that PFOA negatively affects granulosa cell steroidogenesis by impairing mitochondrial function.
Kang, Jae Soon, Jin-Soo Choi, and June-Woo Park. Chemosphere 155 (2016): 436-443.
Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonic acid (PFOS) are two of the most widely used perfluoroalkyl acids (PFAAs). Many in vivo studies suggest that PFOA and PFOS may disrupt the endocrine system.
In this study, the endocrine-related effects of PFOA and PFOS were investigated using in vitro estrogen receptor (ER) and androgen receptor (AR) transcriptional activation assays and steroidogenesis assays. The results showed that both PFOA and PFOS exhibited weak antagonistic effects on ER transcriptional activation, but did not show agonistic effects on either ER or AR transcriptional activation. In the steroidogenesis assay, PFOA and PFOS induced 17β-estradiol (E2) levels while decreasing testosterone levels, which may be due to the induction of aromatase activity. qPCR analysis of genes involved in steroidogenesis revealed that PFOA and PFOS transcriptionally induced the expression of two genes, cyp19 and 3β-hsd2, which are related to sex hormone synthesis. In addition, the transcriptional induction of cyp11b2 by PFOS suggests that this chemical may be the underlying cause of disruptions in multiple physiological functions associated with aldosterone. The findings of this study indicate that PFOA and PFOS are potential endocrine-disrupting chemicals (EDCs) and provide insights into molecular events that could trigger adverse endocrine effects for further investigation.
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