Bisphenol A (BPA), a suspected reproductive biohazard and endocrine disruptor, released from plastics is associated with ED in occupationally exposed workers. However, in rats, despite the induction of hypogonadism, apoptosis of the penile corporal smooth muscle (SM), fat infiltration into the cavernosal tissue and changes in global gene expression with the intraperitoneal administration of high dose BPA, ED was not observed.

Bisphenol-A

Researchers investigated whether BPA administered orally rather than intraperitoneally to rats for longer periods and lower doses will lead to ED. Main outcome measures are ED, histological, and biochemical markers in rat penile tissues. In all, 2.5-month-old rats were given drinking water daily without and with BPA at 1 and 0.1 mg/kg per day.
Two months later, erectile function was determined by cavernosometry and electrical field stimulation (EFS) and serum levels of testosterone (T), estradiol (E2) and BPA were measured.

Penile tissue sections were assayed by Masson (SM/collagen), Oil Red O (fat), terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) (apoptosis), immunohistochemistry for Oct4 (stem cells), and a-SM actin/calponin (SM and myofibroblasts), applying quantitative image analysis.
Other markers were assayed by western blotting. DNA microarrays/microRNA (miR) assays defined transcription profiles.

Orally administered BPA did not affect body weight, but decreased serum testosterone and estradiol; reduced the electrical field stimulation response and increased the drop rate; increased within the corporal tissue the presence of fat, myofibroblasts and apoptosis; lowered the contents of SM and stem cells, but not nerve terminals and caused alterations in the transcriptional profiles for both mRNA and miRs within the penile shaft.

Long-term exposure of rats to oral BPA caused a moderate corporal veno-occlusive dysfunction (CVOD), possibly due to alterations within the corporal tissue that pose gene transcriptional changes related to inflammation, fibrosis and epithelial/mesenchymal transition (EMT).

This is the first demonstration of ED caused by BPA in an animal model. In this experimental design, ED, specifically CVOD, was induced in 10-week-old rats after 4.5 months of the continuous oral ingestion of BPA in the drinking water. In these animals that developed ED, it was estimated that the serum levels of BPA were lower than the serum BPA levels calculated to have been present in those men who developed ED solely from an occupational exposure to BPA.10, 11, 12 As such, the current work suggests that BPA exposure could be the first specific chemical environmental risk identified for ED.

For more information
International Journal of Impotence Research
Oral Bisphenol A (BPA) given to rats at moderate doses is associated with erectile dysfunction, cavernosal lipofibrosis and alterations of global gene transcription

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