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Bisphenol-A Affects Male Fertility via Fertility-related Proteins in Spermatozoa (Feb 2015)

nature
Title:
Bisphenol-A Affects Male Fertility via Fertility-related Proteins in Spermatozoa
Journal:
Scientific Reports 5, Article number: 9169
Author(s):
Md Saidur Rahman, Woo-Sung Kwon, June-Sub Lee, Sung-Jae Yoon, Buom-Yong Ryu, Myung-Geol Pang
Author(s) affiliation:
Department of Animal Science and Technology, Chung-Ang University, Anseong, Gyeonggi-do 456-756, Republic of Korea.
 

 

Short description:
Bisphenol-A (BPA) is an endocrine disruptor (ED) that possesses weak estrogenic, anti-androgenic, and anti-thyroid activities, and it is a prominent environmental pollutant due to its use in the manufacture of food packaging, industrial materials, and dental sealant. Owing to its extensive use, toxicity, and environmental persistence, BPA has become a significant public health concern. The major route of BPA exposure for humans and animals is ingestion of contaminated food and water, but exposure can also occur via dermal and respiratory routes.
Link to the journal
 

 

Abstract taken from PubMed

Abstract:
The xenoestrogen bisphenol-A (BPA) is a widespread environmental contaminant that has been studied for its impact on male fertility in several species of animals and humans. Growing evidence suggests that xenoestrogens can bind to receptors on spermatozoa and thus alter sperm function. The objective of the study was to investigate the effects of varying concentrations of BPA (0.0001, 0.01, 1, and 100 μM for 6 h) on sperm function, fertilization, embryonic development, and on selected fertility-related proteins in spermatozoa. Our results showed that high concentrations of BPA inhibited sperm motility and motion kinematics by significantly decreasing ATP levels in spermatozoa. High BPA concentrations also increased the phosphorylation of tyrosine residues on sperm proteins involved in protein kinase A-dependent regulation and induced a precocious acrosome reaction, which resulted in poor fertilization and compromised embryonic development. In addition, BPA induced the down-regulation of β-actin and up-regulated peroxiredoxin-5, glutathione peroxidase 4, glyceraldehyde-3-phosphate dehydrogenase, and succinate dehydrogenase. Our results suggest that high concentrations of BPA alter sperm function, fertilization, and embryonic development via regulation and/or phosphorylation of fertility-related proteins in spermatozoa. We conclude that BPA-induced changes in fertility-related protein levels in spermatozoa may be provided a potential cue of BPA-mediated disease conditions.
Link to the paper on PubMed
 




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