Picture of mobile phone running fintech app

Fintech: Open Access research exploring new frontiers in financial technology

Strathprints makes available Open Access scholarly outputs by the Department of Accounting & Finance at Strathclyde. Particular research specialisms include financial risk management and investment strategies.

The Department also hosts the Centre for Financial Regulation and Innovation (CeFRI), demonstrating research expertise in fintech and capital markets. It also aims to provide a strategic link between academia, policy-makers, regulators and other financial industry participants.

Explore all Strathclyde Open Access research...

Fertility-disrupting potential of synthetic peptides derived from the beta-subunit of follicle-stimulating hormone

Ferro, Valerie A. and Stimson, William H. (1998) Fertility-disrupting potential of synthetic peptides derived from the beta-subunit of follicle-stimulating hormone. American Journal of Reproductive Immunology, 40 (3). pp. 187-197. ISSN 1600-0897

Full text not available in this repository. Request a copy from the Strathclyde author


PROBLEM: Hormone immunoneutralization is hampered by immunologic cross-reactivity caused by close-sequence homology between related molecules. One solution is to use smaller fragments to induce antibodies of greater specificity. METHOD OF STUDY: A number of peptides selected from beta-follicle-stimulating hormone (FSH) were conjugated to tetanus toxoid and were used to immunize female rats. The antisera were examined for FSH cross-reactivity by immunoassays and in an in vitro bioassay. RESULTS: In the immunoassays, the antisera did not react with FSH but did react with their respective peptides. In the bioassay, sera from VYKDPARPC- and CDSLYTYP-immunized animals inhibited FSH-receptor interaction by 73% and 68%, respectively. These animals also showed reduced estradiol levels. Sequences were synthesized around VYKDPARPC and were tested on a FSH-receptor-bearing Chinese hamster ovary cell line. LVYKDPARPC, VYKDPARPC, YKDPARPIC, CLVYKDPARP, and LVYKDPARP inhibited FSH-receptor interaction by greater than 50%. In female mice, TRDLVYKDPARPKI and LVYKDPARP disrupted estrous cycling in all animals; LVYKDPARPC and CLVYKDPARP disrupted cycling in three of five animals, whereas VYKDPARPC disrupted cycling in one of four animals. CONCLUSIONS: Peptides from two areas of beta-FSH (VYKDPARP and DSLYTYP) were shown to raise FSH-neutralizing antibodies, which were able to suppress estradiol levels. An additional leucine residue to VYKDPARP greatly enhanced the peptide's ability to inhibit FSH-receptor binding and caused fertility disruption in vivo.