Dissertation/Thesis Abstract

The Effect of Endocrine Disrupting Chemical Bisphenol a on Testosterone Biosynthesis
by Alharthy, Saif Abdullah, M.S., The University of Texas Health Science Center at San Antonio, 2014, 59; 10137595
Abstract (Summary)

Endocrine disrupting chemicals are a group of exogenous compounds which disrupt the endocrine functions of human and wildlife. This disruption might be in the synthesis, storage, release, and actions of specific hormones. Endocrine disrupting chemicals encompass a variety of chemical classes including drugs, compounds used in plastic consumer products manufacturing, pollutants, insecticides, herbicides, and even naturally-occurring botanical products like phytoestrogens. Most of these disrupters produce estrogenic properties because of having structural similarity to endogenous 17 beta estradiol. Mimicking estradiol, they can interfere with its actions resulting in the development of several diseases, such as nervous system, diabetes, obesity, breast cancers, and reproductive impairments. One of the endocrine disrupting chemicals of most interest is bisphenol A.

Bisphenol A is a carbon-based synthetic compound and it is used in epoxy resins, polycarbonate plastics, fungicides, antioxidants, stabilizers in rubber, and as a component of dental sealants. Numerous studies have found that bisphenol A may accidentally leak into canned foods or plastic bottled drinks ingested by humans. Studies indicate that bisphenol A effects are due to its estrogenic activity and the ability to bind and activate the estrogen receptor specifically. A growing number of studies have indicated that bisphenol A might be responsible for reduction in sperm count, spermatogenesis, aromatase, seminal fluid, 17 beta hydroxysteroid dehydrogenase activity, and testosterone biosynthesis. The primary objective of this capstone project is to review the available literature in order to determine the mechanism of bisphenol A action on testosterone biosynthesis. The working hypothesis was that bisphenol A-induced reduction in testosterone production may be due predominantly to inhibition of 17 beta beta hydroxysteroid dehydrogenase rather than an increase in aromatase enzyme activity. This study had the following specific aims: 1) review the sex steroid biosynthesis pathway, 2) review the endocrine disrupting chemicals; 3) determine a mechanism by which bisphenol A mimics estrogen and affects testosterone synthesis. Literature review was conducted using the databases PubMed, Ovid Medline, CINAHL Plus, as well as the search engine Google Scholar for the period 1940 to present. The keywords used: bisphenol A, testosterone, luteinizing hormone, 17 beta hydroxysteriod dehydrogenase enzymes. It was found that human studies were limited to urine measurements in which increased bisphenol A correlated with decreased sperm account and seminal fluid volume. In animal studies, bisphenol A reduced testosterone production by direct action on the leydig cells. In the ovarian granulosa cells, bisphenol A reduced aromatase enzyme activity but unlikely to be the method, in the testes as, a decrease in aromatase activity would cause an increase in testosterone level. Since bisphenol A causes significant decrease in testosterone biosynthesis, this suggests that the inhibition of 17 beta hydroxysteroid dehydrogenase, the enzyme that converts androstenedione to testosterone, is probably the principal target for bisphenol A. In conclusion, the literature supports a strong threat from bisphenol A on male reproductive function and every action must be taken seriously to reduce the exposure of male to this endocrine disrupting chemical.

Indexing (document details)
Advisor: Kudolo, George B.
Commitee: Al-Ghoul, Mohammad, Burns, Cheryl, Papa, Vincent
School: The University of Texas Health Science Center at San Antonio
Department: Pharmacology
School Location: United States -- Texas
Source: MAI 55/05M(E), Masters Abstracts International
Subjects: Toxicology, Endocrinology, Environmental science
Publication Number: 10137595
ISBN: 978-1-339-93284-2
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