This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. One's gender, advanced aging, racial origin, affected first-degree relatives and the so-called 'Western life-style' have all been cited as significant risk factors for the development of prostate cancer. In addition, epidemiological and animal studies suggest that the incidence of prostate cancer and prostate disease is tremendously influenced by diet. If we recognize that specific diet components alter prostate risk in a predictable fashion raises the possibility that this disease could be prevented by the use of pharmacological regimes aimed at mimicking dietary phytoestrogens. Androgenic stimulation of males over long periods of time has been suggested as a cause of prostate cancer in adult life. Thus, if dietary phytoestrogen can lower androgenic stimulation over time, they may prevent or delay the onset of prostate disease in later life. We surmise that early exposure to phytoestrogens may confer a lasting protection against prostate cancer by programming the gland to be less susceptible to cancer. We hypothesized that exposure to dietary phytoestrogen during fetal and or neonatal life will alter the gene expression of 5-alpha-R or AR (androgen receptor), thus decreasing the time and exposure to androgens. This altered gene expression will be imprinted on the prostate from fetal or neonatal life and become irreversible throughout adult life. To test the above hypothesis the following two specific aims were developed.
Aim one will determine whether prenatal exposure of dietary phytoestrogen alters or modulates the levels of expression, structure, or function of the 5-alpha-R and AR genes in rat neonates.
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