The prostate is an accessory gland of the reproductive system responsible for producing an alkaline liquid that provides capacity and survival of spermatozoa. Its development occurs under the influence of a regulated and precise androgenic and estrogenic control, so sensitive interference may predispose the gland to develop diseases such as benign prostatic hyperplasia and cancer during adulthood and senile. Current research has shown that many environmental pollutants when in contact with the human body, have hormonal activity. Among these environmental chemicals, we highlight the bisphenol A and cadmium. The Bisphenol is a monomer released from plastic polymers widely used today. Cadmium is a toxic heavy metal used in industry and also released by tobacco burning. These two substances can interfere with the morphogenesis of the prostate, because they mimic estrogens and competing for their receptors. Several studies have demonstrated that intrauterine and neonatal exposure to these estrogenic disruptors alters the normal pattern of prostate morphogenesis, favoring the development of lesions in adult and senile. However, little attention has been focused on the effects that exposure to these environmental chemicals may cause in prostate during postnatal development. Puberty is an important period of postnatal development of the prostate, because the androgen testicular secretion initiated in this period induces an outbreak of prostatic growth and differentiation. Therefore, it is fundamental to evaluate how the exposure to this environmental substances such acts in the prostate pubertal development, observing what is the relevance of this period for the overall process of gland formation. The objective of this study is to evaluate whether exposure to bisphenol A and cadmium during puberty can cause changes in the patterns of proliferation and cell death in the prostate of normal and castrated male gerbils. To fulfill this purpose will be used immunocytochemical and statistical methods. From the results obtained may be elucidated the possible mechanisms involved in the change of these indices, making it possible to associate these mechanisms with the development of prostatic diseases during adulthood and senescence.
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