Evidence indicates that prolactin plays a crucial role in the normal function and development of the prostate, but abnormal high levels of the hormone are associated with hyperplasia and cancer of the gland. Aims: the present study was designed to describe the progressive specific histological abnormalities in the prostate of rats with chronic hyperprolactinemia. Prolactin was administered during 4; 12 or 24 weeks, and the resulting prostatic alterations were compared with control rats, and also with those treated with testosterone, or the combination of prolactin + testosterone. Rats treated with prolactin, testosterone or prolactin + testosterone expressed precancerous histological abnormalities in the dorsolateral and ventral portions of the prostate as early as in 4 weeks of treatment, but in all cases the malignancy increased after 12 or 24 weeks of treatment. Conclusion: our study confirms that chronic hyperprolactinemia is a cause of prostate precancerous pathologies.

Індекс рубрикатора НБУВ: Р569.696.2

Рубрики:

Пухлини передміхурової залози

Шифр НБУВ: Ж14160 Пошук видання у каталогах НБУВ 

Puberty can be a critical period for the long-term development of diseases, especially for stress-related disorders that depend on neuroendocrine and immune responses. Some organs like the prostate are prone to diseases that result from neuroendocrine or immune challenges, such as cancer. Aim - in the present study, we assessed the long-term effects of an acute pubertal stressor (immune-challenge) on the development of precancerous lesions in adult rats, and compared them with testosterone-induced prostatic lesions. Pubertal male rats received a single injection of lipopolysaccharide (LPS) or saline during puberty (5 weeks old). At adulthood (8 weeks old) males were subcutaneously implanted with either an empty capsule or filled with testosterone propionate (100 mg/kg). This resulted in a total of five groups: intact untreated, saline-treated and implanted with a blank capsule, saline-treated and implanted with a testosterone capsule, LPS-treated and implanted with a blank capsule, LPS-treated and implanted with a testosterone capsule. Four weeks later, the rats were sacrified and their prostates processed for histology (hematoxylin and eosin stain) and blood serum processed for hormone analysis (testosterone and corticosterone). Males treated with LPS (stressed during puberty via immune challenge) expressed epithelium dysplasia (specially in the ventral prostate), anisocytosis, presence of mononuclear cells, anisokariosis, non-basal polarity, abnormal nucleus-cytoplasm ratio, proplastic myoepithelium, and granular content in the lumen. These histological alterations were similar, but less severe than those observed in males implanted with testosterone during adulthood. Conclusion: these results indicate that pubertal exposure to an immune challenge (stress) facilitates the long-term development of prostatic lesions in adult male rats.

Stress during puberty and obesity can represent conditions that facilitate the long-term development of diseases, especially for stress-related disorders that depend on neuroendocrine and immune responses. The prostate is prone to diseases that result from neuroendocrine or immune challenges, such as cancer. Aim - in the present study, we assessed the long-term effects of an acute pubertal stressor (immune-challenge) or obesity on the development of precancerous lesions in rats. Pubertal male rats received a single injection of lipopolysaccharide (LPS) or saline during puberty (5 weeks of age). In adulthood (8 weeks old), subgroups of males were fed with hypercaloric liquid diet to induce obesity. This resulted in a total of six subgroups: intact-non obese, intact-obese, saline-non obese, saline-obese, LPS-non obese, and LPS-obese. At 16 weeks of age the rats were sacrified for prostate histology (hematoxylin and eosin stain) and hormone analysis (testosterone, corticosterone and prolactin). As compared to intact-non obese rats, males treated with LPS and those with obesity expressed histological alterations in both the dorsolateral and ventral portions of the prostate. Only prolactin was altered in LPS-treated males, whereas corticosterone was altered in LPS-obese rats. Conclusions: these results indicate that puberal exposure to an immune challenge or obesity facilitate the development of prostatic lesions in adult male rats. We discuss the role of hormones in the development of precancerous lesions.