1α,25-dihydroxyvitamin D3 (1,25-D3), the active form of vitamin D, is synthetized from cholesterol by skin exposure to the sun. This hormone’s actions are mediated by vitamin D receptor (VDR) in the nucleus and in the plasma membrane, resulting in genome actions like gene expression regulation. VDR can also be found in the plasmatic membrane, and together with PDIA3 receptor they mediate 1,25-D3 non-genomic actions. Vitamin D has an important role in reproductive function, since fertility reduction was observed in vitamin D deficient rats, as well as VDR and 1α-hydroxylase deficiency. In these animals, calcium and estrogen supplementation was able to reverse the deleterious effects in reproductive function, indicating that there is a relation between 1,25-D3 and estrogens signalling pathways. Estradiol (E2) is synthetized from testosterone by aromatase enzyme (CYP19). E2 is found in high levels in the male reproductive function, and like 1,25-D3 can induce genomic and non- genomic actions, mediated by ESR1, ESR2 and GPER receptors. Bisphenol A (BPA) is a xenoestrogen utilized in plastic industry, capable of modulating the endocrine system through E2 receptors. The aim of this work was to study metabolism and signaling pathways interactions between 1,25-D3 and E2, as well as BPA influence in testicular cells. In the first line of work, three treatment protocols (TP) were realized, where E2 and BPA were administrated in rats between 15th and 30th days, were a portion of the animals were euthanized at the last day of treatment (TP1) and another portion was kept alive after the treatment until euthanized at adult age with 75 days (TP2). A third animal group also received the same treatments when adults (TP3). In TP1, E2 treatment decreased CYP27A1 gene expression. E2 and BPA decreased VDR gene expression. This effect was not verified in VDR protein expression. In TP2, E2 increased VDR, PDIA3 and CYP27A1 gene expression, and VDR and CYP27A1 protein expression, indicating a compensatory effect over gene expression inhibition in prepubertal age. In TP3, treatments did not change gene expression, indicating that prepubertal age is more susceptible to estrogen exposure. In the second line of work, non-genomic effects of BPA were studied through 45Ca2+ influx in prepubertal rat testis. BPA stimulated 45Ca2+ influx in a similar manner to E2. This effect was independent of classical ERs, consistent with a G protein-coupled receptor mechanism, probably GPER. This effect involves the modulation of ionic channels, such as K+, TRPV1 and Cl- channels. Furthermore, BPA is able to modulate calcium from intracellular storages by inhibiting SERCA and activating IP3 receptor/Ca2+ channels at the endoplasmic reticulum and activate kinase proteins, such as PKA and PKC. The rapid responses of BPA on calcium influx could, in turn, trigger a cross talk by MEK and p38MAPK activation and also mediate genomic responses. In the third line of work, the expression of some genes involved in 1,25-D3 and E2 metabolism and signalling were analysed in Leydig cells. 1,25-D3 decreased CYP27A1 gene expression, an effect that was also observed when cells were coincubated with 1,25-D3 and E2. E2 decreased ESR1 and CYP19 gene expression. Both hormones demonstrated an negative feedback mechanism over their on metabolism in these cells. Non-genomic effects were also studied in these cells, where E2 seems to have an inhibitory effect while 1,25-D3 was able to stimulate calcium influx. From these results we can conclude that 1,25-D3, E2 and BPA have important molecular effects in the male reproductive system, through gene expression control over receptors and enzymes involved in the metabolism of the steroid hormones studied. These results also reinforce the theory that there is a relationship between 1,25-D3 and E2 signalling pathways, as well as 1,25-D3, E2 and BPA also have non-genomic actions in calcium signalling.