The
nephrotic syndrome is a renal disease characterized by
proteinuria,
hypoproteinemia,
edema and
hyperlipidemia. It has been reported that female nephrotic rats are characterized by loss of the oestrus cycle, follicle atresia, low
gonadotropin and
steroid concentrations; particularly, undetectable
estradiol levels. Therefore, to determine the mechanisms involved in the ovarian steroidogenesis impairment, in this present study we evaluated the ovarian expression of the essential steroidogenesis components:
cytochrome P450 side
cholesterol chain cleavage
enzyme (P450scc) and
steroidogenic acute regulatory protein (StAR). The experiments were conducted in the rat experimental model of
nephrosis induced by
puromycin aminonucleoside (PAN) and in control groups. The evaluation of the expression of P450scc and StAR
mRNA were performed during the acute phase of
nephrosis as well as after the exogenous administration of 1 or 4 doses of human chorionic gonadotrophin (hCG), or a daily dose of FSH or FSH+hCG for 10 days. In addition, serum
hormone concentrations, intra-ovarian
steroid content, and the reproductive capacity were determined. The results revealed a decreased expression of
mRNA of P450scc
enzyme and StAR during
nephrosis, and eventhough they increased after
gonadotropins treatment, they did not conduce to a normal cycling rat period or fertility recovery. This study demonstrates that the mechanism by which ovarian
steroid biosynthesis is altered during acute
nephrosis involves damage at the P450scc and StAR
mRNA synthesis and processing.