Absence of relaxin immunostaining in the male reproductive tracts of the rat and mouse.

Abstract

By use of the biotin-avidin immunohistochemical method and a homologous antiserum as the primary antiserum, relaxin immunostaining was absent in the testes, prostate, seminal vesicles, and epididymides of the rat. Relaxin immunostaining was also lacking when anti-porcine relaxin serum was employed as the primary antiserum. Furthermore, immunohistochemical studies for relaxin localization in the reproductive tract of the male mouse using both anti-rat and anti-porcine relaxin sera also revealed an absence of the hormone in the reproductive system of this species. Although this study suggests that immunoreactive relaxin is absent in the male reproductive tracts of both the rat and mouse, it raises some questions concerning the reports in the literature of the presence of relaxin-like substances in the male reproductive tracts of other species. These reports are discussed in relation to our current results.

Efficacy of relaxin for cisplatin-induced testicular dysfunction and epididymal spermatotoxicity

“…Previous studies have reported the antioxidant effects of RLN in myocardial ischemia/reperfusion-induced damage by showing a significant reduction of MDA levels following RLN administration in animal models [50,51]; however, the mechanisms associated with RLN-mediated suppression of oxidative stress remain unclear. Endogenous RLN appears to be at extremely low levels in the rat testis based on the difficulty of antibody detection [20], which as confirmed by detection of weak Rln expression according to RT-PCR in a preliminary study. Additionally, it is possible that endogenous RLN does not play a pivotal role in the testis, as suggested by study of Rxfp1-deficient male mice [52]; however, another study reported impaired spermatogenesis due to increased germ-cell apoptosis in Rln-knockout mice [24].…”

“…In particular, the potential of RLN as a therapeutic agent for renal [11] and heart failure [11][12][13] has attracted substantial attention, since it has been reported to have antifibrotic, anti-apoptotic, antiinflammatory, and antioxidant effects in various clinical applications in studies using animal models of acute kidney [14][15][16] and heart injury [17][18][19]. Alternatively, RLN has been identified to potentially influence testis function, given that small amounts of RLN appears to be produced in the testis [20,21] and that its receptor, RLN family peptide receptor 1 (RXFP1; originally called LGR7, leucine-rich G-protein-coupled receptor 7) [22] has been detected therein [21]. Although the precise effect of RLN on the testis remains unclear, there is evidence that it may be involved in the regulation of testosterone production in Leydig cells and in the reduction of germ cell apoptosis; an earlier study indicated that the addition of RLN to the nucleus-free tissue homogenate from adult macaque testes inhibited testosterone production [23].…”

Relaxin exerts a protective effect during ischemia‐reperfusion in the rat model

“…Extremely low levels of endogenous RLN appears to be present in the rat testis based on the difficulty of antibody detection. 48 Additionally, endogenous RLN may not play a critical role in the testis, as suggested by a study on Rxfp1-deficient male mice 49 ; however, another study reported impaired spermatogenesis owing to increased germ cell apoptosis in Rln-knockout mice. 50 Of note, the present study provided evidence that RLN administration in rats with IR injury tended to upregulate the expression of genes encoding the RLN receptor Rxfp1, which bears signaling.…”

“…However, despite the importance of understanding how RLN improves testicular function in IR−injured rats, the mechanisms associated with RLN‐mediated suppression of oxidative stress, inflammation, and apoptosis have remained unclear to date. Extremely low levels of endogenous RLN appears to be present in the rat testis based on the difficulty of antibody detection 48 . Additionally, endogenous RLN may not play a critical role in the testis, as suggested by a study on Rxfp1 ‐deficient male mice 49 ; however, another study reported impaired spermatogenesis owing to increased germ cell apoptosis in Rln ‐knockout mice 50 .…”