Effects of Dexmedetomidine on the Localization of α2A-Adrenergic and Imidazoline Receptors in Mouse Testis

Abstract

Dexmedetomidine (DEX) used for sedation was reported to have organ-protecting effects in ischemia–reperfusion injury model animals. However, no testicular cell-protecting effect was observed with DEX treatment. The effects of DEX on a normal testis in vivo have not been reported. Therefore, DEX was administered to mice for 14 days to investigate the reproductive toxicology of DEX on the testis and the localization of DEX-responsive receptors. The testes, pituitary glands, and serum were examined and analyzed using real-time PCR, immunofluorescence staining, and liquid chromatography–mass spectrometry. In the testis, α2A-adrenergic receptors were observed in the cytoplasm of Leydig cells, while imidazoline receptors were observed in germ cells and Leydig cell cytoplasm. The levels of luteinizing hormone and follicle-stimulating hormone mRNA in the pituitary gland significantly temporarily decreased. Serum DEX could not be detected 26 h after DEX administration. DEX administration did not affect serum testosterone levels, some testicular mRNA related to spermatogenesis, and oxidative stress factors. Therefore, although DEX receptors are present in the testis, DEX is metabolized relatively quickly, and DEX administration has no damaging effects on the testis. This study is the first in vivo report about the effects of DEX administration on the testis.