## 4 Discussion  
To investigate the reproductive toxicity of DEX, 10 \(\upmu\)g/kg and 40 \(\upmu\)g/kg of DEX alone were administered intraperitoneally to normal mice daily for two weeks. No changes in mRNA expression were observed in cells within the interstitium or semifierous tubules of the testis. In the pituitary gland, the expression of LH and FSH mRNAs was significantly decreased 2 h after DEX administration, and the expression of \(\alpha\)2A-adrenergic receptor mRNA was significantly increased, but it rapidly recovered thereafter. Furthermore, in the testis, the site of action of DEX was localized to the cytoplasm of Leydig cells and vascular endothelial cells for adrenergic receptors and to the cytoplasm of Leydig cells and germ cells for IRs. In general, \(\alpha\)2A-adrenergic receptors are present in the cell membrane, and the sympathetic neurotransmitter noradrenaline responds to the receptors by inhibiting the release of noradrenaline and exerting sedation, hypnosis, and sympatholytic effects [15; 16; 17; 18; 19; 20]. \(\alpha\)2A  
Figure 6: Effects of DEX administration on oxidant stress factors in the mouse testes. The expression levels of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase 2 (SOD2), caspase3, adrenoleukodystrophy protein from subfamily D, member 1 (ABCD1), ABCD, member 3 (ABCD3), glucose-regulated protein, 78 kDa (GRP78), and 8-oxoguanine DNA glycosylase 1 (OGG1) at each testis collection point were measured by RT-PCR. The values in the graph are presented as means \(\pm\) SDs. The sampling points after 14 days of continuous DEX administration were 9:00 on day 14 (D14-9), 13:00 on day 15 (D15-9), and 13:00 on day 15 (D15-13). adrenergic receptors are localized in pancreatic \(\beta\)-cells, platelets, and vascular smooth muscle cells and induces various physiological responses, such as insulin release suppression, platelet aggregation activation, and vasoconstriction [15]. [PERSON] et al. reported that \(\alpha\)2A-adrenergic receptors are localized in the cell membranes of nerve cell bodies, axons, and dendrites in the superior cervical ganglion of mice based on immunofluorescence sustaining [17]. They also reported that pretreatment with DEX suppresses the increase in cytosolic calcium flux after potassium administration [17]. [PERSON] et al. reported that \(\alpha\)2A-adrenergic receptors are localized in the cytoplasm of nerve fibers and neuronal cell bodies in guinea pig neurons and in the cytoplasm of glial cells and neuronal cell bodies in mice and rats [18]. In Madin-Darby canine kidney cells (a cell line derived from canine renal tubular epithelial cells), \(\alpha\)2A adrenergic receptors were reported to be localized in the cell membrane [21]. It was reported that \(\alpha\)2A-adrenergic receptors are localized in ciliary smooth muscle cells and in the cytoplasm [22]. Thus, \(\alpha\)2A-adrenergic receptors are localized in the cell membrane and cytoplasm. IRs were reported to be present on cell membranes [23] and are involved in the regulation of several functions, such as blood pressure and heart rate reduction, sodium excretion from the kidneys, and catecholamine release from adrenal chromaffin cells [24; 25; 26]. In addition, IR mRNA expression was also reported in rat tissues, such as the brain, liver, testis, and skeletal muscle [27]. IRs are expressed in the brainstem of rats, and are localized in the facial nucleus, inferior olive (dorsal nucleus), lateral reticular nucleus, axons, dendrites, and astrocytes based on immunohistochemical staining, which appears to be stained around the nucleus [28]. In a report investigating the localization of IRs in HEK293 cells transplanted with pEGFP1-IRAS plasmid, they were found to be punctate in the cytoplasm [29]. Therefore, imidazoline receptors are localized both in the plasma membrane and cytoplasm. In the testis, it is present in the tunica alubinea of rats, and noradrenaline reacts with \(\alpha\)2A-adrenergic receptors to cause contraction of the tunica alubinea of the testis.