ABSTRACT
In order to investigate the effects of Rutin against restraint stress, 50 adult male mice were divided into five groups: control, restraint stress (RS), and RS with 2 doses of Rutin treatments. Mice were restrained in a conical tube for 4â¯h daily and Rutin was injected intraperitoneally for 15 consecutive days. Restraint stress significantly decreases body weights, testis and epididymis weights, thymus weights, visceral fats, serum concentrations of testosterone, sperm counts, sperm motility and sperm viability, while it increases serum epinephrine levels, adrenal gland weights and abnormal sperms. In addition, restraint stress severely damages the testicular histoarchitecture and spermatogenesis. Stressed groups also showed broken seminiferous tubules, few spermatozoa in lumen, less population of Leydig cells between the interstitial spaces, spermiation arrest in stage I-III and degenerated population of round spermatids in the lumen; as well as missing cells in stages IV-VI. Furthermore, lumen sizes increased in stages VII, VIII, IX and X. Residual bodies increased in stages IV-VI, VII-VIII and vacuoles found in stages XI-XII after restraint stress. PARP1 signaling is involved in apoptosis. In this study, expressional levels of cleaved PARP1 and cleaved Caspase-3 are significantly increased in testes after restraint stress. We demonstrate that Rutin significantly ameliorates the side effects induced by restraint stress.
Subject(s)
Rutin/administration & dosage , Spermatogenesis/drug effects , Spermatozoa/drug effects , Testis/drug effects , Animals , Caspase 3/genetics , Gene Expression Regulation, Developmental/drug effects , Injections, Intraperitoneal , Male , Mice , Poly (ADP-Ribose) Polymerase-1/genetics , Restraint, Physical/adverse effects , Spermatogenesis/genetics , Spermatozoa/growth & development , Spermatozoa/pathology , Testis/growth & developmentABSTRACT
To expand our understanding of the roles of thyroid hormones on female reproduction, we induced hypo- and hyper-T rat models to investigate the roles of thyroid hormones on estrous cyclicity, as well as the antioxidative status in the ovaries of rats. In the current study, our data show that hypothyroidism (hypo-T) and hyperthyroidism (hyper-T) led to significantly reduced body weights and ovarain weights and delayed vaginal opening day. For hyper-T, thyroxine (T4), tri-iodothyronine (T3), progesterone (P4) and follicle-stimulating hormone (FSH) were significantly increased, while estradiol (E2) and luteinizing hormone (LH) were significantly decreased. For hypo-T rats, serum levels of total T4 and T3, E2, P4, FSH and LH were significantly increased, while concentrations of E2 and LH were significantly decreased. For ovary morphology, the numbers of secondary and antral follicles were significantly decreased with more atretic antral follicles and less corpora lutea in both hyper- and hypo-T groups. Both hyper-T and hypo-T treatment significantly decreased the expressions of thyroid hormone receptor α1 in the ovary. Hypo-T significantly reduced nitric oxide (NO), total NO synthase (tNOS), inducible NOS and constitutive NOS activities, but hyper-T increased them. For antioxidative parameters, hypo-T and hyper-T treatment significantly increased malondialdehyde (MDA) contents. The activities of both glutathione peroxidase (GSH-Px) and catalase (CAT) significantly decreased in the hypo-T group but increased in the hyper-T group. Total superoxide dismutase (T-SOD) activity was significantly increased in the hyper-T group. In summary, thyroid hormones alter estrous cyclicity and antioxidative status in the ovary of the rat may act through the NOS signaling pathway.
Subject(s)
Antioxidants/metabolism , Estrous Cycle , Ovary/metabolism , Ovary/physiology , Thyroid Hormones/physiology , Animals , Body Weight , Catalase/metabolism , Estradiol/metabolism , Female , Follicle Stimulating Hormone/metabolism , Glutathione Peroxidase/metabolism , Hyperthyroidism/metabolism , Hypothyroidism/metabolism , Luteinizing Hormone/metabolism , Malondialdehyde/metabolism , Nitric Oxide/metabolism , Nitric Oxide Synthase/metabolism , Organ Size , Ovary/anatomy & histology , Ovary/pathology , Rats, Sprague-Dawley , Superoxide Dismutase/metabolism , Thyroid Hormone Receptors alpha/metabolismABSTRACT
Thyroid hormones are important in the development and regulation of testes. This study was conducted to determine the effects of hyper- and hypothyroidism on testicular development in prepubertal rats aged 20-70 days. Weaning male rats (20 days old) until day 70 age were randomly divided into four groups: control, hyperthyroid (hyper-T), hypothyroid (hypo-T) and hypothyroid treated with thyroxine (T4) (hypo-T+T4). The results indicated that thyroid hormones caused a significant effect in body and testis weights, and food and water consumption. In addition there were changes in serum concentrations of tri-iodothyronine, T4, thyroid stimulating hormone (TSH) and testosterone. Histomorphology showed a significant decrease in seminiferous tubule diameter in hyper-T compared to the other groups. Leydig cell numbers showed a significant elevation in hyper-T but not in hypo-T groups. Immunostaining indicated that TSH receptor (TSHR), thyroid hormone receptors α/ß (TRαß) and proliferating cell nuclear antigen (PCNA) have the roles in testicular development. Our findings suggest that hyper- and hypo-thyroidism regulate testicular cell proliferation and spermatogenesis in prepubertal rats, indicating that expression of TSHR, TRαß and PCNA may be regulated by thyroid hormones that are involved in testicular development; and that the administration of T4 to the hypo-T+T4 group leads to an improvement in the testicular condition.
