Thyroid hormones are involved in the development of several tissues and organs and are essential for the normal growth and reproductive function. The aim of this study was to determine the effects of thyroid hormones on the development of testis and progression of spermatogenesis. Lactating mothers were treated with oral thyroxine (T4; 20 µg/100 g) for 20 days after parturition. The pups were decapitated at the age of 20, 40 and 60 days post partum. Neonatal hyperthyroidism resulted in a decrease in body and testis mass, an increase of free thyroxine and a decrease of testosterone concentrations in plasma of treated rats. The treatment was associated with a significant decrease of the diameter of seminiferous tubules and a slowdown in spermatogenesis, following a delay in the maturation of germ cells. We conclude that thyroid hormones affect the progression of postnatal spermatogenesis.

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The aim of this study was to investigate the effects of castration and testosterone supplementation on nitroso-redox status, cardiac metabolism markers, and S100 proteins expression in the heart of male rats. 50 male Wistar rats were randomized into five groups with ten animals each: group 1: control intact (CON); group 2: sham operated (Sh-O); group 3: sesame oil-treated rats (S-oil); group 4: gonadoectomized (GDX); and group 5: gonadoectomized rats treated with testosterone (GDX-T) for 8 weeks. Our results showed myofibrillar weaving, apoptosis, inflammation, and fibrosis (as reflected by increased activity of MMP 9 and MMP 2) in the heart of gonadoectomized rats. Testosterone supplementation restored the normal structure of the heart. In addition, a state of nitroso-redox imbalance was observed in the heart of castrated rats with increased NO (425.1 ± 322.8 vs. 208 ± 67.06, p ˂ 0.05) and MDA (33.18 ± 9.45 vs. 22.04 ± 7.13, p ˂ 0.05) and decreased GSH levels (0.71 ± 0.13 vs. 1.09 ± 0.19, p = 0.001). Testosterone treatment leads to a re-establish of only NO levels (425.1 ± 322.8 vs. 210.4 ± 114.3, p > 0.05). Markers of cardiac metabolism showed an enhancement of LDH activity (12725 ± 4604 vs. 5381 ± 3122, p ˂ 0.05) in the heart of castrated rats. This was inversed by testosterone replacement (12725 ± 4604 vs. 5781 ± 5187, p ˂ 0.05). Furthermore, castration induced heart's accumulation of triglycerides (37.24 ± 6.17 vs. 27.88 ± 6.47, p ˂ 0.05) and total cholesterol (61.44 ± 3.59 vs. 54.11 ± 7.55, p ˂ 0.05), which were significantly reduced by testosterone supplementation (29.03 ± 2.47 vs. 37.24 ± 6.17, p ˂ 0.05) and (47.9 ± 4.15 vs. 61.44 ± 3.59, p ˂ 0.001). Cardiomyocytes of castrated rats showed a decreased immunoexpression of S100 proteins compared to control animals. A restoration of S100 proteins immunostaining in cardiomyocyte cytoplasm was observed after testosterone supplementation. These findings confirm the deleterious effects of testosterone deficiency on cardiac function and highlight the involvement of nitric oxide, metalloproteinases 2 and 9, and S100 proteins.

The results of the study indicate that phytotherapy using Citrullus colocynthis alkaloids may correct metabolic and hormonal perturbations as well as adrenal medulla structure of rats maintained on HFD.