The Concept of Male Reproductive Anatomy

The human reproductive system is made up of the primary and secondary organs, which helps to enhances reproduction. The male reproductive system is designed to produce male gametes and convey them to the female reproductive tract through the use of supportive fluids and testosterone synthesis. The paired testis (site of testosterone and sperm generation), scrotum (compartment for testis localisation), epididymis, vas deferens, seminal vesicles, prostate gland, bulbourethral gland, ejaculatory duct, urethra, and penis are the parts of the male reproductive system. The auxiliary organs aid in the maturation and transportation of sperm. Semen is made up of sperm and the secretions of the seminal vesicles, prostate, and bulbourethral glands (the ejaculate). Ejaculate is delivered to the female reproduc¬tive tract by the penis and urethra. The anatomy, embryology and functions of the male reproductive system are discussed in this chapter

Endocrine Functions of the Testes

The testes, also known as the male gonads are found in the scrotal sacs. In addition to their spermatogenic functions, they also secrete steroids and protein hormones. The steroid hormones are the androgens, testosterone and dihydrotestosterone as well as estrogen, while the protein hormones are inhibins, activins, and anti-Mullerian hormone (AMH). This chapter therefore discusses the role of the testis in the production and functions of the testicular androgens as well as testicular protein hormones

High dietary consumption of iodine induced thyroid cytotoxicity in diabetic intoxicated rats and oxidonitrergic stress in non-diabetic rats

This study aimed to investigate the role of iodine intake in thyroid function ofdiabetic rats. Twenty-four (24) male Wistar rats were placed into four groups (n=6): Group (non-diabetic without iodine), Group 2 (non-diabetic + iodine), Group 3 (diabetic without iodine) and Group 4 (diabetic + iodine). 10mg/kg bw of iodine were mixed with the feeds. Serum triodothyronine (T3), thyroxine (T4), Thyroid Stimulating Hormone (TSH), thyroglobulin and thyroperoxidase antibodies were assessed using ELISA. Serum MDA, SOD, and NO levels were assessed with spectrophotometry. In the diabetic rats, lower mean serum T4 and TSH concentrations were observed (T4: 13.16±0.55 Vs 11.75±0.21 mg/dL, TSH: 2.62±0.11 Vs 2.28±0.08 IU/mL). Iodine treatment further reduced T4 and increased TSH concentrations (T4: 11.75±0.21 vs 6.75±0.22 mg/dL, TSH: 2.28±0.08 Vs 3.08±0.15 IU/mL). Thyroglobulin and thyroperoxidase antibodies were absent in all the rats. It was also observed that iodine intake caused an increase in oxidative stress in both diabetic and non-diabetic treated rats (MDA; 18.4±1.3 Vs 22.2±2.7 μmol/l X 10-5, NO; 14.08±0.38 Vs 13.24±0.07μm/l) and increased SOD levels in diabetic rats (44.44±2.94 Vs 68.94±0.91 mg/ml); this increase could be due to the increased TSH. Consumption of excess iodine suppressed thyroid function in diabetic rats and induced oxidative stress in both diabetic and non-diabetic treated rats

Testosterone: The Male Sex Hormone

Males primarily use testosterone as a sex hormone. Through its effects on the androgen receptor, it is released by the interstitial cells of the testes and is in charge of the male external genitalia development as well as the internal reproductive glands and ducts during adolescence and maturity. Additionally, testosterone is required for the descent of testes via the inguinal canal in the last 2 months of fetal development. When a Y chromosome and consequently the SRY gene are missing from an embryo, ovaries form. The Wolffian ducts do not mature because the fetal ovaries do not release enough testosterone. It is mostly used to treat male hypogonadism. Notably, this chapter addresses the following context: historical view of testosterone research, biosynthesis, secretion, metabolism, transport mechanism, biological actions, health benefit of testosterone, factors that promote and inhibit testosterone secretion, therapeutic implication as well as pathophysiology of testosterone secretion

Exploring the medicinal significance of l-Arginine mediated nitric oxide in preventing health disorders

l-Arginine is an essential amino acid that plays a crucial role in various physiological processes. It serves as a precursor for nitric oxide (NO), which has potent antioxidant and anti-inflammatory properties. This review aims to comprehensively examine the medicinal importance of l-arginine as a natural antioxidant in preventing human health disorders. A comprehensive literature search was conducted using PubMed, Google Scholar, and other databases. Studies investigating the antioxidant effects of l-arginine and its potential role in preventing various diseases were included. l-Arginine has been shown to mediate NO production with strong antioxidant properties, scavenging free radicals and reducing oxidative stress. It has demonstrated therapeutic potential in preventing and mitigating various health conditions, including: Cardiovascular diseases, Neurodegenerative diseases, Metabolic disorders, Immune function and Anti-aging effects. l-Arginine is a potent natural antioxidant with significant medicinal importance. Its ability to scavenge free radicals, improve endothelial function, and support immune function makes it a promising therapeutic agent for preventing and treating a wide range of human health disorders. Further research is warranted to fully elucidate the mechanisms of action and optimal dosage for specific conditions

Adverse hematological profiles associated with chlorpromazine antipsychotic treatment in male rats: Preventive and reversal mechanisms of taurine and coenzyme-Q10

Chlorpromazine (CPZ) is one of the most effective antipsychotic drugs used for managing psychotic related disorders owing to its dopamine receptor blocking action. However, pharmacological investigations against CPZ’s cytotoxic effect have remained scarce. Hence, this study investigated the preventive and reversal effects of taurine and coenzyme-Q10 (COQ-10), which are compounds with proven natural antioxidant properties, against CPZ-induced hematological impairments in male rats. In the preventive study, rats received oral saline (10 ml/kg), taurine (150 mg/kg/day), COQ-10 (10 mg/kg/day) or in combination for 56 days, alongside CPZ (30 mg/kg, p.o.) between days 29–56. In the reversal protocol, rats had CPZ repeatedly for 56 days before taurine and COQ-10 treatments or their combination from days 29–56. Rats were also given taurine (150 mg/kg/day), and COQ-10 (10 mg/kg/day) alone for 56 days. Serums were extracted and assayed for hematological, with oxidative and inflammatory markers. CPZ induced decreased red/white blood cells, erythropoietin, platelet count, packed cell volume and hemoglobin, neutrophil, and lymphocyte, which were prevented and reversed by taurine and COQ-10, or their combination. Taurine and COQ-10 improved mean corpuscular volume, hemoglobin concentration, with increased erythropoietin levels relative to CPZ groups. CPZ-induced increased malondialdehyde, tumor necrosis factor-alpha and interleukin-6 levels with decreased interleukin-10, glutathione, and superoxide-dismutase were prevented and reversed by taurine and COQ-10 in comparison with CPZ groups. Taurine and COQ-10 alone notably improved the antioxidant/anti-inflammatory status relative to controls. Among other mechanisms, taurine and COQ-10 abated CPZ-induced hematological deficiencies, via decreased serum levels of oxidative stress, and pro-inflammatory cytokines release, with increased antioxidants and anti-inflammation function

Possible mechanisms involved in the protective effect of lutein against cyclosporine-induced testicular damage in rats

Oxidative stress and aberrant inflammatory response have important implications in cyclosporin-induced reproductive functions. Previous studies have shown that agents with antioxidant and anti-inflammatory activities might be beneficial in reversing cyclosporin-induced reproductive impairment. Lutein is a naturally occurring compound with antioxidant and anti-inflammatory properties. However, the effect of lutein against cyclosporin-induced reproductive impairment remains in complete. Hence, we investigated the protective effect of lutein, specifically focusing on the role of nuclear factor erythroid 2 related factor-2 (Nrf2)/heme-oxygenase-1 (HO-1)/connexin-43 (Cx-43) upregulation system against cyclosporine-induced reproductive impairment. Six male Wistar rats were allotted into 5 groups and given daily gavage of cyclosporine (40 mg/kg) and/or lutein (30 mg/kg) for four (4) weeks or in combination, respectively. The testicular antioxidant scaffolds: superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), add to sulfhydryl (T-SH), non-protein sulfhydryl (NP-SH), glutathione reductase (GR), glutathione-S -transferase (GST), glutathione peroxidase (GSH-Px), thiobarbituric acid reactive substances (TBARS), myeloperoxidase (MPO), testicular proinflammatory cytokines, apoptotic related protein, nucleic acids, sialic acid, testicular proton pump ATPase, stress responsive protein, BTB-related protein and total protein levels in the testes were assayed thereafter. Cyclosporin significantly increased NOX-1, TNF-α, IL-1β, MPO, caspase-3 and -9 levels, which were reversed by lutein. Lutein reversed cyclosporin-induced decreases in Nrf2, HO-1, BCL-2, cytochrome C, with corresponding increase in CAT, SOD, GSH, T-SH, NP-SH, GST, GR, GSH-Px, and Cx-43 levels compared to cyclosporin groups. Lutein also abates cyclosporin-induced alterations Na + -K + -ATPase activities. Our findings showed that lutein's protective effect against cyclosporin-induced reproductive impairment might be associated with mechanisms linked to its antioxidant, anti-apoptotic, and anti-inflammatory properties, notably through up-regulation of Nrf2/HO-1/Cx-43 signaling and down-regulation of NOX-1 signaling