Abstract:Diabetes is a rising global health concern and an increasingly common cause of male infertility. Although the definitive pathophysiological mechanisms underpinning the association between diabetes and infertility is unclear, there are several animal studies showing diabetes to be a detrimental factor on reproductive health through apoptosis, oxidative stress and impairment of steroidogenesis. Furthermore, as reflected in animal models, antidiabetic strategies and relevant treatments are beneficial in the manag… Show more
“…Twenty seminiferous tubules from each sample were magnified at 400× to determine the testicular maturity and damage using the Johnsen's tubular biopsy score (JTBS) method [117]. Each seminiferous tubule was given a score between 1 and 10 to indicate its level of germinal epithelial maturity according to the following description: score (1), no cells appear in the tubular section; score (2), no germ cells exist; score (3), just the spermatogonia can be seen; score (4), limited primary spermatocytes; score (5), numerous primary spermatocytes but no spermatozoa or spermatids; score (6), only a few spermatids; score (7), a large number of early spermatids deprived of differentiation; score (8), a few differentiated spermatids; score (9), several differentiated spermatids; and finally, score (10), regular tubules with lots of sperms.…”
Section: Histological Study On the Testesmentioning
confidence: 99%
“…Multiple body organs are affected by micro-and/or macrovascular diabetic complications, resulting in their damage, dysfunction, and eventual failure [4,5]. Reproductive dysfunction is one of the adverse effects of diabetes in both humans and animal models [6][7][8][9]. Recently, it was reported that type 1 and type 2 diabetes (T1DM and T2DM, respectively) adversely affected the sperm quality and histopathology of reproductive organs in T1DM and T2DM mice with a great extent of similarity.…”
Diabetes mellitus is a metabolic disorder associated with various complications encompassing male reproductive dysfunction. The present study aimed to investigate the therapeutic potential of biologically active Lepidium sativum seed oil (LSO) against the testicular dysfunction associated with streptozotocin (STZ)-induced diabetes. Male adults (n = 24) were divided into four groups: control, LSO-administered, diabetic (D), and LSO-treated diabetic (D+LSO) groups. LSO was extracted from L. sativum seeds, and its chemical composition was determined using GC-MS. Serum testosterone levels, testicular enzymatic antioxidants (catalase (CAT) and superoxide dismutase (SOD)), an oxidative stress (OS) biomarker, malondialdehyde (MDA), pro-inflammatory markers (NF-kB, IL-1, IL-6, and TNF-α), and the expression level of NF-kB were assessed. In addition, histopathological changes were evaluated in testicular tissues. The results obtained showed that the chemical composition of LSO indicated its enrichment mainly with γ-tocopherol (62.1%), followed by 2-methylhexacosane (8.12%), butylated hydroxytoluene (8.04%), 10-Methylnonadecane (4.81%), and δ-tocopherol (3.91%). Moreover, LSO administration in the D+LSO mice significantly increased testosterone levels and ameliorated the observed testicular oxidative damage, inflammatory response, and reduced NF-kB expression compared to the diabetic mice. Biochemical and molecular analyses confirmed the histological results. In conclusion, LSO may prevent the progression of diabetes-induced impairment in the testes through inhibition of the OS- and NF-kB-mediated inflammatory response.
“…Twenty seminiferous tubules from each sample were magnified at 400× to determine the testicular maturity and damage using the Johnsen's tubular biopsy score (JTBS) method [117]. Each seminiferous tubule was given a score between 1 and 10 to indicate its level of germinal epithelial maturity according to the following description: score (1), no cells appear in the tubular section; score (2), no germ cells exist; score (3), just the spermatogonia can be seen; score (4), limited primary spermatocytes; score (5), numerous primary spermatocytes but no spermatozoa or spermatids; score (6), only a few spermatids; score (7), a large number of early spermatids deprived of differentiation; score (8), a few differentiated spermatids; score (9), several differentiated spermatids; and finally, score (10), regular tubules with lots of sperms.…”
Section: Histological Study On the Testesmentioning
confidence: 99%
“…Multiple body organs are affected by micro-and/or macrovascular diabetic complications, resulting in their damage, dysfunction, and eventual failure [4,5]. Reproductive dysfunction is one of the adverse effects of diabetes in both humans and animal models [6][7][8][9]. Recently, it was reported that type 1 and type 2 diabetes (T1DM and T2DM, respectively) adversely affected the sperm quality and histopathology of reproductive organs in T1DM and T2DM mice with a great extent of similarity.…”
Diabetes mellitus is a metabolic disorder associated with various complications encompassing male reproductive dysfunction. The present study aimed to investigate the therapeutic potential of biologically active Lepidium sativum seed oil (LSO) against the testicular dysfunction associated with streptozotocin (STZ)-induced diabetes. Male adults (n = 24) were divided into four groups: control, LSO-administered, diabetic (D), and LSO-treated diabetic (D+LSO) groups. LSO was extracted from L. sativum seeds, and its chemical composition was determined using GC-MS. Serum testosterone levels, testicular enzymatic antioxidants (catalase (CAT) and superoxide dismutase (SOD)), an oxidative stress (OS) biomarker, malondialdehyde (MDA), pro-inflammatory markers (NF-kB, IL-1, IL-6, and TNF-α), and the expression level of NF-kB were assessed. In addition, histopathological changes were evaluated in testicular tissues. The results obtained showed that the chemical composition of LSO indicated its enrichment mainly with γ-tocopherol (62.1%), followed by 2-methylhexacosane (8.12%), butylated hydroxytoluene (8.04%), 10-Methylnonadecane (4.81%), and δ-tocopherol (3.91%). Moreover, LSO administration in the D+LSO mice significantly increased testosterone levels and ameliorated the observed testicular oxidative damage, inflammatory response, and reduced NF-kB expression compared to the diabetic mice. Biochemical and molecular analyses confirmed the histological results. In conclusion, LSO may prevent the progression of diabetes-induced impairment in the testes through inhibition of the OS- and NF-kB-mediated inflammatory response.
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