Exogenous oestradiol benzoate induces male mice azoospermia through modulation of oxidative stress and testicular metabolic cooperation

Abstract

in most cases, exogenous oestradiol benzoate (eB) inhibits spermatogenesis, however, the mechanism underlying this process has not been fully elucidated. The present study investigated the effect of eB on redox equilibrium and glycometabolism in mouse testes. Male Kunming mice were divided into 3 groups and injected with 0, 5 and 10 mg/kg eB, respectively. Histological analysis revealed no sperm and far fewer spermatogenic cells in the testes of eB-treated mice. additionally, transmission electron microscopy revealed that mitochondria in Sertoli cells were transformed to vacuoles with irregular cristae in the eB-treated group. eB also significantly decreased the activities and mRNA expression of catalase, superoxide dismutase, and glutathione peroxidase and increased the activity of nitric oxide synthase and nitric oxide concentration in the testes compared with the control. These results indicated that oxidative damage was caused by eB treatment. With regard to glycometabolism, aTP content and activities of hexokinase and pyruvate kinase were significantly reduced in the eB-treated group. although glucose and pyruvate concentrations were significantly increased by eB treatment, levels of lactate, the main energy source of spermatogenic cells, were unchanged. Monocarboxylate transporter 2 (McT2) and McT4, which are responsible for lactate transportation, were downregulated by eB. in conclusion, the results of the present study indicated that azoospermia induced by eB in male mice was associated with oxidative damage and the disorder of testicular metabolic cooperation.

Evaluation of Glutathione Peroxidase Enzymatic Activity in Seminal Plasma of Patients Treated at the Institute Pasteur in Cote d’Ivoire

“…Azoospermia may be associated with oxidative damage. Indeed, Le mice was associated with oxidative stress [31]. Also subjects carrying heterozygous defects in the gene SECISBP2 have synthesis reduced of most of the 25 known human selenoproteins.…”

Effect of spermidine on ameliorating spermatogenic disorders in diabetic mice via regulating glycolysis pathway

“…The membranes were incubted via primitive antibodies overnight at 4 °C with horseradish peroxidase-conjugated goat anti-rabbit IgG (H + L) secondary antibody, Alexa Fluor 594 (R37117) and immersed in ECL Plus Western Blotting detection reagent and displayed on Hyperfilm ECL (both from Amersham, Piscataway, NJ, USA). The band’s intensity was determined using Lab Works 4.5 software (UVP, Upland, CA, USA) [ 18 ]. The primary antibodies used for Western blotting were tubulin, HK2, PKM2, LDHA.…”

Molecular insights into Sertoli cell function: how do metabolic disorders in childhood and adolescence affect spermatogonial fate?

“…In detail, estrogens appear to modulate glucose transporter type 3 (Glut3) and Ldh mRNAs 108 . One study demonstrated that exogenous estradiol benzoate treatment in 4-week-old (prepubertal) rats caused subsequently azoospermia 109 . Furthermore, Glut3 mRNA was upregulated, while monocarboxylate transporter 2 (Mct2) and monocarboxylate transporter 4 (Mct4) mRNAs were downregulated 109 , suggesting that estrogens may promote the internalization of glucose but inhibit the export of lactate which is essential to support GCs.…”

“…One study demonstrated that exogenous estradiol benzoate treatment in 4-week-old (prepubertal) rats caused subsequently azoospermia 109 . Furthermore, Glut3 mRNA was upregulated, while monocarboxylate transporter 2 (Mct2) and monocarboxylate transporter 4 (Mct4) mRNAs were downregulated 109 , suggesting that estrogens may promote the internalization of glucose but inhibit the export of lactate which is essential to support GCs. Another study showed that both E 2 and bisphenol A increased oxidative stress and decreased insulin, Ir, Irs1, PI3K, and Glut2 protein levels in 3-month-old rat testis 110 .…”