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Ethnopharmacological Relevance: Crassostrea gigas Thunberg and other oysters have been traditionally used in China as folk remedies to invigorate the kidney and as natural aphrodisiacs to combat male impotence., Aim of the Study: Erectile dysfunction (ED) has become a major health problem for the global ageing population. The aim of this study is therefore to evaluate the effect of peptide-rich preparations from C. gigas oysters on ED and related conditions as increasing evidence suggests that peptides are important bioactive components of marine remedies and seafood., Materials and Methods: Crassostrea oyster peptide (COP) preparations COP1, COP2 and COP3 were obtained from C. gigas oysters by trypsin, papain or sequential trypsin-papain digestion, respectively. The contents of testosterone, cyclic adenosine monophosphate (cAMP) and nitric oxide (NO) and the activity of nitric oxide synthase (NOS) in mice and/or cells were measured by enzyme-linked immunosorbent assays. Real-time PCR was used to assess the expression of genes associated with sex hormone secretion pathways. The model animal Caenorhabditis elegans was also used to analyze the gene expression of a conserved steroidogenic enzyme. In silico analysis of constituent peptides was performed using bioinformatic tools based on public databases., Results: The peptide-rich preparation COP3, in which >95% peptides were <3000 Da, was found to increase the contents of male mouse serum testosterone and cAMP, both of which are known to play important roles in erectile function, and to increase the activity of mouse penile NOS, which is closely associated with ED. Further investigation using mouse Leydig-derived TM3 cells demonstrates that COP3 was able to stimulate the production of testosterone as well as NO, a pivotal mediator of penile erection. Real-time PCR analysis reveals that COP3 up-regulated the expression of Areg and Acvr2b, the genes known to promote sex hormone secretion, but not Fst, a gene involved in suppressing follicle-stimulating hormone release. Furthermore, COP3 was also shown to up-regulate the expression of let-767, a well-conserved C. elegans gene encoding a protein homologous to human 17-β-hydroxysteroid dehydrogenases. Preliminary bioinformatic analysis using the peptide sequences in COP3 cryptome identified 19 prospective motifs, each of which occurred in more than 10 peptides., Conclusions: In this paper, Crassostrea oyster peptides were prepared by enzymatic hydrolysis and were found for the first time to increase ED-associated biochemical as well as molecular biology parameters. These results may help to explain the ethnopharmacological use of oysters and provide an important insight into the potentials of oyster peptides in overcoming ED-related health issues., (Copyright © 2020 Elsevier B.V. All rights reserved.)

In this study, we investigated the effect of acute administration of gold nanorods (AuNRs) on testicular function, sexual hormones, and oxidative stress parameters in male albino rats. Forty mature male albino rats were divided into two equal groups (n = 20/each). The first group received 1 ml saline solution intraperitoneally (i.p.). The second group received single i.p. injection of 75 μg 50 nm AuNRs/kg/bwt. Five rats from each group were sacrificed on days 1, 3, 7, and 14 post treatment and blood samples were collected for hormonal and biochemical analysis. Testes were collected from each group at each time point for histopathology, morphometric, and transmission electron microscope analyses of testis and epididymis. Results indicated that i.p. injection of AuNRs did not produce any histopathological changes. Morphometric analysis of testicular samples revealed that the height of lining epithelium was significantly (P < 0.05) higher in AuNR group on days 3 and 14 post treatment, and the minor axis of seminiferous tubules was higher (P < 0.05) in AuNR-injected rats than in control group. For the epididymis, the number of spermatozoa was significantly (P < 0.05) higher on days 7 and 14 after AuNR injection when compared with control rats. AuNRs were not detected by TEM at all time points of the experiment. Serum analysis demonstrated that total and free testosterone values significantly (P < 0.05) increased on days 1, 3, 7, and 14 post AuNR injection. LH was higher (P < 0.05) in AuNRs-injected rats on days 3, 7, and 14 post injection, while FSH values were higher (P < 0.05) in AuNR group on days 3 and 14. Malondialdehyde significantly (P < 0.05) decreased on days 3, 7, and 14 in AuNR group, while catalase, glutathione peroxidase, and superoxide dismutase values were significantly (P < 0.05) elevated on days 3, 7, and 14 in AuNRs-injected rats compared with control group. In conclusion, intraperitoneal injection of 50 nm AuNRs is safe on the reproductive function and has an antioxidant action.

Aims: Endocrinological abnormalities, including low testosterone levels, are prevalent in cirrhosis. We assessed sexual hormone status in regard to hemodynamic abnormalities and its impact on hepatic decompensation and survival. Methods: Males with cirrhosis were prospectively included in this study since 2010. Sexual hormones including bioavailable testosterone, total testosterone, luteinizing hormone, follicle‐stimulating hormone, prolactin, and sex hormone‐binding globulin as well as Child–Pugh score, Model for End‐stage Liver Disease (MELD) score, and hepatic venous pressure gradient were recorded. Sarcopenia was also assessed in patients with available computed tomography scans. Clinical follow‐up for hepatic decompensation, liver transplantation, and death was recorded until May 2017. Results: One hundred fourteen male cirrhotic patients were included: age 55 ± 9.4 years, MELD 13.5 (range, 7–20.7). Etiologies were alcoholic liver disease in 61(53.5%) patients, viral in 30 (26.3%) patients, and other in 23 (20.2%). Child–Pugh scores were A in 32 (28.1%) patients, B in 48 (42.1%), and C in 34 (29.8%). Levels of bioavailable testosterone and total testosterone decreased with advanced Child–Pugh score (P < 0.001 and P < 0.001) whereas prolactin increased (P = 0.002). Median bioavailable testosterone (0.8 ng/mL [0.1–2] vs. 1.68 ng/mL [0.07–2.65]; P = 0.004) and total testosterone (2.7 ng/mL [0.23–12.34] vs. 7 ng/mL [0.25–10]; P = 0.041) levels were lower in patients with severe portal hypertension (hepatic venous pressure gradient >12 mmHg). Median bioavailable testosterone (0.25 ng/mL [0.07–1.7] vs. 0.97 ng/mL [0.15–2.74)]; P = 0.017) and total testosterone levels (1.28 ng/mL [0.25–7.32] vs. 4.32 ng/mL [0.43–13.47]; P = 0.031) were significantly lower in sarcopenic patients. Median follow‐up was 13 months (0.2–75 months) and liver‐related events were recorded in 46 patients (40.4%; death, 31 [27.2%]). Low total testosterone was associated with an increased risk for hepatic decompensation and/or death, even after adjusting for Child–Pugh score, MELD, and other relevant factors (Child–Pugh score model: hazard ratio 2.503, 95% confidence interval, 1.214–5.157, P = 0.013; MELD model: hazard ratio 3.065, 95% confidence interval, 1.523–6.169, P = 0.002). Conclusion: In parallel to increasing severity of cirrhosis, levels of testosterone decline whereas prolactin levels increase. However, low testosterone levels are independently associated with a higher risk for hepatic decompensation and mortality. [ABSTRACT FROM AUTHOR]

Abstract: Testosterone (TES; 4-androstene-17β-ol-3-on) is found for the first time to eject electrons from its singlet excited state in water–ethanol solvent mixture. This ability was very recently also observed for 17β-estradiol (17βE2) and progesterone (PRG)/1/. With increasing TES-concentration, the yield of solvated electrons () is decreasing, because of “associate” formation. At higher absorbed UV-doses (λ =254nm) the yield is passing a sharp maximum by formation of TES–ethanol adducts, which are able likewise to emit electrons when excited. At prolonged irradiation the resulting photolytic products of TES–ethanol adducts are also able to emit electrons. The capability of the hormones: 17βE2, PRG and TES to eject electrons and the resulting metabolites, some of which can induce cancer, is discussed. [Copyright &y& Elsevier]