Moringa oleifera-based feed supplement protects against renal ischaemia/reperfusion injury via downregulation of Bax/caspase 3 signaling.

Introduction: Ischaemia/reperfusion (I/R) may lead to acute kidney injury via the induction of oxidative stress. On the other hand, Moringa oleifera has been reported to exert antioxidant activities. This study was designed to assess whether or not Moringa oleifera-based feed supplement could prevent I/R-induced renal injury. Materials and methods: Renal I/R was induced by occluding the right renal artery for 30 min followed by a 2-h reperfusion. Results: Renal I/R led to increased absolute renal weight and renal organo-somatic weight index. Renal I/R also caused distortion of renal histoarchitecture and impaired renal function evidenced by elevated serum creatinine and blood urea nitrogen. In addition, renal I/R significantly elevated renal levels of hydrogen peroxide, MDA, and advanced oxidation protein products, but suppressed the levels of reduced glutathione, protein thiol, and non-protein thiol, and the activities of superoxide dismutase and glutathione peroxidase. In addition, renal I/R up-regulated myeloperoxidase activity and the renal levels of NO, TNF-α, and IL-6. Renal I/R also up-regulated Bax and caspase 3 expression in the kidney. Furthermore, I/R-driven structural and biochemical alterations were markedly inhibited by Moringa oleifera-based feed supplement. Discussion: These results suggest that Moringa oleifera-based feed supplement may preserve the gross and histoarchitectural integrity of the kidney as well as renal function via downregulation of Bax/caspase 3 signaling by targeting oxidative stress, inflammation and apoptosis in the kidney of I/R rat.

Impact of organophosphate pesticides exposure on human semen parameters and testosterone: a systematic review and meta-analysis.

Background: Organophosphate (OP) pesticides have been associated with a decline in semen quality, although there are still considerable arguments about the magnitude of the association. Objective: This study provides a systematic review and meta-analysis of the impacts of OP pesticides on semen quality and male reproductive hormones. Methods: This study was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) protocols. Strategic search was conducted using combined text words as search terms. The eligibility criteria were developed based on Population, Exposure, Comparator, Outcome, and Study designs (PECOS) framework. Relevant data were extracted, risk of bias was evaluated by The Office of Health Assessment and Translation (OHAT) tool, and certainty of evidence was assessed by the Grading of Recommendations Assessment, Development and Evaluation (GRADE) Working Group guidelines. Quantitative meta-analysis was performed by using Review Manager. Results: A total of 766 male subjects (349 exposed to OP pesticides and 417 unexposed controls) were included in the meta-analysis. There was no significant difference in the ejaculate volume, seminal fluid volume, sperm multiple anomaly index, sperm, and leukocytes levels of the OP-exposed subjects compared to the control. In addition, OP pesticides exposure did not significantly affect serum concentrations of FSH, LH, and testosterone in subjects who were exposed to OP pesticides compared to their unexposed counterparts. However, we found a significant reduction in the sperm count, sperm concentration, progressive sperm motility, total sperm motility, and normal sperm morphology of OP pesticides-exposed subjects compared to the unexposed subjects. However, after subtype and sensitivity analyses, exposure to OP pesticides did not reduce sperm count. Also, after sensitivity analysis, OP pesticides exposure did not alter progressive sperm motility. Conclusion: This study demonstrates that OP pesticides exposure reduced sperm count, concentration, total and progressive motility, and normal sperm morphology, possibly via a testosterone-independent mechanism.

Impact of stress on male fertility: role of gonadotropin inhibitory hormone.

Studies have implicated oxidative stress-sensitive signaling in the pathogenesis of stress-induced male infertility. However, apart from oxidative stress, gonadotropin inhibitory hormone (GnIH) plays a major role. The present study provides a detailed review of the role of GnIH in stress-induced male infertility. Available evidence-based data revealed that GnIH enhances the release of corticosteroids by activating the hypothalamic-pituitary-adrenal axis. GnIH also mediates the inhibition of the conversion of thyroxine (T4) to triiodothyronine (T3) by suppressing the hypothalamic-pituitary-thyroidal axis. In addition, GnIH inhibits gonadotropin-releasing hormone (GnRH), thus suppressing the hypothalamic-pituitary-testicular axis, and by extension testosterone biosynthesis. More so, GnIH inhibits kisspeptin release. These events distort testicular histoarchitecture, impair testicular and adrenal steroidogenesis, lower spermatogenesis, and deteriorate sperm quality and function. In conclusion, GnIH, via multiple mechanisms, plays a key role in stress-induced male infertility. Suppression of GnIH under stressful conditions may thus be a beneficial prophylactic and/or therapeutic strategy.

Viral Infections and Male Infertility: A Comprehensive Review of the Role of Oxidative Stress.

Viral infections have been a part of human existence to date, though viruses have posed a huge threat with various outbreaks lately. These threats are associated with reproductive health challenges, especially male infertility. The prime focus of this review is to highlight the mechanisms associated with viral infection-induced male infertility/subfertility and identify new treatment strategies with the aim to preserve male fertility. The reviewed data showed that viral infections stimulate inflammatory responses, resulting in the release of proinflammatory cytokines, which induces oxidative stress. This oxido-inflammatory cycle could continue in a vicious cycle and threaten male fertility. Existing data from human and experimental studies show that viral infection-induced oxido-inflammatory response results in testicular damage, atrophy of the seminiferous tubules and Sertoli cells, and reduced Leydig cell mass. This is accompanied by reduced circulatory testosterone, impaired spermatogenesis, reduced sperm motility, lipid peroxidation, DNA fragmentation and apoptosis of the sperm cells. Based on the available pieces of evidence, antioxidant therapy, in vivo and in vitro, may be beneficial and protects against the potential risk of male infertility from viral infection. It is, however recommended that more clinical studies be conducted to demonstrate the possible protective roles of antioxidants used as adjuvant therapy in viral infections, and in the in vitro treatment of semen samples for those utilizing semen washing and artificial reproductive techniques.

Influence of ejaculatory abstinence period on semen quality of 5165 normozoospermic and oligozoospermic Nigerian men: A retrospective study.

Background and Aims: Several studies have shown that the length of ejaculatory abstinence alters sperm quality. However, the available data are conflicting and none seems to exist in a Nigerian population. The present study aims to compare the semen quality in normozoospermic and oligozoospermic semen samples of a homogenous Nigerian population, following varying ejaculatory abstinence days (EAD); less than 2, 2-3, and 3-7 days. Methods: The present retrospective study included 5165 semen samples collected over 5 years, from April 2015 to April 2020. Results: In normozoospermic samples, sperm count and total sperm count were significantly higher in prolonged EAD. In oligozoospermic patients, semen volume significantly increased with prolonged EAD, while sperm count, total sperm count, and progressive motility were significantly reduced with prolonged EAD. In addition, EAD and sperm volume positively correlated in oligozoospermic patients. Conclusion: Our findings indicate that EAD affects sperm quality in both normozoospermic and oligozoospermic men with varying impacts. Prolonged EAD increased sperm count and total sperm count in normozoospermic patients, while EAD increased semen volume but reduced sperm count, total sperm count, and progressive motility in oligozoospermic patients.