Ritalinic Acid Stimulates Human Sperm Motility and Maintains Vitality In Vitro

Proteomic Signatures in Spermatozoa Reveal the Role of Paternal Factors in Recurrent Pregnancy Loss

Proteomic analysis reveals dysregulated cell signaling in ejaculated spermatozoa from infertile men / 亚洲男科学杂志(英文版)

Dysfunctional sperm maturation is the primary reason for the poor sperm motility and morphology in infertile men. Spermatozoa from infertile men were fractioned on three-layer density gradient (80%, 60%, and 40%). Fraction 1 (F1) refers to the least mature stage having the lowest density, whereas the fraction 4 (F4) includes the most dense and morphologically mature motile spermatozoa. Fraction 2 (F2) and fraction 3 (F3) represent the intermediate stages. Proteins were extracted and separated by 1-dimensional gel. Bands were digested with trypsin and analyzed on a LTQ-Orbitrap Elite hybrid mass spectrometer system. Functional annotations of proteins were obtained using bioinformatics tools and pathway databases. A total of 1585 proteins were detected in the four fractions of spermatozoa. A dysregulated protein turnover and protein folding may lead to accumulation of defective proteins or proteins that otherwise would have been eliminated during the process of maturation, resulting in the impairment of sperm function. Aberrant chaperone expression may be a major contributing factor to the defective sperm function. Androgen receptor was predicted as a transcription regulator in one of the networks and the affected pathways were chaperone-mediated stress response, proteosomal pathway, and sperm function. The downregulation of key pathways and proteins which compromises the fertilizing potential of spermatozoa may provide insight into the mechanisms that lead to male infertility.

Male Oxidative Stress Infertility (MOSI): Proposed Terminology and Clinical Practice Guidelines for Management of Idiopathic Male Infertility

Despite advances in the field of male reproductive health, idiopathic male infertility, in which a man has altered semen characteristics without an identifiable cause and there is no female factor infertility, remains a challenging condition to diagnose and manage. Increasing evidence suggests that oxidative stress (OS) plays an independent role in the etiology of male infertility, with 30% to 80% of infertile men having elevated seminal reactive oxygen species levels. OS can negatively affect fertility via a number of pathways, including interference with capacitation and possible damage to sperm membrane and DNA, which may impair the sperm's potential to fertilize an egg and develop into a healthy embryo. Adequate evaluation of male reproductive potential should therefore include an assessment of sperm OS. We propose the term Male Oxidative Stress Infertility, or MOSI, as a novel descriptor for infertile men with abnormal semen characteristics and OS, including many patients who were previously classified as having idiopathic male infertility. Oxidation-reduction potential (ORP) can be a useful clinical biomarker for the classification of MOSI, as it takes into account the levels of both oxidants and reductants (antioxidants). Current treatment protocols for OS, including the use of antioxidants, are not evidence-based and have the potential for complications and increased healthcare-related expenditures. Utilizing an easy, reproducible, and cost-effective test to measure ORP may provide a more targeted, reliable approach for administering antioxidant therapy while minimizing the risk of antioxidant overdose. With the increasing awareness and understanding of MOSI as a distinct male infertility diagnosis, future research endeavors can facilitate the development of evidence-based treatments that target its underlying cause.

Response of testicular antioxidant enzymes to hexachlorocyclohexane is species specific / 亚洲男科学杂志(英文版)

<p><b>AIM</b>To find out whether the response of testicular oxidative stress parameters to hexachlorocyclohexane (HCH) is species specific.</p><p><b>METHODS</b>In rats and mice (n=5 in each group), HCH was administered at a dose of 20 mg/kg/day intraperitoneally for 30 days in 0.1 ml of refined groundnut oil. The control groups received equal volume of the vehicle. Animals were sacrificed 24 hours after the last injection and various oxidative stress parameters were measured immediately.</p><p><b>RESULTS</b>The level of both endogenous as well as FeSO4 and ascorbic acid-stimulated lipid peroxidation was increased significantly in the HCH-treated rats, whereas the pattern was just the reverse in case of mice. Although the level of H2O2 content increased in response to HCH in both groups, a totally different trend was observed for the activity of the principal H2O2-metabolising enzyme, catalase. In case of rats, a significant decline in the activity of catalase was recorded in response to HCH whereas a sharp augmentation in the enzyme activity was noticed in mice. Similarly, the decreased activity of superoxide dismutase observed in rats remained unaltered in mice.</p><p><b>CONCLUSION</b>HCH induces oxidative stress in the testis of both rats and mice. However, the pattern of response of testicular oxidative stress parameters seems to be species specific.</p>