Development of in Vitro Systems for the Diagnosis of Human Sperm Function

1988 ◽  
pp. 99-111 ◽  
Author(s):  
R. J. Aitken ◽  
D. S. Irvine ◽  
J. S. Clarkson ◽  
D. W. Richardson
Andrologia ◽  
2006 ◽  
Vol 38 (2) ◽  
pp. 39-47 ◽  
Author(s):  
S. Pflieger-Bruss ◽  
S. Heitkamp ◽  
S. Hagemann ◽  
W. Korner ◽  
F.-M. Kohn ◽  
...  
Keyword(s):  

2017 ◽  
Vol 29 (6) ◽  
pp. 1169 ◽  
Author(s):  
Nicola A. Pascarelli ◽  
Antonella Fioravanti ◽  
Elena Moretti ◽  
Giacomo M. Guidelli ◽  
Lucia Mazzi ◽  
...  

Tumour necrosis factor (TNF)-α is primarily involved in the regulation of cell proliferation and apoptosis; in addition it possesses pro-inflammatory properties. Anti-TNF-α strategies involve either administration of anti-TNF-α antibody or soluble TNF receptor to mop up circulating TNF-α. Etanercept, a recombinant human TNF-α receptor, was found to be effective in the treatment of rheumatoid arthritis. The impact of TNF-α inhibitors on human fertility is of notable interest. This in vitro study investigated the effect of different concentrations of TNF-α and etanercept used alone or in combination on sperm viability, motility, mitochondrial function, percentage of apoptosis and chromatin integrity in swim-up selected human spermatozoa. A negative effect of TNF-α (300 and 500 ng mL–1) and etanercept (from 800 µg mL–1 to 2000 µg mL–1) individually on sperm viability, motility, mitochondrial function, percentage of apoptotic spermatozoa and sperm DNA integrity was demonstrated. However, at concentrations of 100 and 200 µg mL–1, etanercept can block, in a significant way, the toxic effects of TNF-α (500 ng mL–1) on studied sperm characteristics. Our results confirm that TNF-α has a detrimental effect on sperm function and suggest, for the first time, that etanercept may counteract the in vitro toxic action of TNF-α. This data appears to be quite promising, although further studies, both in vivo and in vitro, are needed to understand the exact mechanism of action of TNF-α and TNF-α antagonists on sperm function.


1988 ◽  
Vol 49 (2) ◽  
pp. 272-277 ◽  
Author(s):  
De Yi Liu ◽  
Yvonne P. Du Plessis ◽  
Penny L. Nayudu ◽  
W. Ian H. Johnston ◽  
H.W. Gordon Baker

Reproduction ◽  
2015 ◽  
Vol 150 (1) ◽  
pp. 77-84 ◽  
Author(s):  
J M D Portela ◽  
R S Tavares ◽  
P C Mota ◽  
J Ramalho-Santos ◽  
S Amaral

Diabetes mellitus (DM) represents one of the greatest concerns to global health and it is associated with diverse clinical complications, including reproductive dysfunction. Given the multifactorial nature of DM, the mechanisms that underlie reproductive dysfunction remain unclear. Considering that hyperglycemia has been described as a major effector of the disease pathophysiology, we used anin vitroapproach to address the isolated effect of high glucose conditions on human sperm function, thus avoiding otherin vivoconfounding players. We performed a complete and integrated analysis by measuring a variety of important indicators of spermatozoa functionality (such as motility, viability, capacitation status, acrosomal integrity, mitochondrial superoxide production and membrane potential) in human sperm samples after incubation withd- andl-glucose (5, 25, or 50 mM) for 24 and 48 h. No direct effects promoted by 25 or 50 mMd-glucose were found for any of the parameters assessed (P>0.05), except for the acrosome reaction, which was potentiated after 48 h of exposure to 50 mMd-glucose (P<0.05). Interestingly, non-metabolizablel-glucose drastically increased superoxide production (P<0.05) and suppressed sperm motility (P<0.05) and capacitation (P<0.05) after 24 h of treatment, whereas mitochondrial membrane potential (P<0.05), acrosomal integrity (P<0.01) and viability (P<0.05) were later decreased. The overall results suggest that high glucose levelsper sedo not influence human sperm functionin vitro, which stresses the importance of other factors involved in DM pathology. Nevertheless, the absence of metabolizable glucose contributes to a severe impairment of sperm function and thus compromises male fertility.Free Portuguese abstract: A Portuguese translation of this abstract is freely available athttp://www.reproduction-online.org/content/150/1/77/suppl/DC1.


2020 ◽  
Vol 32 (6) ◽  
pp. 629
Author(s):  
Xinyi Sun ◽  
Wenqiong Chen ◽  
Shiqi Weng ◽  
Tingting Pan ◽  
Xiaonian Hu ◽  
...  

Di-2-ethylhexyl phthalate (DEHP), a plastic-derived, endocrine-disrupting chemical, has been shown to exhibit male reproductive toxicity. However, its effects on human mature spermatozoa are largely unknown. In this study we investigated the invitro effects of DEHP and mono-2-ethylhexyl phthalate (MEHP; the main metabolite of DEHP) on sperm function and the mechanisms involved. Human spermatozoa were exposed to phthalates invitro at the doses that cover the concentrations detected in human semen: 20nM–8 μM DEHP, 1nM–20 μM MEHP or a mixture of 20nM–8 μM DEHP and 1nM–20 μM MEHP. DEHP and MEHP, alone or in combination, had no effect on the viability, membrane integrity, motility, homeostasis of reactive oxygen species or mitochondrial activity of human spermatozoa. Interestingly, 1nM–20 μM MEHP and combinations of 20nM–8 μM DEHP and 1nM–20 μM MEHP enhanced penetration ability, hyperactivation and the spontaneous acrosome reaction of human spermatozoa, and increased intracellular free Ca2+ concentrations ([Ca2+]i) and tyrosine phosphorylation, two key signalling pathways that regulate sperm function. The findings of this study suggest that invitro exposure to MEHP metabolised from DEHP affects human sperm function by inducing increases in sperm [Ca2+]i and tyrosine phosphorylation, which adds to our understanding of the effects of DEHP on male reproduction.


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