Effect of monensin on the enzymes of oxidative stress, thiamine pyrophosphatase and DNA integrity in rat testicular cells in vitro

2006 ◽  
Vol 58 (2-3) ◽  
pp. 203-208 ◽  
Author(s):  
Malti Singh ◽  
N.R. Kalla ◽  
S.N. Sanyal
Reproduction ◽  
2013 ◽  
Vol 146 (5) ◽  
pp. 433-441 ◽  
Author(s):  
Renata Simões ◽  
Weber Beringui Feitosa ◽  
Adriano Felipe Perez Siqueira ◽  
Marcilio Nichi ◽  
Fabíola Freitas Paula-Lopes ◽  
...  

Sperm chromatin fragmentation may be caused by a number of factors, the most significant of which is reactive oxygen species. However, little is known about the effect of sperm oxidative stress (OS) on DNA integrity, fertilization, and embryonic development in cattle. Therefore, the goal of this study was to evaluate the influence of sperm OS susceptibility on the DNA fragmentation rate and in vitro embryo production (IVP) in a population of bulls. Groups of cryopreserved sperm samples were divided into four groups, based on their susceptibility to OS (G1, low OS; G2, average OS; G3, high OS; and G4, highest OS). Our results demonstrated that the sperm DNA integrity was compromised in response to increased OS susceptibility. Furthermore, semen samples with lower susceptibility to OS were also less susceptible to DNA damage (G1, 4.06%; G2, 6.09%; G3, 6.19%; and G4, 6.20%). In addition, embryo IVP provided evidence that the embryo cleavage rate decreased as the OS increased (G1, 70.18%; G2, 62.24%; G3, 55.85%; and G4, 50.93%), but no significant difference in the blastocyst rate or the number of blastomeres was observed among the groups. The groups with greater sensitivity to OS were also associated with a greater percentage of apoptotic cells (G1, 2.6%; G2, 2.76%; G3, 5.59%; and G4, 4.49%). In conclusion, we demonstrated that an increased susceptibility to OS compromises sperm DNA integrity and consequently reduces embryo quality.


Cells ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 1789
Author(s):  
Simon Schneider ◽  
Farhad Shakeri ◽  
Christian Trötschel ◽  
Lena Arévalo ◽  
Alexander Kruse ◽  
...  

Protamines are the safeguards of the paternal sperm genome. They replace most of the histones during spermiogenesis, resulting in DNA hypercondensation, thereby protecting its genome from environmental noxa. Impaired protamination has been linked to male infertility in mice and humans in many studies. Apart from impaired DNA integrity, protamine-deficient human and murine sperm show multiple secondary effects, including decreased motility and aberrant head morphology. In this study, we use a Protamine-2 (Prm2)-deficient mouse model in combination with label-free quantitative proteomics to decipher the underlying molecular processes of these effects. We show that loss of the sperm’s antioxidant capacity, indicated by downregulation of key proteins like Superoxide dismutase type 1 (SOD1) and Peroxiredoxin 5 (PRDX5), ultimately initiates an oxidative stress-mediated destruction cascade during epididymal sperm maturation. This is confirmed by an increased level of 8-OHdG in epididymal sperm, a biomarker for oxidative stress-mediated DNA damage. Prm2-deficient testicular sperm are not affected and initiate the proper development of blastocyst stage preimplantation embryos in vitro upon intracytoplasmic sperm injection (ICSI) into oocytes. Our results provide new insight into the role of Prm2 and its downstream molecular effects on sperm function and present an important contribution to the investigation of new treatment regimens for infertile men with impaired protamination.


2018 ◽  
Vol 30 (10) ◽  
pp. 1359 ◽  
Author(s):  
L. Bittner ◽  
S. Wyck ◽  
C. Herrera ◽  
M. Siuda ◽  
C. Wrenzycki ◽  
...  

Oxidative stress in spermatozoa has effects on subsequent embryo development. The aim of the present study was to elucidate whether sperm oxidative stress results in increased DNA damage in the embryo. To this end, bovine spermatozoa were incubated for 1 h at 37°C without or with 100 µM H2O2, resulting in non-oxidised (NOX-S) and oxidised (OX-S) spermatozoa respectively. Non-incubated spermatozoa served as the control group (CON-S). After IVF, developmental rates 30, 46 and 60 h and 7 days after IVF were assessed. DNA damage was analysed in embryos using the comet assay and a DNA damage marker (γH2AX immunostaining); the apoptotic index was determined in blastocysts. Exposure of spermatozoa to H2O2 induced a significant amount of sperm chromatin damage. The use of OX-S in IVF resulted in significantly reduced cleavage and blastocyst rates compared with the use of CON-S and NOX-S. Furthermore, in embryos resulting from the use of OX-S, a developmental delay was evident 30 and 46 h after IVF. γH2AX immunostaining was lower in blastocysts than in early embryos. In blastocysts, the comet and apoptotic indices were significantly higher in embryos resulting from the use of OX-S than CON-S and NOX-S. In conclusion, oxidative stress in spermatozoa induces developmental abnormalities and is a source of DNA damage in the resulting embryos.


2021 ◽  
Author(s):  
Roland Eghoghosoa Akhigbe ◽  
Moses Agbomhere Hamed ◽  
Lydia Oluwatoyin Ajayi ◽  
Davinson Chuka Anyogu ◽  
Ayodeji Folorunsho Ajayi

Abstract Purpose This study assessed the in vitro effect of codeine, a popular drug of abuse, on human spermatozoa motility, plasma membrane integrity, DNA integrity, and oxidative stress. Materials and Methods Semen samples were collected from fifteen healthy donors and conventional semen analysis was carried out per the guideline of the World Health Organization. Direct Swim-up technique was performed to obtain highly motile sperm. Samples were incubated at 34.5°C with different concentrations (0, 0.1, 1, 5 and 10 mM) of codeine. The non-exposed (0 mM) was used as the control group. Sperm motility and DNA integrity were assessed at 30, 60, and 90 minutes, while sperm membrane integrity and sperm 8-OHdG level were determined at 90 minutes. Results Codeine at any tested concentration significantly reduced sperm motility and plasma membrane integrity but increased sperm 8-OHdG level compared to the control in a time-dependent manner. Furthermore, codeine at 1, 5, and 10 mM markedly increased sperm DNA damage. In addition, correlation study showed that sperm 8OHdG level was negatively associated with sperm motility, plasma membrane integrity, and DNA integrity. Conclusions Codeine may impair human spermatozoa fertilization capacity by inducing sperm dysmotility and damage to the sperm plasma membrane and DNA through an oxidative stress-dependent mechanism.


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