Sperm lipid peroxidation and pro-inflammatory cytokines

Martínez, Pedro A.; Proverbio, Fulgencio; Camejo, María Isabel

doi:10.1016/j.jri.2006.08.064

Cited by 24 publications

(35 citation statements)

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“…Moreover, infection-inflammation concentrations of some cytokines, such as IL-8 and TNF-alpha, either alone or in the presence of leukocytes could drive the LPO of the spermatozoa plasma membrane to a level that can affect the ability of sperm to fertilize [Martinez et al 2007].…”

Section: Discussionmentioning

confidence: 99%

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Lipid Peroxidation in Human Spermatozoa from Men with Genitourinary Infections

Cosci

Moretti

Collodel

2008

Systems Biology in Reproductive Medicine

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A fluorescent assay was used to reveal the presence of lipid peroxidation (LPO) in spermatozoa from individuals with genitourinary infections (GI). The incidence of LPO was compared with sperm pathologies (apoptosis, immaturity, necrosis) evaluated by transmission electron microscopy (TEM) and motility. A C11-BODIPY 581/591 probe was used to detect and localize LPO in sperm from 34 individuals. The sperm morphological characteristics were studied by TEM and the results were mathematically assessed. Using the LPO percentage we divided the patients into four groups. Group 1 included ten patients with GI with almost normal progressive motility, a very low percentage of LPO and sperm pathology values that were not far from the standard ranges. Group 2 had eleven infected patients showing reduced motility, LPO of 10 to 20% and sperm pathologies that were just out of normal range. Group 3 included 6 infected patients with progressive motility r22%, low levels of LPO with a higher percentage of apoptosis and necrosis. Group 4 had 7 patients showing normal semen parameters, without GI, LPO ranged from 0% to 1% and a normal incidence of sperm pathologies. In all groups, LPO was inversely correlated with sperm motility and directly correlated with low semen quality. However, the LPO percentage was low in Group 3, in which sperm necrosis, concomitant with GI, was the predominant pathology. C11-BODIPY 581/591 is a useful labeling method for quantifying and localizing LPO in spermatozoa from patients with GI. The detection of LPO could be questionable in cases of sperm necrosis because in this pathology the plasma membrane is often disrupted and the lipidic probe is unable to intercalate within the phospholipidic bilayer.

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Section: Discussionmentioning

confidence: 99%

“…It has been postulated that the effects produced by ROS depend on their nature, quantity and on the moment and length of exposure. Mammalian spermatozoa membranes are rich in polyunsaturated fatty acid and this makes them very susceptible to oxygen-induced damage, mediated by lipid peroxidation (LPO) [Sikka 2001;Martinez et al 2007].…”

Section: Introductionmentioning

confidence: 99%

Lipid Peroxidation in Human Spermatozoa from Men with Genitourinary Infections

Cosci

Moretti

Collodel

2008

Systems Biology in Reproductive Medicine

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“…The adverse effect of cytokines on sperm membrane properties might constitute one of the several mechanisms by which these immune factors interfere with sperm quality during semen bacterial infection. An increase in lipid sperm membrane peroxidation, as judged by MDA levels, has been demonstrated in the presence of some proinflammatory cytokines under both in situ [139,140] and in vitro conditions following the incubation of sperm with human recombinant proinflammatory cytokines [141,142]. However, the harmful effect of cytokines on sperm membranes appears to be closely associated with the accompanying leukocytospermia.…”

Section: Role Of the Immune/autoimmune Reactionsmentioning

confidence: 99%

Mechanisms of the harmful effects of bacterial semen infection on ejaculated human spermatozoa: potential inflammatory markers in semen

Frączek

Kurpisz

2015

Folia Histochem Cytobiol.

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The invasion of the male reproductive tract by microorganisms, and its subsequent consequences for sperm fertilizing potential, has been intensely discussed. The role of the bacteria that are responsible for the colonization and contamination of the male urogenital tract, rather than its infection, in diminished sperm parameters raises the most controversy. There are numerous premises suggesting that bacterial semen infection is associated with male infertility. However, the molecular mechanism by which the fertility is affected is complex and multifactorial, and still presents a puzzle. Some authors have suggested that direct interactions between bacteria and human spermatozoa facilitate sperm immobilization, affect sperm morphology, and thus weaken the ability of sperm to fertilize. On the other hand, the massive infiltration of activated leukocytes into the inflammatory site may be associated with impairment of sperm fertilizing potential, due to oxidative, apoptotic, and immune processes. This review presents current research trends and aims to summarize the present knowledge of semen inflammation and causative bacterial agents in the male urogenital tract, with its consequence on seminological parameters, and male fertility status.

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“…Notably, it has been reported that TNFα can induced sperm membrane lipid peroxidation by increasing ROS releasing within spermatozoa (Buch et al, 1994;Martinez et al, 2007), this may support that the TNFα plays a key role in regulation of apoptosis process throughout binding with type-1 TNFα receptor (TNFR1) within sperm membrane, this linking cause trimerazation of certain adaptor proteins, which aid to recruits and activates of caspase-8, which considered as a trigger of apoptotic cascade initiation. This process probably mediated by existence of ROS, lastly, sperm death can be occurred due to these activities (Aitken et al, 1992;Barroso et al, 2000).…”

Section: Resultsmentioning

confidence: 92%

“…Instead of, the releasing of TNFα depend on NFATC2 rather than NFAT/AP-1 pathway, (Bhushan et al, 2008;Cirl et al, 2008). In addition, other investigations were reported that TNFα can induced sperm membrane lipid peroxidation by increasing ROS releasing within spermatozoa (Buch et al, 1994;Martinez et al, 2007).…”

Section: Introductionmentioning

confidence: 99%