Sperm viability, apoptosis, and intracellular reactive oxygen species levels in human spermatozoa before and after induction of oxidative stress

Mahfouz, R.; Plessis, Stefan S. du; Aziz, Nabil; Sharma, Rakesh; Sabanegh, Edmund; Agarwal, Ashok

doi:10.1016/j.fertnstert.2008.10.068

Cited by 149 publications

(100 citation statements)

References 40 publications

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“…This is in agreement with the ultrastructural findings of Collodel et al [110], who observed a high percentage of sperm with anomalies typical of apoptosis, as well as of necrosis, from individuals affected by urogenital bacterial infection, although the percentage of necrotic sperm was predominant in the majority of infected semen samples. Moreover, sperm apoptosis and necrosis were also induced under experimental high-ROS conditions [111]. These observations are supported by a recent report that showed a lack of correlation between ROS and DNA fragmentation in semen, as well as a correlation between sperm-damaged DNA and mitochondrial depolarization, suggesting that intrinsic mitochondrial-dependent apoptotic pathways might not have a major impact on sperm DNA fragmentation [112].…”

Section: Apoptosis/necrosissupporting

confidence: 70%

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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Section: Apoptosis/necrosissupporting

confidence: 70%

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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“…Mitochondria are the main source of sperm-produced ROS, notably via the formation of superoxide in the ETC, although NADPH oxidase may also be an additional source (Koppers et al 2008, Kothari et al 2010. Importantly, controlled ROS levels are needed for proper sperm function (notably for motility, capacitation, the acrosome reaction, hyperactivation and fertilising ability), while ROS can also have a pathological effect on the male gamete, if in excess, or if there is an imbalance with available antioxidant defences, resulting in a decrease in viability, motility, MMP, and increases in DNA damage, morphology defects and lipid peroxidation, possibly resulting in apoptosis-like phenomena, as will be discussed below (Kothari et al 2010, Mahfouz et al 2010, Aitken et al 2012b. The recent development of specific probes for mitochondria-produced ROS (mROS) shows that excessive production results in membrane peroxidation and loss of motility (Koppers et al 2008, Aitken et al 2012a).…”

Section: Ros Productionmentioning

confidence: 99%

Mitochondria functionality and sperm quality

Amaral¹,

Lourenço²,

Marques³

et al. 2013

Reproduction

402

309

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Although mitochondria are best known for being the eukaryotic cell powerhouses, these organelles participate in various cellular functions besides ATP production, such as calcium homoeostasis, generation of reactive oxygen species (ROS), the intrinsic apoptotic pathway and steroid hormone biosynthesis. The aim of this review was to discuss the putative roles of mitochondria in mammalian sperm function and how they may relate to sperm quality and fertilisation ability, particularly in humans. Although paternal mitochondria are degraded inside the zygote, sperm mitochondrial functionality seems to be critical for fertilisation. Indeed, changes in mitochondrial integrity/functionality, namely defects in mitochondrial ultrastructure or in the mitochondrial genome, transcriptome or proteome, as well as low mitochondrial membrane potential or altered oxygen consumption, have been correlated with loss of sperm function (particularly with decreased motility). Results from genetically engineered mouse models also confirmed this trend. On the other hand, increasing evidence suggests that mitochondria derived ATP is not crucial for sperm motility and that glycolysis may be the main ATP supplier for this particular aspect of sperm function. However, there are contradictory data in the literature regarding sperm bioenergetics. The relevance of sperm mitochondria may thus be associated with their role in other physiological features, particularly with the production of ROS, which in controlled levels are needed for proper sperm function. Sperm mitochondria may also serve as intracellular Ca 2C stores, although their role in signalling is still unclear.

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“…For each sample, 10 000 events were collected. 25 Measurement of DNA damage Genomic DNA damage was measured using a single cell gel electrophoresis assay (comet assay). Briefly, rat Leydig cells from each of the three groups were embedded in 0.6% (w/v) low melting point agarose and then lysed in 2.5 mol l 21 NaCl, 100 mmol l 21 EDTA, 10 mmol l Tris-HCl (pH 10), 1% (v/v) Triton X-100 at 4 uC overnight.…”

Section: Electron Microscope Analysismentioning

confidence: 99%

Chronic stress induces ageing-associated degeneration in rat Leydig cells

Wang¹,

Wang²,

Chen³

et al. 2012

Asian J Androl

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Several studies have suggested that stress and ageing exert inhibitory effects on rat Leydig cells. In a pattern similar to the normal process of Leydig cell ageing, stress-mediated increases in glucocorticoid levels inhibit steroidogenic enzyme expression that then results in decreased testosterone secretion. We hypothesized that chronic stress accelerates the degenerative changes associated with ageing in Leydig cells. To test this hypothesis, we established a model of chronic stress to evaluate stress-induced morphological and functional alterations in Brown Norway rat Leydig cells; additionally, intracellular lipofuscin levels, reactive oxygen species (ROS) levels and DNA damage were assessed. The results showed that chronic stress accelerated ageing-related changes: ultrastructural alterations associated with ageing, cellular lipofuscin accumulation, increased ROS levels and more extensive DNA damage were observed. Additionally, testosterone levels were decreased. This study sheds new light on the idea that chronic stress contributes to the degenerative changes associated with ageing in rat Leydig cells in vivo.

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Sperm viability, apoptosis, and intracellular reactive oxygen species levels in human spermatozoa before and after induction of oxidative stress

Cited by 149 publications

References 40 publications

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

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

Mitochondria functionality and sperm quality

Chronic stress induces ageing-associated degeneration in rat Leydig cells

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