17β-estradiol modifies human spermatozoa mitochondrial function in vitro

Kotwicka, Małgorzata; Skibinska, Izabela; Jendraszak, Magdalena; Jȩdrzejczak, Piotr

doi:10.1186/s12958-016-0186-5

Cited by 20 publications

(12 citation statements)

References 43 publications

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“…It appears because of the proven middle piece localization of ERs in sperm. This region of sperm cell is characteristic for mitochondrial incidence, and mitochondria are possibly target organelles for oestrogen action [98]. In addition, there is proof that mitochondrial enzymes in the testis such as succinate dehydrogenase, malate dehydrogenase, isocitrate dehydrogenase, monoamine oxidase and NAD dehydrogenase decreased after BPA exposure [99].…”

Section: Spermatogenesis and Sperm Function Affected By Bpamentioning

confidence: 98%

Male Reproduction: One of the Primary Targets of Bisphenol

Jambor¹,

Bistakova²,

Greifova³

et al. 2017

Bisphenol a Exposure and Health Risks

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Infertility is a major health issue affecting human life. The most notable factors causing male infertility is exposure to environmental contaminants. Bisphenol A (BPA) is a common toxic environmental contaminant. Human population is exposed to bisphenol A through air, water, food and a variety of industrial products. Growing evidence from research on laboratory animals supports the hypothesis that bisphenol A is able to adversely affect male reproductive function. The specific mechanisms of action of bisphenol A are wide but not definite. Bisphenol A interferes with the hormonal metabolism and regulation, binding affinity or enzymatic activity, resulting in a deviation from a normal reproductive behaviour. Binding ability to androgen and oestrogen receptors, as well as other properties, is currently investigated. A decreased sperm count, inhibition of sperm motility and reduction of organ weights were observed and linked with oxidative stress after bisphenol A treatment. In addition, prenatal exposure to bisphenol A may lead to adverse effects in the offspring. In this review, we address the topic of BPA effects on male reproductive function and emphasize its effects on testicular steroidogenesis and spermatogenesis. A considerably more detailed and systematic research focusing on bisphenol A toxicology is required for a better understanding of risks associated with exposure to this endocrine disruptor.

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Section: Spermatogenesis and Sperm Function Affected By Bpamentioning

confidence: 98%

Male Reproduction: One of the Primary Targets of Bisphenol

Jambor¹,

Bistakova²,

Greifova³

et al. 2017

Bisphenol a Exposure and Health Risks

View full text Add to dashboard Cite

show abstract

“…As a consequence, emphasis has shifted away from dihydroethidium and toward a charged version of this molecule, MitoSox™ Red, which is able to localize within sperm mitochondria and reflect the capacity of these organelles to generate

{normalO}_{2}^{- •}

. As an example, Kotwicka and colleagues recently used this probe to demonstrate that estradiol‐17β is able to stimulate mitochondrial ROS generation in populations of human spermatozoa (Kotwicka, Skibinska, Jendraszak, and Jedrzejczak, 2016).…”

Section: Detection Of Ros In the Male Germ Linementioning

confidence: 99%

Reactive oxygen species as mediators of sperm capacitation and pathological damage

Aitken

2017

Molecular Reproduction Devel

472

370

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Oxidative stress plays a major role in the life and death of mammalian spermatozoa.These gametes are professional generators of reactive oxygen species (ROS), which appear to derive from three potential sources: sperm mitochondria, cytosolic L-amino acid oxidases, and plasma membrane Nicotinamide adenine dinucleotide phosphate oxidases. The oxidative stress created via these sources appears to play a significant role in driving the physiological changes associated with sperm capacitation through the stimulation of a cyclic adenosine monophosphate/Protein kinase A phosphorylation cascade, including the activation of Extracellular signal regulated kinase-like proteins, massive up-regulation of tyrosine phosphorylation in the sperm tail, as well as the induction of sterol oxidation. When generated in excess, however, ROS can induce lipid peroxidation that, in turn, disrupts membrane characteristics that are critical for the maintenance of sperm function, including the capacity to fertilize an egg.Furthermore, the lipid aldehydes generated as a consequence of lipid peroxidation bind to proteins in the mitochondrial electron transport chain, triggering yet more ROS generation in a self-perpetuating cycle. The high levels of oxidative stress created as a result of this process ultimately damage the DNA in the sperm nucleus; indeed, DNA damage in the male germ line appears to be predominantly induced oxidatively, reflecting the vulnerability of these cells to such stress. Extensive evaluation of antioxidants that protect the spermatozoa against oxidative stress while permitting the normal reduction-oxidation regulation of sperm capacitation is therefore currently being undertaken, and has already proven efficacious in animal models. | INTRODUCTIONCapacitation is a key feature of mammalian sperm cell biology, and was independently reported by Chang (1951) and Austin (1951); its discovery was a sentinel for unwrapping the mysteries of mammalian fertilization.Completion of capacitation provides sperm with a series of behaviours that are essential for the achievement of fertilization, including hyperactivated motility, sperm-zona pellucida recognition, and acrosome exocytosis. Despite being aware of capacitation for more than half a century, the molecular mechanisms that underpin this process at a physiological level are still far from resolved (Aitken & Nixon, 2013). We do know that capacitation involves an efflux of cholesterol from the sperm plasma membrane (Davis, 1981) and a global increase in tyrosine phosphorylation (Visconti et al., 1995). Yet, our understanding of how these elements are controlled is still quite embryonic. In this context, one insight that has emerged in the relatively recent past is that sperm capacitation is a reduction-oxidation (redox)-regulated event, promoted by the de novo generation of low levels of reactive oxygen species (ROS). One of the first scientists to discover this association was the late Claude Gagnon, who published an important paper in 1993 citing the ability of superoxide to...

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“…In addition, bisphenol A, a chemical produced in large quantities for use in the production of polycarbonate plastics and epoxy resins [ 70 ], has been found to stimulate mitochondrial ROS generation, but only when high doses (>300 µM) and prolonged exposure periods (4 h) were used. Similarly, the parent estrogen (estradiol-17β) has been found to induce mitochondrial ROS generation in high doses [ 71 ], possibly after being converted to catechol estrogens that are much more redox active than estradiol-17β and constitute powerful inducers of mitochondrial ROS generation by human spermatozoa, as well as other cell types [ 66 , 69 , 72 ]. All of these oestrogen-like compounds that are capable of eliciting mitochondrial ROS generation by human spermatozoa share a key structural feature, which is a hydroxylated aromatic ring ( Figure 1 ).…”

Section: Sources Of Ros In the Human Ejaculatementioning

confidence: 99%

Male Infertility and Oxidative Stress: A Focus on the Underlying Mechanisms

et al. 2022

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Reactive oxygen species (ROS) play a critical role in defining the functional competence of human spermatozoa. When generated in moderate amounts, ROS promote sperm capacitation by facilitating cholesterol efflux from the plasma membrane, enhancing cAMP generation, inducing cytoplasmic alkalinization, increasing intracellular calcium levels, and stimulating the protein phosphorylation events that drive the attainment of a capacitated state. However, when ROS generation is excessive and/or the antioxidant defences of the reproductive system are compromised, a state of oxidative stress may be induced that disrupts the fertilizing capacity of the spermatozoa and the structural integrity of their DNA. This article focusses on the sources of ROS within this system and examines the circumstances under which the adequacy of antioxidant protection might become a limiting factor. Seminal leukocyte contamination can contribute to oxidative stress in the ejaculate while, in the germ line, the dysregulation of electron transport in the sperm mitochondria, elevated NADPH oxidase activity, or the excessive stimulation of amino acid oxidase action are all potential contributors to oxidative stress. A knowledge of the mechanisms responsible for creating such stress within the human ejaculate is essential in order to develop better antioxidant strategies that avoid the unintentional creation of its reductive counterpart.

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17β-estradiol modifies human spermatozoa mitochondrial function in vitro

Cited by 20 publications

References 43 publications

Male Reproduction: One of the Primary Targets of Bisphenol

Male Reproduction: One of the Primary Targets of Bisphenol

Reactive oxygen species as mediators of sperm capacitation and pathological damage

Male Infertility and Oxidative Stress: A Focus on the Underlying Mechanisms

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