Protein Glycation

Wautier, Jean‐Luc; Schmidt, Ann Marie

doi:10.1161/01.res.0000137876.28454.64

Cited by 364 publications

(79 citation statements)

References 54 publications

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“…In diabetes, there is evidence both in men and in animal models, whether spontaneously occurring (O'Neill et al 2009) or chemically induced diabetic mice (Shrilatha & Muralidhara 2007a, O'Neill et al 2009) and rats (Shrilatha & Muralidhara 2007b), that the condition is associated with marked increases in oxidative stress and sperm nDNA damage. Hyperglycaemia is known to cause oxidative stress (Wautier & Schmidt 2004, Chekir et al 2006 and to accelerate the accumulation of advanced glycation end products and their receptor RAGE, both of which are capable of generating, promoting and/or amplifying oxidative stress and its detrimental consequences. It is this amplification and extension of the injurious oxidative environment that may be responsible for the damage seen in the previously mentioned studies.…”

Section: Discussionmentioning

confidence: 99%

Spermatogenic and sperm quality differences in an experimental model of metabolic syndrome and hypogonadal hypogonadism

Mallidis¹,

Czerwiec²,

Filippi³

et al. 2011

Reproduction

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The synergistic effect of the co-morbidities that comprise metabolic syndrome (MetS) is increasingly being recognised as an important contributor in the pathology of a broad spectrum of seemingly disparate conditions. However, in terms of male reproductive function, beyond erectile dysfunction, little is known about the influence of this cohort (collectively or separately) on spermatogenesis and sperm quality. The aims of this study were to assess the reproductive tract of a MetS animal model for detrimental changes, to determine whether a group of compounds (advanced glycation end products and their receptor) known to cause cell dysfunction and DNA damage was present and assess whether hypogonadotropic hypogonadism was the main contributing factor for the changes seen. Animals fed a high-fat diet were found to have significantly increased cholesterol, triglycerides, blood glucose, mean arterial pressure and visceral fat levels. Although serum testosterone was decreased, no changes were seen in either testicular or epididymal histology. Immunolocalisation of N 3 -carboxymethyl-lysine and the receptor for advanced glycation end products was found in the testes, epididymides and sperm of the two treated groups of animals; however, ELISA did not show any difference in protein levels. Similarly, assessment of sperm nuclear DNA (nDNA) fragmentation by acridine orange test did not find significant differences in nDNA integrity. We conclude that the minimal effect on spermatogenesis and sperm quality seen in our model is probably due to the moderate increase of blood glucose rather than the hypogonadism.

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Section: Discussionmentioning

confidence: 99%

Spermatogenic and sperm quality differences in an experimental model of metabolic syndrome and hypogonadal hypogonadism

Mallidis¹,

Czerwiec²,

Filippi³

et al. 2011

Reproduction

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“…Interestingly, diabetic men who presented normal semen parameters showed significantly higher levels of damage in sperm nuclear and mitochondrial DNA, probably resulting from supraphysiological glucose levels and related oxidative stress . Additionally, advanced glycation end products that result from oxidative damage have been implicated in an increasing number of diabetic complications and have been detected at higher levels in the reproductive tract, seminal plasma and sperm of type 1 and type 2 diabetic males (Wautier & Schmidt 2004), which suggests their involvement in reactive oxygen species (ROS)-initiated sperm DNA damage.…”

Section: Introductionmentioning

confidence: 99%

High glucose concentrations per se do not adversely affect human sperm function in vitro

et al. 2015

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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 an in vitro approach to address the isolated effect of high glucose conditions on human sperm function, thus avoiding other in vivo confounding 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 with D-and L-glucose (5, 25, or 50 mM) for 24 and 48 h. No direct effects promoted by 25 or 50 mM D-glucose were found for any of the parameters assessed (PO0.05), except for the acrosome reaction, which was potentiated after 48 h of exposure to 50 mM D-glucose (P!0.05). Interestingly, non-metabolizable L-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 levels per se do not influence human sperm function in 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 at

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“…However, increased RBC adhesion to endothelial cells has been observed in various clinical states such as sickle cell disease, ␤-thalassemia, and diabetes mellitus, and the degree of RBC-EC adhesiveness has been linked to the vascular complications associated with these diseases (1)(2)(3)(4)(5). There is now general agreement that various cell surface alterations control the increased RBC adhesiveness in such disease states.…”

mentioning

confidence: 99%

Specific Binding of Red Blood Cells to Endothelial Cells Is Regulated by Nonadsorbing Macromolecules

Yang

Koo

Lin

et al. 2010

Journal of Biological Chemistry

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Abnormal adhesion of red blood cells to the endothelium has been linked to the pathophysiology of several diseases associated with vascular disorders. Various biochemical changes, including phosphatidylserine exposure on the outer membrane of red blood cells as well as plasma protein levels, have been identified as being likely to play a key role, but the detailed interplay between plasma factors and cellular factors remains unknown. It has been proposed that the adhesionpromoting effect of plasma proteins originates from ligand interaction, but evidence substantiating this assumption is often missing. In this work, we identified an alternative pathway by demonstrating that nonadsorbing macromolecules can also have a marked impact on the adhesion efficiency of red blood cells with enhanced phosphatidylserine exposure to endothelial cells. It is concluded that this adhesion-promoting effect originates from macromolecular depletion interaction and thereby presents an alternative mechanism by which plasma proteins could regulate cell-cell interactions. These findings should thus be of potential value for a detailed understanding of the pathophysiology of diseases associated with vascular complications and might be applicable to a wide range of cellcell interactions in plasma or plasma-like media. The adhesion of red blood cells (RBC)2 to endothelial cells (EC) is usually insignificant. However, increased RBC adhesion to endothelial cells has been observed in various clinical states such as sickle cell disease, ␤-thalassemia, and diabetes mellitus, and the degree of RBC-EC adhesiveness has been linked to the vascular complications associated with these diseases (1-5). There is now general agreement that various cell surface alterations control the increased RBC adhesiveness in such disease states. For example, an enhanced phosphatidylserine (PS) exposure on the outer leaflet of the RBC membrane has been linked to abnormal RBC-EC adhesion in sickle cell disease, hereditary hydrocytosis, and chronic uremia (6 -8). Usually this anionic phospholipid is located exclusively on the inner leaflet of the RBC membrane but is translocated to the outer leaflet in hemoglobinopathies and oxidative stress states (9). The role of PS in adhesion has not been fully understood, but RBC with enhanced PS exposure have been identified to establish specific interactions with EC or the endothelial matrix via several receptors including thrombospondin, ␣ V ␤ 3 , CD36, and PS receptor (6, 10, 11).Moreover, several plasma factors have been identified to be involved in abnormal RBC adhesion to EC. For example, fibrinogen enhances the adhesion of pathological RBC to EC (12, 13), which is consistent with the observation that the onset of vaso-occlusive crisis in sickle cell disease is always accompanied by a temporally elevated level of this acute phase protein (12,14). However, the underlying mechanisms behind the increased adhesion efficiency in the presence of this acute phase protein remain obscure. It has been suggested that fibrinogen acts...

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Protein Glycation

Abstract: Abstract-The

Cited by 364 publications

References 54 publications

Spermatogenic and sperm quality differences in an experimental model of metabolic syndrome and hypogonadal hypogonadism

Spermatogenic and sperm quality differences in an experimental model of metabolic syndrome and hypogonadal hypogonadism

High glucose concentrations per se do not adversely affect human sperm function in vitro

Specific Binding of Red Blood Cells to Endothelial Cells Is Regulated by Nonadsorbing Macromolecules

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