glyoxal/atrophy

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A novel source of methylglyoxal and glyoxal in retina: implications for age-related macular degeneration.

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Aging of retinal pigment epithelial (RPE) cells of the eye is marked by accumulations of bisretinoid fluorophores; two of the compounds within this lipofuscin mixture are A2E and all-trans-retinal dimer. These pigments are implicated in pathological mechanisms involved in some vision-threatening

Effects of advanced glycation end products-inductor glyoxal and hydrogen peroxide as oxidative stress factors on rat retinal organ cultures and neuroprotection by UK-14,304.

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Retinal ganglion cell degeneration is supposed to be mediated by reactive oxygen species (ROS) and advanced glycation end products (AGEs). The alpha2-adrenergic agonist, 5-bromo-N-(4,5-dihydro-1H-imidazol-2-yl)-6-quinoxalinamine (brimonidine; UK-14,304), is said to exert a neuroprotective effect. To

Stress responses of human retinal pigment epithelial cells to glyoxal.

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OBJECTIVE Intracellular formation of advanced glycation end products (AGEs) is a crucial pathological process in retinal diseases such as age-related macular degeneration (AMD) or diabetic retinopathy (DR). Glyoxal is a physiological metabolite produced during formation of AGEs and has also been

Calcium staining by the glyoxal-bis-(2-hydroxyanil)-method in the livers of rats treated with CCl4, diltiazem, and with both agents together.

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We studied the histochemistry of Ca in livers treated with CCl4, diltiazem (one of the Ca antagonists), and both agents together to determine whether hepatocytes or other parts of the liver lesions show Ca staining and whether the grade or location of Ca in these injuries varies. For Ca staining,

Oxidation chemistry of catecholamines and neuronal degeneration: an update.

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Aberrant oxidative pathways of catecholamine neurotransmitters, i.e. dopamine and norepinephrine, are an important biochemical correlate of catecholaminergic neuron loss in some disabling neurodegenerative diseases of the elderly, notably Parkinson's disease. In an oxidative stress setting, under

Metformin Protects ARPE-19 Cells from Glyoxal-Induced Oxidative Stress

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The protective effects and mechanisms of metformin against oxidative stress were evaluated both in vivo and in vitro. ARPE-19 cells comprised the normal group, the glyoxal-treated group (0.5 mM glyoxal), and the glyoxal+metformin group (0.5 mM glyoxal and 0.1 mM metformin). In the

Alteration of the intracellular pH and apoptosis induction in a retinal cell line by the AGE-inducing agent glyoxal.

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BACKGROUND Methylglyoxal and glyoxal, intermediate products of glycation, are known to accelerate glycation and the formation of advanced glycation endproducts (AGEs). These mechanisms may play a role in the degenerative progression of diabetic retinopathy and macular degeneration. The present study

Identification of alpha-dicarbonyl scavengers for cellular protection against carbonyl stress.

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Tissue deterioration and aging have long been associated with the accumulation of chemically induced protein and DNA damage. Reactive oxygen species (ROS) and reactive carbonyl species (RCS), especially alpha-dicarbonyl compounds, are key mediators of damage caused by oxidative stress, glycation,

High-density areas on muscle CT in childhood-onset Pompe disease are caused by excess calcium accumulation.

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We report two patients with childhood-onset Pompe disease showing striking changes with high-density areas on skeletal muscle CT, not seen in adult- or infantile-onset forms of this disease. While the anterior compartment of the thigh muscles was less affected in the adult-onset form, the rectus

P301 L, an FTDP-17 Mutant, Exhibits Enhanced Glycation in vitro.

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Frontotemporal dementia and parkinsonism-linked to chromosome-17 are a group of diseases with tau mutations leading to primary tauopathies which include progressive supranuclear palsy, corticobasal syndrome, and frontotemporal lobar degeneration. Alzheimer's disease is a non-primary

Glucose degradation product methylglyoxal enhances the production of vascular endothelial growth factor in peritoneal cells: role in the functional and morphological alterations of peritoneal membranes in peritoneal dialysis.

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Peritoneal membrane permeability deteriorates in peritoneal dialysis (PD) patients. We test whether glucose degradation products (GDPs) in PD fluids, glyoxal, methylglyoxal and 3-deoxyglucosone, stimulate the production of vascular endothelial growth factor (VEGF), a factor known to enhance vascular

Effect of dwell time on carbonyl stress using icodextrin and amino acid peritoneal dialysis fluids.

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BACKGROUND Deterioration of the peritoneal membrane limits the technical survival of peritoneal dialysis (PD). Advanced glycation of the membrane has been incriminated in this evolution. Advanced glycation end products (AGEs) develop under the influence of glucose and of its degradation products,

Efficient in vitro lowering of carbonyl stress by the glyoxalase system in conventional glucose peritoneal dialysis fluid.

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BACKGROUND Reactive carbonyl compounds (RCOs) present in heat-sterilized peritoneal dialysis (PD) fluid have been incriminated in the progressive deterioration of the peritoneal membrane observed in long-term PD patients. The present study utilized the glyoxalase I (GLO I) system as a new approach

Affinity adsorption of glucose degradation products improves the biocompatibility of conventional peritoneal dialysis fluid.

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BACKGROUND Reactive carbonyl compounds (RCOs) present in peritoneal dialysis (PD) fluid have been incriminated in the progressive deterioration of the peritoneal membrane in long-term PD patients. They are initially present in fresh conventional heat-sterilized glucose PD fluid and are supplemented

Possible role of methylglyoxal and glyoxalase in arthritis.

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OA (osteoarthritis) and RA (rheumatoid arthritis) lead to deterioration of the joints. Early OA is associated with loss of bone due to increased bone remodelling. A role for inflammation is thought to be integral to the pathology. RA is a chronic inflammatory disease of the synovium, a membrane

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