galactosemias/glutathione

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The protective effect of L-cysteine and glutathione on the adult and aged rat brain (Na+,K+)-ATPase and Mg2+-ATPase activities in galactosemia in vitro.

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The aim of this study was to evaluate whether the addition of the antioxidants L-cysteine (Cys) or the reduced glutathione (GSH) could reverse the alterations of brain total antioxidant status (TAS) and the modulated activities of the enzymes (Na+,K+)-ATPase, and Mg2+-ATPase in adult or aged rat

Mg2+-ATPase activity in suckling rat brain regions in galactosaemia in vitro. L-Cysteine and glutathione effects.

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Mg2+-ATPase activity is implicated with Mg2+ homeostasis, maintaining high brain intracellular Mg2+ content. We determined the in vitro effects of galactose-1-phosphate (Gal-1-P), galactitol (Galtol) and galactose (Gal) {mix A=Gal-1-P(2 mM)+Galtol(2 mM)+Gal(4 mM) concentrations commonly found in

Suckling rat brain regional distribution of Na+,K+-atpase activity in the in vitro galactosaemia: the effect of L-cysteine and glutathione.

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Inhibition of Na+,K+-ATPase activity causes edema and cell death in central nervous system. We determined the in vitro effects of galactose-l-phosphate (Gal-1-P), galactitol (Galtol) and galactose (Gal) (mix A = classical galactosaemia) or Galtol and Gal (mix B = galactokinase deficiency

Abnormalities of retinal metabolism in diabetes or galactosemia: ATPases and glutathione.

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OBJECTIVE Experimental galactosemia and diabetes are known to result in diabetic-like retinopathy in animals, but the mechanism by which the retinopathy develops remains unclear. Defects of retinal metabolism that are common to galactosemia and diabetes are closely associated with the development of

Protective effect of L-cysteine and glutathione on the modulated suckling rat brain Na+, K+, -ATPase and Mg2+ -ATPase activities induced by the in vitro galactosaemia.

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Galactosaemia is an inborn error of galactose (Gal) metabolism characterized by irreversible brain damage. The aim of this study was to evaluate whether the antioxidants L-cysteine (Cys) and the reduced glutathione (GSH) could reverse the alterations of brain total antioxidant status (TAS) and the

Non-enzymic glycosylation (glycation) of lens proteins by galactose and protection by aspirin and reduced glutathione.

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Radioactive galactose becomes attached covalently to lens proteins in the same way as glucose. Simultaneous incubation with aspirin inhibits the reaction with galactose in a dose-related manner. Incubation with aspirin before incubation with galactose in the absence of aspirin showed that aspirin

Glutathione depletion in the lens of galactosemic and diabetic rats.

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Depletion of lens glutathione (GSH) occurs quickly and drastically following induction of diabetes or galactosemia in rats as well as in lens culture. The explanation for this dramatic loss of GSH has been investigated by many laboratories but the solution has been elusive. There are several

Abnormalities of retinal metabolism in diabetes or experimental galactosemia VIII. Prevention by aminoguanidine.

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OBJECTIVE Aminoguanidine has been found to inhibit the development of some retinal lesions in diabetic rats and diabetic dogs, thereby raising a possibility that the formation of glycation end products (AGEs) may be an essential step in the pathogenesis of the retinopathy. The purpose of this study

Termination of experimental galactosemia in rats, and progression of retinal metabolic abnormalities.

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OBJECTIVE To investigate the effect of termination of galactose feeding after a very short duration of experimental galactosemia on the biochemical abnormalities that are postulated to contribute to the development of retinopathy. METHODS Experimentally galactosemic rats (normal rats fed a 30%

The effect of diet on total antioxidant status, erythrocyte membrane Na+,K+-ATPase and Mg2+-ATPase activities in patients with classical galactosaemia.

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OBJECTIVE Classical galactosaemia is characterized by high levels of galactose-1-phosphate (Gal-1-P), galactose and galactitol. In vitro studies have shown modulation of the rat brain Na+,K+-ATPase and Mg2+-ATPase activities by Gal-1-P. The aim of this study was to evaluate the erythrocyte membrane

Impaired NADPH oxidase activity in peripheral blood lymphocytes of galactosemia patients.

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Galactosemia is an autosomal recessive disorder with a wide range of clinical abnormalities. Cellular oxidative stress is considered as one of the pathogenic mechanisms of galactosemia. In this study, we examined the activity of NADPH oxidase (NOX), a major superoxide-generating enzyme system, in

Abnormalities of retinal metabolism in diabetes or galactosemia. II. Comparison of gamma-glutamyl transpeptidase in retina and cerebral cortex, and effects of antioxidant therapy.

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Levels of the intracellular antioxidant, glutathione, become subnormal in retina in diabetes or experimental galactosemia. In order to investigate the cause and significance of this abnormality, activity of gamma-glutamyl transpeptidase (an enzyme important in the synthesis and degradation of

Abnormalities of retinal metabolism in diabetes or experimental galactosemia. IV. Antioxidant defense system.

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Activities of enzymes that protect the retina from reactive oxygen species were investigated in experimentally diabetic rats and experimentally galactosemic rats, two animal models known to develop vascular lesions consistent with diabetic retinopathy. Diabetes or experimental galactosemia of 2

Combination of glycemic and oxidative stress in lens: implications in augmentation of cataract formation in diabetes.

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It is well known that the incidence of cataract is higher in diabetics as compared to non-diabetics. Its rate of maturation is also faster in the diabetics. The precise mechanism of this acceleration is not clearly understood. It is hypothesized that this could be a result of the combination of the

Oxidative stress in rats after 60 days of hypergalactosemia or hyperglycemia.

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Two of the models used in current diabetes research include the hypergalactosemic rat and the hyperglucosemic, streptozotocin-induced diabetic rat. Few studies, however, have examined the concurrence of these two models regarding the effects of elevated hexoses on biomarkers of oxidative stress.

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