Deficiency of glucose-6-phosphate dehydrogenase activity in the development of contrast-induced acute kidney injury

Glucose-6-phosphate dehydrogenase is a key enzyme of the pentose phosphate pathway and the main source of the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH). NADPH is a leading cellular reducing agent that plays a central role in cell survival. In a study conducted on 200 white mongrel male rats, the dynamics of changes in the concentration of reduced glutathione, malondialdehyde, as well as the activity of antioxidant defense enzymes (glucose-6-phosphate dehydrogenase, glutathione peroxidase, glutathione reductase, and catalase) in kidney tissues and erythrocytes of laboratory animals under the conditions of intoxication with an X-ray contrast preparation were determined. It was found that the use of the nonionic radiopaque drug omnipak-350 (yogexol) in an average lethal dose leads to a deficiency of glucose-6-phosphate dehydrogenase activity, a decrease in NADPH level, and damage to kidney tissue and endothelial cells. NADPH deficiency, in turn, can affect glutathione reductase activity since this enzyme uses NADPH to convert oxidized glutathione into reduced. The relative insufficiency of reduced glutathione, which is the main low-molecular-weight free radical scavenger and substrate of the glutathione peroxidase reaction, leads to an imbalance in pro-oxidant processes. In the erythrocytes and kidney tissues of rats, against the background of the introduction of the radiopaque drug, activation of oxidative stress was noted in the form of a decrease in the concentration of reduced glutathione and the activity of antiradical protection enzymes, as well as an increase in the content of lipid peroxidation products. These shifts in the activity of antioxidant defense enzymes (catalase, glutathione peroxidase, and glutathione reductase) in animal kidney tissues against the background of the use of radiopaque preparation should be considered as characteristic signs of depletion of adaptive reserves of the cell. The tendency to increase the content of creatinine and urea in the blood plasma of poisoned animals, indicating a decrease in the functional activity of nephrons, and morphological examination of kidney tissues, which revealed signs of activation of apoptosis in renal tissue, served as confirmation of the adequacy of the selected experimental model on animals to study the mechanisms of development of contrast-induced acute kidney injury. The results obtained allow us to conclude that a decrease in the activity of G-6-FDG can serve as a trigger factor for the activation of free radical processes that play an important role in the development of contrast-induced acute kidney injury.

глюкозо-6-фосфатдегидрогеназа, пентозофосфатный путь, контраст-индуцированное острое повреждение почек, почка, белые беспородные крысы, glucose-6-phosphate dehydrogenase, pentose phosphate pathway, contrast-induced acute kidney injury, kidney, white mongrel rats

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