Bìol. Tvarin, 2018, volume 20, issue 4, pp. 9–15

COPPER METABOLISM IN RATS UNDER TOXIC INJURY BY ACETAMINOPHEN ON THE BACKGROUND OF ALIMENTARY PROTEIN DEFICIENCY

O. M. Voloshchuk, G. P. Kopylchuk

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Institute of Biology, Chemistry and Bioresources
of Chernivtsi national university named by Yurii Fedkovych,
Biochemistry and biotechnology department,
2 Kotsyubinskogo str., Chernivtsi 58000 Ukraine

The indices of copper metabolism in rats with toxic liver injury on the background of alimentary protein deficiency were studied in the research.

The animals were separated into the following 4 groups: I intact animals (C); II — animals receiving low-protein ration (LPR); III animals subjected to acetaminophen-induced liver lesions receiving complete ration (H); IV animals subjected to acetaminophen-induced liver lesions that were previously fed semi-synthetic low-protein ration (LPR+H). The level of ceruloplasmin in blood plasma was determined by Ravin method based on a photocolorimetrical evaluation of the products of n-phenylamide oxidation by ceruloplasmin. Determination of copper level in blood plasma and urea was conducted using set of reagents (“BIO-LA-TEST”, Czech Republic). Albumin level in blood plasma was evaluated using set of reagents (“Filisit-Diagnostics”, Ukraine).

It is established that in rats with protein deficiency there is a decrease in copper level by 1.6 times comparing to control, along with a significant reduction of ceruloplasmin plasma level as well as an increased loss of copper with urine. The similar changes are found in animals with a modeled toxic liver injury, maintained on a full-value diet.

It is established that the most significant disturbances of copper metabolism are observed in rats with protein deficiency and acetaminophen-induced liver injury. In rats of III group there is a 3-fold decrease in copper level in blood plasma on the background of hypoalbuminemia, and a 2-fold reduction of ceruloplasmin level in blood plasma accompanied by an increased copper content in urine. A depletion of pool of the biologically available copper may further lead to changes in functioning of the copper-dependent enzymes. Thus, it may be considered as a possible mechanism of disturbances of the metabolic processes in conditions of drug-induced intoxications against the background of alimentary protein deficiency.

Obtained changes in copper metabolism indices under the conditions of toxic liver injury on a background of alimentary deprivation of protein open the new prospects for the further research into the activity of copper-containing enzymes and their role in the formation of the metabolic disturbances in the given conditions.

Keywords: ACETAMINOPHEN, LIVER, ALIMENTARY PROTEIN DEFICIENCY, COPPER, CERULOPLASMIN

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