The Animal Biology

Bìol. Tvarin. 2020; 22(1): 10–14.
https://doi.org/10.15407/animbiol22.01.010
Received 26.12.2019 ▪ Accepted 22.03.2020 ▪ Published online 01.05.2020

Energy supply of laboratory rats tissues at combined action of cadmium chloride and sodium nitrite

Ivano-Frankivsk National Medical University,
2 Halytska str., Ivano-Frankivsk, 76018, Ukraine

The mechanism of action of Cadmium and nitrites is different: Cadmium inhibits the enzyme systems of energy supply by replacing divalent metals; and nitrites enhance the formation of methemoglobin, which disrupts oxygen transport to cells. However, to date, the combined effect of these xenobiotics, in particular on energy metabolism, remains poorly understood. Taking into account the foregoing, the purpose of this study was to find out the state of energy metabolism in the brain and liver of rats under conditions of combined action of cadmium chloride and sodium nitrite. The intoxication was modeled as follows: cadmium chloride was administered intramuscularly. Sodium nitrite was administered with drinking water at a dose of 1/10 of LD₅₀ once a day for 10 days. Animals were divided into two groups: intact and experimental. The material was collected after decapitation under thiopental anesthesia at 1^st, 14^th, 28^th day after the completion of the introduction of toxicants. Indicators of energy metabolism were determined as follows: activity of ATPase, lactate dehydrogenase — enzymatic method; glucose concentration — glucose oxidase method; the level of pyruvic, lactic, adenosine triphosphate (ATP) acids — spectrophotometrically; content of Zn, Cu, Mg — by atomic absorption spectrophotometer. The conducted researches indicate disturbance of energy supply of brain and liver tissues by cadmium-nitrite intoxication, which is confirmed by activation of aerobic oxidation of glucose in the brain, increase of ATP content and activity of ATPase in the investigated organs.

Key words: rats, energy metabolism, cadmium chloride, sodium nitrite, Na⁺, K⁺-activation, Mg²⁺-dependent ATPase, adenosine triphosphate, glucose, lactate dehydrogenase, liver, brain

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