Tag Archives: chromium picolinate

Extracellular matrix degradation products in the heart of rats with metabolic syndrome under chromium picolinate administration

10.09.2025   Uncategorized   No comments

O. Ye. Akimov1*, A. O. Mykytenko2, V. O. Kostenko1

1Department of Pathophysiology, Poltava State Medical University, Poltava, Ukraine;
*e-mail: o.akimov@pdmu.edu.ua;
2Department of Biological and Bioorganic Chemistry,
Poltava State Medical University, Poltava, Ukraine

Received: 22 May 2025; Revised: 24 July 2025;
Accepted: 12 September 2025; Available on-line: 17 September 2025

The populace of Ukraine shows a trend of increasing percentage of persons with obesity, complicated by metabolic syndrome (MetS), which causes damage to the heart extracellular matrix. According to recent studies chromium, picolinate (CrPIC) has the potential to attenuate lipid metabolism disorders and protect the extracellular matrix from degradation. The aim of this research was to estimate the blood lipid profile and the content of glycosaminoglycans, L-hydroxyproline and sialic acids in the heart of rats with simulated metabolic syndrome under Chromium picolinate administration. Mature male Wistar rats were divided into 4 groups of 6 animals each – control; metabolic syndrome induction; CrPIC administration; metabolic syndrome + CrPIC administration. Metabolic syndrome was reproduced by using a 20% fructose solution as the only source of water for 60 days. CrPIC was administered orally at a dose of 80 µg/kg daily for 60 days. The concentration of the heart extracellular matrix degradation proteins was determined spectrophotometrically in a 10% heart homogenate. CrPIC administration to healthy animals stimulated the accumulation of glycosaminoglycans chondroitin fraction in the rat heart. Metabolic syndrome modeling resulted in an increase in TG, TC and LDL-C blood levels, intensification of collagenolysis, degradation of glycoproteins and glycosaminoglycans with a predominance of the keratan-dermatan fraction. CrPIC administration to animals with metabolic syndrome reduced collagenolysis and glycoproteins degradation, changed the dominating fraction of glycosaminoglycans from keratan-dermatan to chondroitin in rat heart connective tissue indicating its potential to prevent cardiac tissue remodeling during metabolic syndrome.

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Chromium picolinate prevents the development of oxidative-nitrosative stress and restores endogenous H(2)S production in the rat brain under rotenone-induced toxicity

05.05.2025   Uncategorized   No comments

A. O. Mykytenko1*, I. S. Hrytsenko2, A. Y. Semenchuk2, M. V. Voroniuk2,
V. V. Kovpak2, O. Y. Akimov3, K. S. Neporada1

1Department of Bioorganic and Biological Chemistry,
Poltava State Medical University, Poltava, Ukraine;
2Medical Faculty №1, Poltava State Medical University, Poltava, Ukraine;
3Department of Pathophysiology, Poltava state medical university, Poltava, Ukraine;
*e-mail: mykytenkoandrej18@gmail.com

Received: 19 December 2024; Revised: 03 March 2025;
Accepted: 25 April 2025; Available on-line: 12 May 2025

Energy deficit, mitochondrial dysfunction and oxidative stress induced by rotenone may play a decisive role in the pathogenesis of neurodegenerative disorders. Chromium picolinate has shown neuroprotective activity and efficacy in the treatment of Alzheimer’s disease The effect of chromium picolinate on the brain under the conditions of rotenone influence has not been studied, and such data could shed light on the pathogenesis of neurodegenerative diseases. The aim of the study was to determine the effect of chromium picolinate on the indices of oxidative-nitrosative stress and the content of sulfide anion and sulfites in the brain homogenate under rotenone administration to rats. Experiments were performed on 24 white, sexually mature male Wistar rats. The animals were divided into 4 groups: control group; chromium picolinate group; rotenone group; group of combined exposure to chromium picolinate and rotenone. Chromium picolinate was administered orally at a dose of 80 μg/kg per day for 21 days. Rotenon was injected subcutaneously at a dose of 1.5 mg/kg every other day. The introduction of rotenone into the body of rats was accompanied by the development of oxidative-nitrosative stress mainly due to the increased activity of NO-synthase inducible isoform, and by the decrease in the content of H2S and SO32- in brain tissue. Oral administration of chromium picolinate against the background of rotenone administration prevents the development of oxidative-nitrosative stress in brain tissue by reducing the production of reactive oxygen and nitrogen forms, promotes the restoration of arginase activity and increases the content of H2S and SO32-.

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