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JournalISSN: 0041-610X

Ukraïns'kyĭ biokhimichnyĭ zhurnal 

Naukova Dumka
About: Ukraïns'kyĭ biokhimichnyĭ zhurnal is an academic journal. The journal publishes majorly in the area(s): Lipid peroxidation & Antioxidant. It has an ISSN identifier of 0041-610X. Over the lifetime, 813 publications have been published receiving 2436 citations.


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Journal Article
TL;DR: Findings on vitamin A transport from intestines to target-cell and metabolism of this fat-soluble vitamin are reviewed and possible roles of cellular retinoid-binding proteins in the process of Vitamin A transport and metabolism are reviewed.
Abstract: The present paper is a review of up-to-date findings on vitamin A transport from intestines to target-cell and metabolism of this fat-soluble vitamin. The hypotheses of possible enzymes participation in the process of etherification/hydrolysis and oxidation/reduction of vitamin A are discussed. Furthermore, possible roles of cellular retinoid-binding proteins in the process of vitamin A transport and metabolism are reviewed.

80 citations

Journal Article
TL;DR: The blood of patients with multiple sclerosis shows the signs of a significant oxidative stress, and the possibility of counteracting it by antioxidant administration plus an appropriate diet, might represent a promising way of inhibiting the progression of the disease.
Abstract: It is well known that brain and nervous system cells are prone to oxidative damage because of their relatively low content of antioxidants, especially enzymatic ones, and of the high levels of both membrane polyunsaturated fatty acids (PUFA) and iron easily released from injured cells. We have investigated the oxidative stress in the blood (plasma, erythrocytes and lymphocytes) of 28 patients affected with multiple sclerosis (MS) and of 30 healthy age matched controls, by performing a multiparameter analysis of non-enzymatic and enzymatic antioxidants--Vitamin E (Vit. E), ubiquinone (UBI), reduced and oxidized glutathione (GSH, GS-SG), superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT) and fatty acid patterns of phospholipids (PL-FA). PL-FA and Vit. E were assayed by GC-MS; UBI and GSH/GS-SG by HPLC; SOD, GPX and CAT by spectrophotometry. In comparison to controls, patients with MS showed significantly reduced levels of plasma UBI (0.21 +/- 0.10 vs. 0.78 +/- 0.08 mg/ml, p < 0.001), plasma Vit. E (7.4 +/- 2.1 vs. 11.4 +/- 1.8 mg/ml, p < 0.01), lymphocyte UBI (8.1 +/- 4.0 vs. 30.3 +/- 7.2 ng/ml blood, p < 0.001) and erythrocyte GPX (22.6 +/- 5.7 vs. 36.3 +/- 6.4 U/g Hb, p < 0.001). This blood antioxidant deficiency was associated with plasma levels of PL-PUFA--especially C20:3 n-6 and C20:4 n-6--significantly higher than controls. In conclusion, the blood of patients with MS shows the signs of a significant oxidative stress. The possibility of counteracting it by antioxidant administration plus an appropriate diet, might represent a promising way of inhibiting the progression of the disease. Antioxidant supplements should include not only GSH repleting agents, but also Vit. E, ubiquinol, and selenium.

53 citations

Journal Article
TL;DR: In this paper, the basic components of the death machinery, discuss their interaction in regulation of apoptosis, and describe the main pathways that are used to activate apoptosis in a wide range of pathologic conditions, including neurodegenerative and cardiovascular diseases, cancer and autoimmune diseases.
Abstract: Apoptosis (Programmed Cell Death) is a genetically regulated, morphologically distinct form of cell death that can be initiated by many different physiological and pathological stimuli. Such strategic intracellular programming is initiated in many instances during normal life cycle and development in order to maintain the homeostasis of a multicellular organism, to eliminate unwanted cells. However, apoptosis is also involved in a wide range of pathologic conditions, including neurodegenerative and cardiovascular diseases, cancer and autoimmune diseases. Therefore, the ability to understand and manipulate the cell death machinery is an obvious goal of medical research. Here we review the basic components of the death machinery, discuss their interaction in regulation of apoptosis, and describe the main pathways that are used to activate apoptosis.

31 citations

Journal Article
TL;DR: In this article, the Nomenclature Committee on enzymes of the International Union of Biochemistry described the unit E (U), introduced in 1961 and its derivatives: specific activity, molecular (molar) activity, enzyme catalytic center activity and enzyme solution concentration.
Abstract: Units of enzymes activity, recommended by the Nomenclature Committee on enzymes of the International Union of Biochemistry are described the unit E (U), introduced in 1961 and its derivatives: specific activity, molecular (molar) activity, enzyme catalytic centre activity, enzyme solution concentration; the unit catal, introduced in 1972 and its derivatives Information presented is essential to ensure correct expression of enzyme activity

29 citations

Journal Article
TL;DR: The results' clearly demonstrated overexpression of PFKFB gene family isozymes in the lung cancers and they possible role in the Warburg effect.
Abstract: The 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB) is a family of bifunctional enzymes which is responsible for maintaining the cellular levels of fructose-2,6-bisphosphate, a powerful allosteric activator of glycolysis. Here we report the overexpression of PFKFB-1, -2, -3 and -4 mRNA in the human lung cancers when compared with corresponding normal tissues counterparts as well as PFKFB-4 and -3 protein levels. The lung carcinoma cell line A549, under conditions of normal oxygen tension, has also shown increased transcript levels of PFKFB-2, -3 and -4 when compared to normal tissues. Moreover, hypoxia highly induced the expression of PFKFB-2, PFKFB-3 and especially PFKFB-4 isozymes are highly induced in the lung carcinoma cells. Thus, our results' clearly demonstrated overexpression of PFKFB gene family isozymes in the lung cancers and they possible role in the Warburg effect.

28 citations

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Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
201352
201234
201141
201042
200944
200852