Maria Jurczuk
Medical University of Białystok
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Featured researches published by Maria Jurczuk.
Toxicology | 2007
Malgorzata M. Brzóska; Joanna Rogalska; Malgorzata Galazyn-Sidorczuk; Maria Jurczuk; Alicja Roszczenko; Elżbieta Kulikowska-Karpińska; Janina Moniuszko-Jakoniuk
The aim of the present study is to investigate, based on the rat model of moderate and relatively high human exposure to cadmium (Cd), whether zinc (Zn) supplementation may prevent Cd-induced disorders in bone metabolism. For this purpose, male Wistar rats received Cd (5 and 50mg/l) or/and Zn (30 and 60mg/l) in drinking water for 6 and 12 months. Bone densitometry and biochemical markers of bone turnover were used to assess the effects of Cd or/and Zn. Bone mineral content (BMC) and density (BMD) were measured in the femur. Serum osteocalcin (OC) and alkaline phosphatase in trabecular (bT-ALP) and cortical (bC-ALP) bone were determined as bone formation markers, and carboxy-terminal cross-linking telopeptides of type I collagen (CTX) in serum were measured as bone resorption marker. Serum concentration of calcium (Ca) and its renal handling, as well as Zn and Cd concentrations in the serum/blood, urine and femur were evaluated as well. The exposure to 5 and 50mg Cd/l (0.340+/-0.026 and 2.498+/-0.093mg Cd/kg body wt/24h, respectively), in a dose and duration dependent manner, affected bone turnover (inhibited bone formation and stimulated its resorption) and disturbed bone mineralization (decreased BMC, BMD and Zn concentration). Zn supply at the concentration of 30 and 60mg/l (1.904+/-0.123 and 3.699+/-0.213mg/kg body wt/24h, respectively) during Cd exposure influenced the Cd-induced disorders in bone metabolism. Zn administration to the Cd-exposed rats enhanced the bone ALP activity and prevented Cd-induced bone resorption, but had no statistically significant effect on BMC and BMD; however, mean values of the densitometric parameters in the rats receiving both Cd and Zn were higher than in those treated with Cd alone. Moreover, Zn supplementation at both levels of Cd exposure was found to prevent Cd accumulation in the femur and the Cd-induced decrease in bone Zn concentration. The results of the present study allow the conclusion that Zn supplementation during Cd exposure may partly protect from disorders in bone metabolism. The influence of Zn may be accompanied by its ability to prevent Cd-induced Zn deficiency and to decrease Cd accumulation in bone tissue. The findings seem to indicate that enhanced dietary intake of Zn in subjects chronically exposed to moderate and relatively high Cd levels may have a protective influence on the skeleton.
Chemico-Biological Interactions | 2008
Malgorzata M. Brzóska; Malgorzata Galazyn-Sidorczuk; Joanna Rogalska; Alicja Roszczenko; Maria Jurczuk; Katarzyna Majewska; Janina Moniuszko-Jakoniuk
The present study was aimed at estimate, based on the rat model of human moderate and relatively high chronic exposure to cadmium (Cd), whether zinc (Zn) supplementation may prevent Cd-induced weakening in the bone biomechanical properties. For this purpose, male Wistar rats were administered Cd (5 or 50 mg/l) or/and Zn (30 or 60 mg/l) in drinking water for 6 and 12 months. Bone mineral density (BMD) and biomechanical properties (yield load, ultimate load, post-yield load, displacement at yield and at ultimate, stiffness, work to fracture, yield stress, ultimate stress and Young modulus of elasticity) of the femoral distal end and femoral diaphysis were examined. Biomechanical properties of the distal femur were estimated in a compression test, whereas those of the femoral diaphysis -- in a three-point bending test. Exposure to Cd, in a dose and duration dependent manner, decreased the BMD and weakened the biomechanical properties of the femur at its distal end and diaphysis. Zn supplementation during Cd exposure partly, but importantly, prevented the weakening in the bone biomechanical properties. The favorable Zn influence seemed to result from an independent action of this bioelement and its interaction with Cd. However, Zn supply at the exposure to Cd had no statistically significant influence on the BMD at the distal end and diaphysis of the femur. The results of the present paper suggest that Zn supplementation during exposure to Cd may have a protective influence on the bone tissue biomechanical properties, and in this way it can, at least partly, decrease the risk of bone fractures. The findings seem to indicate that enhanced dietary Zn intake may be beneficial for the skeleton in subjects chronically exposed to Cd.
Food and Chemical Toxicology | 2001
Malgorzata M. Brzóska; Janina Moniuszko-Jakoniuk; Maria Jurczuk; Malgorzata Galazyn-Sidorczuk; J. Rogalska
It has been determined that zinc supplementation (240 microg Zn/ml) during (for 12 weeks) or after (for 2 weeks) cadmium exposure (50 microg Cd/ml for 12 weeks) can prevent the accumulation and toxic action of Cd in the tibia of rats. The exposure to Cd led to disturbances in bone metabolism reflected by changes in the chemical composition of bone and decreased bone mineral density (osteomalacian changes). The Zn supply in conditions of Cd intoxication completely prevented the Cd-induced increase in percentage of water content and decrease in tibia ash weight, ash weight/dry weight, non-org. comp./org. comp., Zn content and concentration. Moreover, Zn partly protected from the decrease in Ca concentration and content, percentage of non-organic components content, Ca/wet weight, Ca/ash weight and Ca/dry weight. Zn administered after Cd exposure partly, but not completely, protected from Cd-induced decrease in percentage of non-organic components content, Ca/wet weight as well as Ca content and concentration. This protective effect on bone was most evident when Zn was administered during Cd exposure. But Zn, independently of the manner of its administration, did not prevent Cd accumulation in the tibia. Our results suggest that Zn supply in conditions of simultaneous exposure can prevent Cd-induced bone loss to some extent, and used after Cd treatment can give therapeutic benefits.
Journal of Trace Elements in Medicine and Biology | 2012
Malgorzata Galazyn-Sidorczuk; Malgorzata M. Brzóska; Joanna Rogalska; Alicja Roszczenko; Maria Jurczuk
It was investigated whether the ability of zinc (Zn) to prevent cadmium (Cd)-induced lipid peroxidation may be connected with its impact on glutathione peroxidase (GPx) activity and selenium (Se) concentration. GPx and Se were determined in the serum, liver and kidney of the rats that received Cd (5 or 50 mg/L) or/and Zn (30 mg/L) in drinking water for 6 months in whose the protective Zn impact was noted (Rogalska J, Brzóska MM, Roszczenko A, Moniuszko-Jakoniuk J. Enhanced zinc consumption prevents cadmium-induced alterations in lipid metabolism in male rats. Chem Biol Interact 2009;177:142-52). Moreover, dependences between these parameters, and indices of lipid peroxidation (F(2)-isoprostane, lipid peroxides, oxidized low density lipoprotein cholesterol) as well as concentrations of Cd and Zn were estimated. The supplementation with Zn during the exposure to 5 mg Cd/L entirely antagonized the Cd-induced increase in GPx activity and Se concentration in the liver and kidney, but not in the serum. Zn administration during the treatment with 50 mg Cd/L totally or partially prevented from the Cd-caused decrease in GPx activity and Se concentration in the serum, liver and kidney. At the higher level of Cd exposure, GPx activity in the serum and tissues positively correlated with Se concentration. Moreover, numerous correlations were noted between GPx and/or Se and the indices of lipid peroxidation. The results indicate that the protective impact of Zn against the Cd-induced lipid peroxidation during the relatively high exposure might be connected with its beneficial influence on Se concentration and GPx activity in the serum and tissues, whereas this bioelement influence at the moderate exposure seems to be independent of GPx and Se.
Chemico-Biological Interactions | 2015
Malgorzata M. Brzóska; Joanna Rogalska; Malgorzata Galazyn-Sidorczuk; Maria Jurczuk; Alicja Roszczenko; Michał Tomczyk
It was investigated, in a female rat model of low and moderate lifetime human exposure to cadmium (Cd), whether polyphenols from Aronia melanocarpa berries (chokeberry; AMP) may offer protection from this heavy metal-induced disorders in bone metabolism. For this purpose, numerous indices of bone formation (osteocalcin, alkaline phosphatase, osteoprotegerin) and resorption (carboxy-terminal cross-linking telopeptides of type I collagen, soluble receptor activator of nuclear factor-κB ligand) in the serum and/or distal femur epiphysis (trabecular bone region), as well as bone mineral status (volumetric bone mineral density of the femur and content of mineral components, including calcium, in the bone tissue at the distal femur epiphysis) were evaluated in female Wistar rats that received a 0.1% aqueous extract of AMP, as the only drinking fluid (prepared from lyophilized extract by Adamed Consumer Healthcare), and/or Cd in diet (1 and 5mg/kg) for 3, 10, 17, and 24 months. Examination of the phytochemical profile of the aronia extract revealed high content of polyphenols (612.40 ± 3.33 mg/g), including anthocyanins, proanthocyanidins, phenolic acids, and flavonoids. Among detected compounds anthocyanins were identified as dominating. The exposure to Cd, dose- and duration-dependently, enhanced resorption and inhibited formation of the bone tissue resulting in its decreased mineralization. The administration of AMP under the exposure to 1 and 5 mgCd/kg diet provided important protection from this heavy metal-induced disturbances in the bone turnover and changes in the bone mineral status, and the beneficial impact of polyphenols resulted from their independent action and interaction with Cd. These findings suggest that consumption of Aronia melanocarpa polyphenols may play a role in prevention against female skeleton damage due to chronic exposure to Cd and that chokeberry represents the good natural plant candidate for further investigations of its prophylactic use under environmental exposure to this heavy metal.
Food and Chemical Toxicology | 2004
Maria Jurczuk; Malgorzata M. Brzóska; Janina Moniuszko-Jakoniuk; Malgorzata Galazyn-Sidorczuk; E Kulikowska-Karpińska
Food and Chemical Toxicology | 2007
Maria Jurczuk; Malgorzata M. Brzóska; Janina Moniuszko-Jakoniuk
Chemico-Biological Interactions | 2009
Malgorzata Galazyn-Sidorczuk; Malgorzata M. Brzóska; Maria Jurczuk; Janina Moniuszko-Jakoniuk
Toxicology | 2006
Maria Jurczuk; Janina Moniuszko-Jakoniuk; Malgorzata M. Brzóska
Polish Journal of Environmental Studies | 2006
Maria Jurczuk; J. Moniuszko-Jakoniuk; J Rogalska