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  1. 14 Cellular and Molecular Biology Letters

  2. 7 Acta Biochimica Polonica

  3. 6 Folia Histochemica et Cytobiologica

  4. 5 Archivum Immunologiae et Therapiae Experimentalis

  5. 4 Journal of Physiology and Pharmacology

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Autorzy help

  1. 6 Gwozdzinski K.

  2. 6 Koceva-Chyla A.

  3. 5 Jozwiak Z.

  4. 3 Gagat M.

  5. 3 Grzanka A.

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  1. 1 2021

  2. 3 2017

  3. 2 2014

  4. 2 2013

  5. 4 2012

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1

Mathematical optimization for liposomal doxorubicin in tumor

100%
Hrynyk R., Langner M.
Cellular and Molecular Biology Letters
|
2005
|
tom 10
|
nr Suppl.
2

Effect of iodothyronine hormone status on doxorubicin related cardiotoxicity

88%
Dudka J., Mandziuk S., Madej-Czerwonka B., Sierocinska-Sawa J., Walczyna B., Korga A., Cendrowska-Pinkosz M., Burdan F.
Folia Morphologica
|
2013
|
tom 72
|
nr 4
The anthracycline anticancer agent doxorubicin has been recognised to induce a dose-dependent cardiotoxicity. The chronic form of such complication is characterised by an irreversible cardiac damage and congestive heart failure. Although the pathogenesis of anthracycline cardiotoxicity seems to be multifactorial, the pivotal role has been attributed to reactive oxygen species formation. Because redox equilibrium in cardiomyocytes may be regulated via iodothyronine hormones, the aim of the study was to appraise the effect of hypothyroidism on heart damages induced by doxorubicin. The rats received methimazole in drinking water (0.001 and 0.025%) after doxorubicin administration (2.0, 5.0 and 15 mg/kg). The cardiac morphology and blood biochemical markers of heart damage were assessed. Decreased levels of iodothyronine hormones had not significant impact on cardiac morphological changes and no effect on the level of B-type natriuretic peptide in rats receiving doxorubicin. Lower hormonal levels had sporadic, diverse effect on blood transaminases, lactate dehydrogenase and creatine kinase levels, but any relation to time, doxorubicin doses and hypothyroid status was found. Hypothyreosis leads to increase in fatty acid binding protein in rats receiving higher dose of doxorubicin. Hypothyreosis had no effect on heart stretching and on necrosis at morphological level, but caused biochemical symptoms of cardiomyocyte necrosis in rats receiving doxorubicin. (Folia Morphol 2013; 72, 4: 340–348)
3

Annamycin, a novel liposomally formulated anticancer agent

88%
Priebe W., Booser D., Perez-Soler R.
Cellular and Molecular Biology Letters
|
1999
|
tom 04
|
nr 2
4

Imatinib inhibits the renewal and tumorigenicity of CT-26 colon cancer cells after cytoreductive treatment with doxorubicin

75%
Przybyszewska M., Miloszewska J., Kotlarz A., Swoboda P., Pysniak K., Szczepek W., Kaczmarek L., Markowicz S.
Archivum Immunologiae et Therapiae Experimentalis
|
2017
|
tom 65
|
nr 1
5

Combination of combretastatin A4 phosphate and doxorubicin-containing liposomes affetcs growth of B16-F10 tumors

75%
Mitrus I., Sochanik A., Cichon T., Szala S.
Acta Biochimica Polonica
|
2009
|
tom 56
|
nr 1
161-165
The study aimed to check the effectiveness of anticancer therapy combining a vascular-disruptive drug (combretastatin phosphate, CA4P) and a liposomal formulation of a chemotherapeutic (doxorubicin). CA4P was synthesized in our laboratory according to a previously described procedure. The antivascular drug and long-circulating doxorubicin-loaded liposomes were used to treat B16-F10 murine melanoma experimental tumors. Seventy-four hours after drug administration, a decrease in the number of tumor blood vessels was apparent and necrotic areas within tumors were visible. Combination therapy consisting of alternate administrations of CA4P and liposomal doxorubicin yielded greater inhibition of tumor growth than monotherapies alone. The best therapeutic results were obtained with the antivascular drug administered intratumorally every second day at 50 mg/kg body mass. In the case of combined therapy, the best results were obtained when the vascular-disruptive agent (CA4P) and the antineoplastic agent (liposomal doxorubicin) were administered in alternation.
6

Cytotoxicity and inhibitory properties against topoisomerase II of doxorubicin and its formamidine derivatives

75%
Kik K., Studzian K., Wasowska-Lukawska M., Oszczapowicz I., Szmigiero L.
Acta Biochimica Polonica
|
2009
|
tom 56
|
nr 1
135-142
 This work was undertaken to compare cytotoxicity, DNA damaging properties and effect on DNA cleavage by topoisomerase II of the anthracycline drug doxorubicin (DOX) and its two derivatives with a formamidino group containing a cyclic amine moiety such as morpholine (DOXM) or hexamethyleneimine (DOXH). The tetrazolium dye colorimetric assay was used to determine the cytotoxic activity of anthracyclines toward L1210 leukemia cells. DNA damage was measured by alkaline elution technique. The effect of anthracyclines on DNA cleavage was studied in a cell-free system containing supercoiled pBR322 DNA and purified human topoisomerase II. The cytotoxicity data and the results of studies on the mechanism of DNA break formation by anthracyclines at the cellular level and in the cell-free system showed that the presence of the formamidino group in the doxorubicin molecule reduced its ability to stimulate DNA cleavage by DNA topoisomerase II. Conclusion: DNA topoisomerase II is not a primary cellular target for DOXM or DOXH. An advantageous feature of formamidinoanthracyclines is their mechanism of cytotoxic action which is not related to the inhibition of DNA topoisomerase II. Therefore this class of anthracyclines seems to be a good source for selection of an anticancer drug directed toward cancer cells with the developed multidrug resistance attributed to the presence of altered DNA topoisomerase II.
7

Effect of hypoxia on toxicity induced by anticancer agents in cardiomyocyte culture

75%
Mandziuk S., Kus P., Dudka J., Madej-Czerwonka B., Cendrowska-Pinkosz M., Iwan M., Luszczewska-Sierakowska I., Korga A.
Medycyna Weterynaryjna
|
2014
|
tom 70
|
nr 05
The main goal of the study was to determine whether hypoxia augments the toxicity of anticancer drugs towards cardiomyocytes. Drugs selected for this experiment were those that disturb the cardiac redox equilibrium. Cardiomyocytes were incubated for 24 h with doxorubicin, tirapazamine, and 5-fluorouracil, each at three doses, under normoxia and under 50% and 90% hypoxia. The cytotoxic effect was evaluated on the basis of the percentage of living cells, cell vitality (assessed by the MTT assay), and morphology. In addition, the oxidative marker and pH value were determined. Varied protective effects of hypoxia on cell morphology were observed in all cases except the medium concentration of tirapazamine. The 50% hypoxia prevented the toxic effects of all tested drugs. The 90% hypoxia, on the other hand, was effective against the cytotoxic action of doxorubicin and 5-fluoruracil, but the cytotoxicity of tirapazamine increased. It was found that under the 90% hypoxia the oxidative stress observed under normoxia and the 50% hypoxia was greatly reduced. The study revealed that the above drugs did not activate anaerobic glycolysis.
8

Aromatic indolinic aminoxyls as antioxidants in cardiac sarcoplasmic reticulum lipid and protein oxidation

75%
Kulawiak-Galaska D., Wozniak M., Greci L.
Acta Biochimica Polonica
|
2002
|
tom 49
|
nr 1
The results presented demonstrate the influence of aromatic indolinic aminoxyls: 1,2-dihydro-2-ethyl-2-phenyl-3.H-indole-3-phenylimino-1-oxyl (IA-C2) and 1,2-dihydro- 2-octadecyl-2-phenyl-3.H-indole-3-phenylimino-1-oxyl (IA-C18) on oxidation of lipids and proteins of cardiac sarcoplasmic reticulum membranes. We have used doxorubicin and t-butyl hydroperoxide as agents inducing oxidative stress in isolated rat cardiac sarcoplasmic reticulum membrane system. Carbonyl groups were measured as the end product of membrane protein oxidation, and thiobarbituric acid reactive substances were assessed as a marker of lipid pero- xidation. Inhibition of peroxidation of certain membrane components depends on the length of acyl chain. Aminoxyl IA-C2 inhibits the lipid peroxidation process while IA-C18 is an efficient protector against protein oxidation.
9

There is no evidence for the existence of complex formation between doxorubicin and glutathione

75%
Marszalek M., Bartosz M., Bartosz G.
Cellular and Molecular Biology Letters
|
2003
|
tom 08
|
nr 2
Doxorubicin is co-transported with glutathione by several multidrug resistance proteins (MRPs). In order to check whether weak non-covalent aggregates between doxorubicin and glutathione can be formed, which might be substrates for the transporter, the effect of glutathione on the partition coefficient of doxorubicin was studied. No evidence of an effect of glutathione (at levels up to 20 mM) on the partition coefficient of doxorubicin was found in the pH range of 4.0-7.4. These results indicate that non-covalent doxorubicin-glutathione complexes do not form.
10

Expression of cyclin B1 after induction of senescence and cell death in non-small cell lung carcinoma A549 cells

63%
Zuryn A., Gagat M., Grzanka A. A., Gackowska L., Grzanka A.
Folia Histochemica et Cytobiologica
|
2012
|
tom 50
|
nr 1
11
Content available remote

Resveratrol protects against acute chemotherapy toxicity induced by doxorubicin in rat erythrocyte and plasma

63%
Hamlaoui S., Mokni M., Limam N., Carrier A., Limam F., Amri M., Marzouki L., Aouani E.
Journal of Physiology and Pharmacology
|
2012
|
tom 63
|
nr 3
12

Combined effects of doxorubicin and STI571 on growth, differentiation and apoptosis of CML cell line K562

63%
Jakubowska J., Stasiak M., Szulawska A., Bednarek A., Czyz M.
Acta Biochimica Polonica
|
2007
|
tom 54
|
nr 4
839-846
STI571 (imatinib mesylate; Gleevec®) is an inhibitor that targets the tyrosine kinase activity of Bcr-Abl present in chronic myelogenous leukemia (CML) cells. Some preclinical studies have demonstrated that the combination of STI571 with chemotherapeutic drugs results in enhanced toxicity in Bcr-Abl-positive leukemias. We investigated the potential benefit of using STI571 to down-regulate Bcr-Abl activity for the enhancement of doxorubicin anti-proliferative action in K562 cell line derived from blast crisis of CML. At low concentrations of both drugs (40 nM doxorubicin combined with STI571 in the range of 100–150 nM), the antiproliferative effects were mainly due to cellular differentiation as assessed by benzidine staining for hemoglobin synthesis level and real-time PCR for γ-globin expression. Higher concentrations of STI571 used in combinations with doxorubicin caused mainly apoptosis as shown by DNA degradation and nuclear fragmentation visualized by fluorescence microscopy after DAPI staining, changes in cell morphology observed after Giemza-May Grünwald staining and cellular membrane organization estimated by flow cytometry after Annexin V staining. As compared with either drug alone, cotreatment with STI571 and DOX induced stronger cellular responses. A low concentration of STI571 in combination with a low concentration of DOX might be tested as an alternative approach to increasing the efficacy of chemotherapy against CML
13

Switching p53-dependent growth arrest to apoptosis via the inhibition of DNA damage-activated kinases

63%
Hublarova P., Greplova K., Holcakova J., Vojtesek B., Hrstka R.
Cellular and Molecular Biology Letters
|
2010
|
tom 15
|
nr 3
473-484
Cisplatin and doxorubicin are widely used anticancer drugs that cause DNA damage, which activates the ATM-Chk2-p53 pathway in cancer cells. This activation leads to cell cycle block or apoptosis, depending on the nature of the DNA damage. In an attempt to enhance the effects of these agents, we inhibited ATM/ATR and Chk2, which are known upstream regulators of p53. The cancer cell lines A2780 and ARN8, bearing the wild-type p53 protein, were used to study changes in p53 activation and trans-activation. Our results suggest that the G1-checkpoint, normally activated by DNA damage, is functionally overcome by the action of kinase inhibitors that sensitize cells to apoptosis. Both inhibitors show these effects, albeit with variable intensity in different cell lines, which is promising for other studies and theoretically for use in clinical practice.
14
Content available remote

The lactate receptor (HCAR1/GPR81) contributes to doxorubicin chemoresistance via ABCB1 transporter up-regulation in human cervical cancer HeLa cells

63%
Wagner W., Kania K. D., Blauz A., Ciszewski W. M.
Journal of Physiology and Pharmacology
|
2017
|
tom 68
|
nr 4
15

The role of exportin 6 in cytoskeletal-mediated cell death and cell adhesion in human non-small-cell lung carcinoma cells following doxorubicin treatment

63%
Izdebska M., Gagat M., Grzanka D., Halas M., Grzanka A.
Folia Histochemica et Cytobiologica
|
2014
|
tom 52
|
nr 3
16

Doxorubicin-transferrin conjugate selectively overcomes multidrug resistance in leukaemia cells

63%
Lubgan D., Jozwiak Z., Grabenbauer G. G., Distel L. V. R.
Cellular and Molecular Biology Letters
|
2009
|
tom 14
|
nr 1
113-127
Neoplastic cells frequently have an increased number of transferrin receptors. Coupling transferrin to an anti-neoplastic drug has the potential to overcome multidrug resistance (MDR). The purpose of this study was to examine the distribution and action of doxorubicin-transferrin conjugate (DOXTRF) in a leukaemia cell line (HL60), a multidrug-resistant leukaemia cell line (HL60ADR) and a normal tissue cell line (human fibroblasts). The intracellular accumulation of DOX and DOX-TRF was monitored by direct fluorescence. More DOX-TRF than free DOX was delivered to the tumour cells, and consecutively the levels of DNA double-strand breaks and apoptosis increased even in the multidrug-resistant cell line. In the normal tissue cell line, DOX-TRF did not accumulate, and therefore, the levels of DNA double-strand breaks and apoptosis did not increase. Cell viability was determined using the MTT assay. The IC50 for DOX-TRF was lower than the IC50 value for the free drug in both leukaemia cell lines. The IC50 values for the HL60 cells were 0.08 μM for DOX and 0.02 μM for DOX-TRF. The IC50 values for HL60ADR cells were 7 μM for DOX and 0.035 μM for DOX-TRF. In conclusion, DOX-TRF was able to overcome MDR in the leukaemia cell lines while having only a very limited effect on normal tissue cells.
17

Nitroxide as an antioxidant in the protection of heart tissue in doxorubicin treated rats

63%
Koceva-Chyla A., Gwozdzinski K., Kochman A., Stolarska A., Jozwiak Z.
Cellular and Molecular Biology Letters
|
2002
|
tom 07
|
nr Suppl.
18

Correlation of histopathological and biochemical appraisal of anthracyclin-induced myocardium damage

63%
Dziegiel P., Surowiak P., Zabel M.
Folia Histochemica et Cytobiologica
|
2002
|
tom 40
|
nr 2
19

The effect of melatonin on the cytotoxic effects of doxorubicin on the myocardium and on transplantable Morris hepatoma in rats

63%
Dziegiel P., Podhorska-Okolow M., Surowiak P., Ciesielska U., Rabczynski J., Zabel M.
Cellular and Molecular Biology Letters
|
2002
|
tom 07
|
nr Suppl.
20

Effects of pyrroline and pyrrolidine nitroxides on lipid peroxidation in heart tissue of rats treated with doxorubicin

63%
Koceva-Chyla A., Gwozdzinski K., Kochman A., Stolarska A., Jozwiak Z.
Cellular and Molecular Biology Letters
|
2003
|
tom 08
|
nr 1
Protection from doxorubicin-induced lipid peroxidation in vivo by two pyrroline and pyrrolidine nitroxides, Pirolin, PL, and Pirolid, PD, was examined in the heart tissue of rats treated with this drug. The level of lipid peroxidation was estimated on the basis of MDA content. A considerable (threefold) increase in the MDA amount was found in heart homogenates from rats injected with doxorubicin, whereas no significant changes in MDA content compared to control were observed in cardiomyocytes treated with the nitroxides (Pirolin or Pirolid) only. Pirolin injected simultaneously with doxorubicin showed antioxidative effect and markedly attenuated lipid peroxidation in the heart tissue caused by this drug. In contrast to Pirolin, structurally related Pirolid was ineffective in the protection of heart myocytes from DOX-induced lipid peroxidation.
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