scholarly journals DNA Damage and Inhibition of Akt Pathway in MCF-7 Cells and Ehrlich Tumor in Mice Treated with 1,4-Naphthoquinones in Combination with Ascorbate

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Fabiana Ourique ◽  
Maicon R. Kviecinski ◽  
Karina B. Felipe ◽  
João Francisco Gomes Correia ◽  
Mirelle S. Farias ◽  
...  
Keyword(s):  
Dna Damage ◽  
Ehrlich Ascites Carcinoma ◽  
Carcinoma Cells ◽  
Parp Cleavage ◽  
Ehrlich Carcinoma ◽  
Ehrlich Ascites ◽  
Molecular Toxicity ◽  
Ct Dna ◽  
Mcf 7

The aim of this study was to enhance the understanding of the antitumor mechanism of 1,4-naphthoquinones and ascorbate. Juglone, phenylaminonaphthoquinone-7, and 9 (Q7/Q9) were evaluated for effects on CT-DNA and DNA of cancer cells. Evaluations in MCF-7 cells are DNA damage, ROS levels, viability, and proliferation. Proteins from MCF-7 lysates were immunoblotted for verifying PARP integrity,γH2AX, and pAkt. Antitumor activity was measured in Ehrlich ascites carcinoma-bearing mice. The same markers of molecular toxicity were assessedin vivo. The naphthoquinones intercalate into CT-DNA and caused oxidative cleavage, which is increased in the presence of ascorbate. Treatments caused DNA damage and reduced viability and proliferation of MCF-7 cells. Effects were potentiated by ascorbate. No PARP cleavage was observed. Naphthoquinones, combined with ascorbate, caused phosphorylation of H2AX and inhibited pAkt. ROS were enhanced in MCF-7 cells, particularly by the juglone and Q7 plus ascorbate. Ehrlich carcinoma was inhibited by juglone, Q7, or Q9, but the potentiating effect of ascorbate was reproducedin vivoonly in the cases of juglone and Q7, which caused up to 60% inhibition of tumor and the largest extension of survival. Juglone and Q7 plus ascorbate caused enhanced ROS and DNA damage and inhibited pAkt also in Ehrlich carcinoma cells.

Trichosanthes dioica seed lectin inhibits Ehrlich ascites carcinoma cells growth in vivo in mice by inducing G 0 /G 1 cell cycle arrest

2021 ◽  
Author(s):  
Shaikh Shohidul Islam ◽  
Md. Rezaul Karim ◽  
A. K. M. Asaduzzaman ◽  
A. H. M. Khurshid Alam ◽  
Zahid Hayat Mahmud ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Ehrlich Ascites Carcinoma ◽  
Carcinoma Cells ◽  
Cycle Arrest ◽  
Ehrlich Ascites ◽  
Trichosanthes Dioica

THE ENZYMIC FORMATION OF 6-(METHYLMERCAPTO)PURINE RIBONUCLEOSIDE 5′-PHOSPHATE

1966 ◽  
Vol 44 (2) ◽  
pp. 229-245 ◽  
Author(s):  
Ian C. Caldwell ◽  
J. Frank Henderson ◽  
A. R. P. Paterson
Keyword(s):  
Tumor Cells ◽  
Blood Cells ◽  
Intraperitoneal Injection ◽  
Ehrlich Ascites Carcinoma ◽  
Carcinoma Cells ◽  
Ehrlich Ascites ◽  
Mouse Tissues ◽  
Enzymatic Methods

6-(Methylmercapto)purine ribonucleoside (Me6MPR) is efficiently phosphorylated in mouse tissues and in Ehrlich ascites carcinoma cells in vivo; tumor cells in vitro and cell-free extracts of the tumor also phosphorylate this analogue ribonucleoside. The product of this reaction has been identified by chemical and enzymatic methods and by its chromatographic behaviour as Me6MPR 5′-phosphate. The evidence presented in this report indicates that no other major metabolites of Me6MPR are formed.The phosphorylation of Me6MPR by cell-free tumor extracts requires ATP and Mn2+ (or Mg2+), and evidence is presented that the reaction is probably mediated by adenosine kinase.Me-14C-6MPR is rapidly taken up by most mouse tissues following its intraperitoneal injection. Forty minutes after injection of the labeled drug, the highest levels of radioactivity were found in intestine, liver, blood cells, lung, and spleen, in descending order; virtually no radioactivity was found in brain tissue or in blood plasma.

THE ROLE OF THIOL GROUPS IN THE DEVELOPMENT OF RADIATION DAMAGE IN THYMOCYTES AND EHRLICH ASCITES CARCINOMA CELLS

1964 ◽  
Vol 42 (12) ◽  
pp. 1717-1727 ◽  
Author(s):  
J. F. Scaife
Keyword(s):  
Ehrlich Ascites Carcinoma ◽  
Carcinoma Cells ◽  
Irradiation Damage ◽  
Thiol Groups ◽  
Protein Thiol ◽  
Ehrlich Ascites ◽  
X Irradiation ◽  
The Difference

The effect of 800–1000 rads of X-irradiation on the thiol content of thymocytes and Ehrlich ascites carcinoma cells has been compared. Four hours after irradiation there was a decrease in the non-protein thiol (NP.SH) content of thymus and thymocytes but no change in ascites cells. In both cells the main NP.SH compound was glutathione. There was no significant effect of irradiation on the protein thiol (P.SH) content of thymus or ascites cells, but there was a slight decrease in P.SH in thymocytes after 4 hours incubation. Isolated thymus nuclei showed an immediate small decrease in P.SH content following 800 rads in vitro. Nuclei isolated from rat thymus 1 hour after 1000 rads in vivo showed an increase in the SH content of the globulin fraction and a decrease in the SH content of the nucleohistones. The total SH content of thymocytes and ascites cells was reduced by slow diffusion of H2O2into the cell suspension, but no effect of prior irradiation on this decrease of SH was found. Inhibition of catalase in vivo and in vitro did not produce any of the morphological signs of irradiation damage in thymocytes. There was no effect of irradiation on the copper content of thymus, thymocytes, or ascites cells. The ratio of NP.SH/P.SH is higher in thymocytes than in ascites cells, but, allowing for the difference in cell size, the overall total thiol concentration was the same. Anoxia produced only a small increase in NP.SH content in both cells and a small and doubtful increase in P.SH. It is concluded that, if thiol groups are involved in cell sensitivity to radiation, only a small fraction of the total SH groups are involved at critical sites.

Iron N-(2-hydroxy acetophenone) glycinate (FeNG), a non-toxic glutathione depletor circumvents doxorubicin resistance in Ehrlich ascites carcinoma cells in vivo

BioMetals ◽  
2011 ◽  
Vol 25 (1) ◽  
pp. 149-163 ◽  
Author(s):  
Avishek Ganguly ◽  
Paramita Chakraborty ◽  
Kaushik Banerjee ◽  
Shilpak Chatterjee ◽  
Soumya Basu ◽  
...  
Keyword(s):  
Ehrlich Ascites Carcinoma ◽  
Carcinoma Cells ◽  
Doxorubicin Resistance ◽  
Ehrlich Ascites

Adaptation of ehrlich ascites carcinoma cells to energy deprivation in vivo can be associated with heat shock protein accumulation

1995 ◽  
Vol 165 (1) ◽  
pp. 1-6 ◽  
Author(s):  
A. E. Kabakov ◽  
A. O. Molotkov ◽  
K. R. Budagova ◽  
Yu M. Makarova ◽  
A. F. Mosin ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Ehrlich Ascites Carcinoma ◽  
Carcinoma Cells ◽  
Protein Accumulation ◽  
Ehrlich Ascites ◽  
Energy Deprivation

Characterization of the pigment from homogentisic acid and urine and tissue from an alkaptonuria patient

1991 ◽  
Vol 69 (4) ◽  
pp. 269-273 ◽  
Author(s):  
I. Aravind Menon ◽  
Suruj D. Persad ◽  
Herbert F. Haberman ◽  
Prasanta K. Basu ◽  
Joseph F. Norfray ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Electron Spin Resonance ◽  
Electron Spin ◽  
Ehrlich Ascites Carcinoma ◽  
Homogentisic Acid ◽  
Carcinoma Cells ◽  
Ehrlich Ascites ◽  
Spin Resonance

When urine samples from alkaptonuria patients are allowed to stand, they turn black, presumably owing to the oxidation of homogentisic acid to a melanin-like substance. We report the characterization of the pigments formed by polymerization of (a) the components in the urine from a patient with alkaptonuria and (b) homogentisic acid. The absorption spectra and electron spin resonance signals of these pigments are similar to those of eumelanins. Irradiation of the pigments with nitroblue tetrazolium caused reduction of the tetrazolium; this was partially inhibited by superoxide dismutase. Irradiation of Ehrlich ascites carcinoma cells with the pigments from homogentisic acid or urine caused cell lysis. Since this lysis was inhibited by catalase, we have concluded that it was mediated by H2O2. A similar pigment was also extracted from the tissue from an alkaptonuria patient. It is suggested that the degeneration of tissue in vivo may be due to the deposition of melanin-like pigments in the tissues, probably in combination with metal ions.Key words: alkaptonuria, homogentisic acid, pigmentation, melanin, photosensitization.

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