TY  - JOUR
AU  - Tabaković, I.
AU  - Davidović, A.
AU  - Müller, W.E.G.
AU  - Zahn, R.K.
AU  - Sladić, Dušan
AU  - Dogović, N.
AU  - Gašić, M.J.
PY  - 1987
UR  - https://cherry.chem.bg.ac.rs/handle/123456789/71
AB  - The redox reactivity of avarone and avarol, a quinone/hydroquinone couple isolated from the marine sponge Dysidea avara, was investigated by cyclic voltammetry, using a glassy carbon electrode. Both oxidation of avarol and reduction of avarone in aqueous ethanol (1:1 V/V) take place by a 2 e- process at a wide range of pH values; in acetonitrile, however, the reduction of avarone occurs as a stepwise electron transfer process. The mechanisms, as well as the scope and limitations of the method are discussed with reference to the biological activity of the two sesquiterpenoids. © 1987.
T2  - Bioelectrochemistry and Bioenergetics
T1  - Electrochemical reactivity of biologically active quinone/hydroquinone sesquiterpenoids on glassy carbon electrodes
VL  - 17
IS  - 3
SP  - 567
EP  - 577
DO  - 10.1016/0302-4598(87)80064-8
ER  - 

@article{
author = "Tabaković, I. and Davidović, A. and Müller, W.E.G. and Zahn, R.K. and Sladić, Dušan and Dogović, N. and Gašić, M.J.",
year = "1987",
abstract = "The redox reactivity of avarone and avarol, a quinone/hydroquinone couple isolated from the marine sponge Dysidea avara, was investigated by cyclic voltammetry, using a glassy carbon electrode. Both oxidation of avarol and reduction of avarone in aqueous ethanol (1:1 V/V) take place by a 2 e- process at a wide range of pH values; in acetonitrile, however, the reduction of avarone occurs as a stepwise electron transfer process. The mechanisms, as well as the scope and limitations of the method are discussed with reference to the biological activity of the two sesquiterpenoids. © 1987.",
journal = "Bioelectrochemistry and Bioenergetics",
title = "Electrochemical reactivity of biologically active quinone/hydroquinone sesquiterpenoids on glassy carbon electrodes",
volume = "17",
number = "3",
pages = "567-577",
doi = "10.1016/0302-4598(87)80064-8"
}

Tabaković, I., Davidović, A., Müller, W.E.G., Zahn, R.K., Sladić, D., Dogović, N.,& Gašić, M.J.. (1987). Electrochemical reactivity of biologically active quinone/hydroquinone sesquiterpenoids on glassy carbon electrodes. in Bioelectrochemistry and Bioenergetics, 17(3), 567-577.
https://doi.org/10.1016/0302-4598(87)80064-8

Tabaković I, Davidović A, Müller W, Zahn R, Sladić D, Dogović N, Gašić M. Electrochemical reactivity of biologically active quinone/hydroquinone sesquiterpenoids on glassy carbon electrodes. in Bioelectrochemistry and Bioenergetics. 1987;17(3):567-577.
doi:10.1016/0302-4598(87)80064-8 .

Tabaković, I., Davidović, A., Müller, W.E.G., Zahn, R.K., Sladić, Dušan, Dogović, N., Gašić, M.J., "Electrochemical reactivity of biologically active quinone/hydroquinone sesquiterpenoids on glassy carbon electrodes" in Bioelectrochemistry and Bioenergetics, 17, no. 3 (1987):567-577,
https://doi.org/10.1016/0302-4598(87)80064-8 . .

TY  - JOUR
AU  - Muller, W.E.G.
AU  - Sladić, Dušan
AU  - Zahn, R.K.
AU  - Bassler, K.-H.
AU  - Dogovic, N.
AU  - Gerner, H.
AU  - Gasic, M.J.
AU  - Schroder, H.C.
PY  - 1987
UR  - https://cherry.chem.bg.ac.rs/handle/123456789/13
AB  - The hydroquinone-containing cytostatic compound avarol inhibits predominantly growth of those cell lines which have a low level of superoxide dismutase. The substrate of this enzyme, the superoxide anion, was found to be formed during the in vitro oxidation reaction of avarol to its semiquinone radical in the presence of oxygen. Under the same incubation conditions plasmid DNA (pBR322) was converted from the fully supercoiled circular form mainly to the nicked circular form, indicating that the compound causes primarily single-strand breaks. Using Friend erythroleukemia cells (FLC) it was found that avarol induces a dose-dependent DNA damage; the maximum number of DNA strand breaks was observed at 5 h after addition of the compound to the cells. Removal of avarol resulted in a rapid DNA rejoining with biphasic repair kinetics [first half-time, 8 min (90% of the breaks) and a second half-time, 40 min (10% of the breaks)]. When the degree of avarol-induced DNA damage in FLC was compared with the drug-caused inhibition of cell growth a close correlation was established. Avarol displayed no effect on dimethyl sulfoxide-induced erythrodifferentiation of FLC as determined by the benzidine reaction and by dot blot hybridization experiments. From incubation studies of FLC with [3H]avarol no hint was obtained for the formation of an adduct between DNA and the compound. The subcellular distribution of [3H]avarol was studied in liver cells after i.v. application of the compound. The predominant amount of the compound was present in the cytosolic fraction; little avarol was associated with plasma membranes, nuclei, and mitochondria. Using (a) oxidative phosphorylation and (b) oxygen uptake as parameters for mitochondrial function, no effect of the compound on the activity of this organelle was determined. These results suggest that avarol forms superoxide anions (and in consequence possibly also hydroxyl radicals) especially in those cells which have low levels of superoxide dismutase. Moreover, evidence is provided that the active oxygen species cause DNA damage resulting in the observed cytotoxic effect.
T2  - Cancer Research
T1  - Avarol-induced DNA strand breakage in vitro and in Friend erythroleukemia cells
VL  - 47
IS  - 24 I
SP  - 6565
EP  - 6571
UR  - https://hdl.handle.net/21.15107/rcub_cherry_13
ER  - 

@article{
author = "Muller, W.E.G. and Sladić, Dušan and Zahn, R.K. and Bassler, K.-H. and Dogovic, N. and Gerner, H. and Gasic, M.J. and Schroder, H.C.",
year = "1987",
abstract = "The hydroquinone-containing cytostatic compound avarol inhibits predominantly growth of those cell lines which have a low level of superoxide dismutase. The substrate of this enzyme, the superoxide anion, was found to be formed during the in vitro oxidation reaction of avarol to its semiquinone radical in the presence of oxygen. Under the same incubation conditions plasmid DNA (pBR322) was converted from the fully supercoiled circular form mainly to the nicked circular form, indicating that the compound causes primarily single-strand breaks. Using Friend erythroleukemia cells (FLC) it was found that avarol induces a dose-dependent DNA damage; the maximum number of DNA strand breaks was observed at 5 h after addition of the compound to the cells. Removal of avarol resulted in a rapid DNA rejoining with biphasic repair kinetics [first half-time, 8 min (90% of the breaks) and a second half-time, 40 min (10% of the breaks)]. When the degree of avarol-induced DNA damage in FLC was compared with the drug-caused inhibition of cell growth a close correlation was established. Avarol displayed no effect on dimethyl sulfoxide-induced erythrodifferentiation of FLC as determined by the benzidine reaction and by dot blot hybridization experiments. From incubation studies of FLC with [3H]avarol no hint was obtained for the formation of an adduct between DNA and the compound. The subcellular distribution of [3H]avarol was studied in liver cells after i.v. application of the compound. The predominant amount of the compound was present in the cytosolic fraction; little avarol was associated with plasma membranes, nuclei, and mitochondria. Using (a) oxidative phosphorylation and (b) oxygen uptake as parameters for mitochondrial function, no effect of the compound on the activity of this organelle was determined. These results suggest that avarol forms superoxide anions (and in consequence possibly also hydroxyl radicals) especially in those cells which have low levels of superoxide dismutase. Moreover, evidence is provided that the active oxygen species cause DNA damage resulting in the observed cytotoxic effect.",
journal = "Cancer Research",
title = "Avarol-induced DNA strand breakage in vitro and in Friend erythroleukemia cells",
volume = "47",
number = "24 I",
pages = "6565-6571",
url = "https://hdl.handle.net/21.15107/rcub_cherry_13"
}

Muller, W.E.G., Sladić, D., Zahn, R.K., Bassler, K.-H., Dogovic, N., Gerner, H., Gasic, M.J.,& Schroder, H.C.. (1987). Avarol-induced DNA strand breakage in vitro and in Friend erythroleukemia cells. in Cancer Research, 47(24 I), 6565-6571.
https://hdl.handle.net/21.15107/rcub_cherry_13

Muller W, Sladić D, Zahn R, Bassler K, Dogovic N, Gerner H, Gasic M, Schroder H. Avarol-induced DNA strand breakage in vitro and in Friend erythroleukemia cells. in Cancer Research. 1987;47(24 I):6565-6571.
https://hdl.handle.net/21.15107/rcub_cherry_13 .

Muller, W.E.G., Sladić, Dušan, Zahn, R.K., Bassler, K.-H., Dogovic, N., Gerner, H., Gasic, M.J., Schroder, H.C., "Avarol-induced DNA strand breakage in vitro and in Friend erythroleukemia cells" in Cancer Research, 47, no. 24 I (1987):6565-6571,
https://hdl.handle.net/21.15107/rcub_cherry_13 .