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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
11

The study of antitumour drugs and their interactions with DNA using X-ray diffraction methods

Thorpe, James Henry January 2000 (has links)
No description available.
12

Aspects of the interaction between cisplatin and renal glutathione

Merazga, Yamina January 1990 (has links)
No description available.
13

The synthesis and evaluation of potential inhibitors of the DNA repair protein #OMICRON#'6-alkylguanine-DNA alkyltransferase

Dalby, Christine January 1993 (has links)
No description available.
14

Mechanisms of enhancement of antimetabolite cytotoxicity by 3-aminobenzamide

Willmore, Elaine January 1994 (has links)
No description available.
15

Selective potentiation of antipurine antifolate activity by dipyridamole

Marshman, Emma January 1999 (has links)
No description available.
16

An investigation into the cytotoxic mechanisms of DNA topoisomerase II poisons and catalytic inhibitors : the role of DNA topoisomerase II alpha and beta

Errington, Fiona January 2001 (has links)
No description available.
17

Design and synthesis of fluorodeoxyuridine derivatives and their conjunction with monoclonal antibody for the purpose of drug targeting

Henn, Thomas Frederic George January 1990 (has links)
No description available.
18

Antibody-targeted methotrexate against methotrexate resistant tumour cells

Affleck, Karen January 1990 (has links)
No description available.
19

The synthesis and evaluation of anti-melanoma drugs

Lant, Neil Joseph January 1998 (has links)
No description available.
20

Free radical formation and DNA damage in the cytotoxicity of alkylaminoanthraquinone antitumour agents

Fisher, Geoffrey Roy January 1989 (has links)
The role of NAD(P)H dependent reductase mediated redox cycling in DNA strand breakage and cytotoxicity by doxorubicin (DOX), mitozantrone (MIT), CI941 and a series of alkylaminoanthraquinones (AQ) based on MIT has been investigated in MCF-7 human breast cancer cells. lAQ, 1,8AQ and DOX were found to redox cycle in MCF-7 cells as evidenced by stimulation of NADPH oxidation, superoxide anion formation and hydroxyl radical formation associated with generation of a drug free radical in MCF-7 S9 cell fraction. Furthermore, DOX formed a free radical, stimulated oxygen consumption and produced hydroxyl radicals in intact viable MCF-7 cells. 1,5AQ formed a free radical species and produced hydroxyl radicals but did not stimulate NADPH oxidation or superoxide anion formation in MCF-7 S9 fraction. Reactive oxygen formation correlated with the DNA strand breakage and cytotoxicity produced by IAQ, I,SAQ, 1,8AQ and DOX in MCF-7 cells. DOX also produced plasmid DNA strand breakage in the presence of purified cytochrome P4S0 reductase or xanthine oxidase. lAQ, 1,SAQ and 1,8AQ mediated plasmid DNA strand breakage only in the presence of purified cytochrome P4S0 reductase. MIT, CI941 and 1,4AQ did not redox cycle in MCF-7 cell S9 fraction yet produced equivalent cellular DNA strand breakage to DOX and AQ's at LDSO concentrations. The order of cytotoxicity of these compounds after a 1 hour exposure ~nd at least 6 d~ys further cell growth was;- (LDSO);- CI941(I.SxlO-lUM) >MIT(S.2xlO- YM) >lAQ(6.0xlO- 8M) >1,8AQ(O.5xlO- 6M) >1,4AQ(I.2xIO- 6M) >DOX(3.0xlO- 6M) >1,SAQ(12.3xIO- 6M). Variation in cellular uptake between the agents did not account for differences in cytotoxicity and DNA strand breakage observed. The 1,4 substitution pattern of MIT, CI941 and 1,4AQ appears to prevent metabolic activation. In further studies;- i) MIT and CI941 were more potent inhibitors of 3 MCF-7 topoisomerase I activity than other quinones, ii) MIT and DOX-Fe + complexes mediated plasmid DNA strand breakage in the presence of reduced glutathione iii) Only MIT was oxidatively activated by horseradish peroxidase!H202' producing plasmid DNA damage. The results indicate that future development of quinone anti tumour agents should concentrate on compounds which do not redox cycle but have functional groups that assist iron binding, activation by peroxidases and/or topoisomerase inhibition. In this respect, these agents should possess chromophore hydroxyl groups as these appear to be responsible for the increased cytotoxicity of MIT and CI941 compared to the other AQ's.

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