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dc.contributor.authorSheweita, S A
dc.contributor.authorEl-Shahat, F G
dc.contributor.authorBazeed, M A
dc.contributor.authorAbu El-Maati, M R
dc.contributor.authorO'Connor, Peter J
dc.date.accessioned2009-08-21T11:26:27Z
dc.date.available2009-08-21T11:26:27Z
dc.date.issued2004-03-08
dc.identifier.citationEffects of Schistosoma haematobium infection on drug-metabolizing enzymes in human bladder cancer tissues. 2004, 205 (1):15-21 Cancer Lett.en
dc.identifier.issn0304-3835
dc.identifier.pmid15036656
dc.identifier.doi10.1016/j.canlet.2003.09.023
dc.identifier.urihttp://hdl.handle.net/10541/78175
dc.description.abstractThe mixed function oxidase system includes the phase I drug oxidation proteins e.g. aryl hydrocarbon hydroxylase (AHH), N-nitrosodimethylamine-N-demethylase I (NDMA-dI) and cytochrome b5 which metabolize most carcinogens and xenobiotics into less and/or more active intermediates. These were determined in human bladder tissues diagnosed as bladder cancer only (10 samples) and bladder cancer associated with Schistosoma haematobium (12 samples) and normal bladder tissues (12 samples). In addition to the above enzymes, agents involved in Phase II drug metabolism e.g. glutathione and glutathione S-transferase as well as free radicals (detected as thiobarbituric acid-reactive substances, TBARS) were also determined in these tissues samples. AAH and NDMA-dI, cytochrome b5, and glutathione S-transferase activity decreased by 42, 28, 47 and 32%, respectively, in human bladder cancer tissues. In bladder cancer tissues associated with S. haematobium infection NDMA-dI and GST activity decreased further by 65 and 56%, respectively, whereas AHH activity increased by 50% and levels of reduced glutathione also increased by 43% in cancer tissue and by 29% in schistocome infected bladder cancer tissue. The level of free radicals also increased significantly (by 57%) in infected bladder cancer tissue but not at all in non-infected cancer tissue. Alterations in the activity of phase I and II of drug-metabolizing enzymes in human bladder tissues as a result of S. haematobium infection may therefore change the bladder's capacity to detoxify many endogenous compounds and may also potentiate the deleterious effects of bladder carcinogens, (e.g. N-nitrosamines) which are known to be present in relatively large quantities in the bladder of patients with schistosomiasis. The present study thus provides new insights into mechanisms for the genesis of bladder cancer initiated in association with schistosomiasis.
dc.language.isoenen
dc.subjectUrinary Bladder Canceren
dc.subject.meshAdult
dc.subject.meshAnimals
dc.subject.meshHumans
dc.subject.meshMiddle Aged
dc.subject.meshMixed Function Oxygenases
dc.subject.meshSchistosomiasis haematobia
dc.subject.meshUrinary Bladder Neoplasms
dc.titleEffects of Schistosoma haematobium infection on drug-metabolizing enzymes in human bladder cancer tissues.en
dc.typeArticleen
dc.contributor.departmentDepartment of Bioscience and Technology, Institute of Graduate Studies and Research, Alexandria University, Alexandria, Egypt. sheweita@hotmail.comen
dc.identifier.journalCancer Lettersen
html.description.abstractThe mixed function oxidase system includes the phase I drug oxidation proteins e.g. aryl hydrocarbon hydroxylase (AHH), N-nitrosodimethylamine-N-demethylase I (NDMA-dI) and cytochrome b5 which metabolize most carcinogens and xenobiotics into less and/or more active intermediates. These were determined in human bladder tissues diagnosed as bladder cancer only (10 samples) and bladder cancer associated with Schistosoma haematobium (12 samples) and normal bladder tissues (12 samples). In addition to the above enzymes, agents involved in Phase II drug metabolism e.g. glutathione and glutathione S-transferase as well as free radicals (detected as thiobarbituric acid-reactive substances, TBARS) were also determined in these tissues samples. AAH and NDMA-dI, cytochrome b5, and glutathione S-transferase activity decreased by 42, 28, 47 and 32%, respectively, in human bladder cancer tissues. In bladder cancer tissues associated with S. haematobium infection NDMA-dI and GST activity decreased further by 65 and 56%, respectively, whereas AHH activity increased by 50% and levels of reduced glutathione also increased by 43% in cancer tissue and by 29% in schistocome infected bladder cancer tissue. The level of free radicals also increased significantly (by 57%) in infected bladder cancer tissue but not at all in non-infected cancer tissue. Alterations in the activity of phase I and II of drug-metabolizing enzymes in human bladder tissues as a result of S. haematobium infection may therefore change the bladder's capacity to detoxify many endogenous compounds and may also potentiate the deleterious effects of bladder carcinogens, (e.g. N-nitrosamines) which are known to be present in relatively large quantities in the bladder of patients with schistosomiasis. The present study thus provides new insights into mechanisms for the genesis of bladder cancer initiated in association with schistosomiasis.


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