Characterization of cisplatin-induced DNA damage in human bladder tumour cell lines

Abstract

sera and aliquots assayed for EH activity. None of the clones expressed more activity than the mouse control cells. When extracts were treated with the anti-human antiserum, however, no greater reduction in EH activity occurred than occurred with the mouse cell pellets. It can be concluded, therefore, that none of the hybrids was expressing human EH activity. There are several possible explanations for this. Firstly, the gene coding for human EH could be located on chromosome 6. It has proved impossible to test for this to date since all clones examined segregated this chromosome. It could also be possible that either chromosome 3 or 22 was segregated from these clones. Finally, it may be that the human EH gene was present in some of these clones but was not expressed. This has been reported for tyrosine aminotransferase expression in hybrid cells but is not the case for aryl hydrocarbon hydroxylase or glutathione S-epoxide transferases (Benedict er a/., 1972; Silberstein & Shows, 1982). Further work is in progress to test these possibilities.