N.W. Gibson

TL;DR: Using polymerase chain reaction (PCR) analysis, it is found that the H596 human non-small-cell lung cancer cell line has elevated NQO1 mRNA, but no detectable enzyme activity, which suggests that the mutation at position 609 represents a polymorphism in an important xenobiotic metabolizing enzyme, which has implications for cancer therapy, chemoprevention and chemoprotection.

TL;DR: Using a cell-free system, it is confirmed that DTD can bioactivate mitomycin C using both purified rat and human DTD and the cytotoxicity of this drug in DTD-rich cell lines is oxygen-independent.

TL;DR: A point mutation at position 609 in the DTD cDNA is characterized, which codes for a proline to serine change in the protein and leads to a loss of enzyme activity and complicates the use of agents designed to target DTD in tumors.

TL;DR: Compounds such as 2,5-dimethyl-3,6-diaziridinyl-1,4-benzoquinone and streptonigrin are still excellent substrates for the human enzyme and may be useful in the therapy of tumors high in DTD activity.

TL;DR: Observations indicate that it is possible to maintain high intracellular levels of selenium, by exposure to methylated selenocompounds, without affecting DNA integrity and suggest that DNA fragmentation resulting from exposure to selenite occurs during its reductive metabolism and not from the accumulation of a methylated metabolite ofSelenium.