Abstract:
:Diethanolamine (DEA), a secondary amine found in a number of consumer products, reportedly induces liver tumors in mice. In an attempt to define the tumorigenic mechanism of DEA, N-nitrosodiethanolamine (NDELA) formation in vivo and development of choline deficiency were examined in mice. DEA was administered with or without supplemental sodium nitrite to B6C3F1 mice via dermal application (with or without access to the application site) or via oral gavage for 2 weeks. Blood levels of DEA reflected the dosing method used; oral greater than dermal with access greater than dermal without access. No NDELA was observed in the urine, blood or gastric contents of any group of treated mice. Choline, phosphocholine and glycerophosphocholine were decreased =62-84% in an inverse relation to blood DEA levels. These data demonstrated a lack of NDELA formation in vivo at tumorigenic dosages of DEA but revealed a pronounced depletion of choline-containing compounds in mice. It is suggested that the latter effect may underlie DEA tumorigenesis in the mouse.
journal_name
Toxicol Lettjournal_title
Toxicology lettersauthors
Stott WT,Bartels MJ,Brzak KA,Mar M,Markham DA,Thornton CM,Zeisel SHdoi
10.1016/s0378-4274(99)00197-6keywords:
subject
Has Abstractpub_date
2000-04-03 00:00:00pages
67-75issue
1-3eissn
0378-4274issn
1879-3169pii
S0378427499001976journal_volume
114pub_type
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