Potential mechanisms of tumorigenic action of diethanolamine in mice

Diethanolamine (DEA), a secondary amine found in a number of consumer produ cts, reportedly induces liver tumors in mice. In an attempt to define the t umorigenic mechanism of DEA, N-nitrosodiethanolamine (NDELA) formation in v ivo and development of choline deficiency were examined in mice. DEA was ad ministered with or without supplemental sodium nitrite to B6C3F1 mice via d ermal application (with or without access to the application site) or via o ral gavage for 2 weeks. Blood levels of DEA reflected the dosing method use d; 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 de creased less than or equal to 62-84% in an inverse relation to blood DEA le vels. These data demonstrated a lack of NDELA formation in vivo at tumorige nic dosages of DEA but revealed a pronounced depletion of choline-containin g compounds' in mice. It is suggested that the latter effect may underlie D EA tumorigenesis in the mouse. (C) 2000 Elsevier Science Ireland Ltd. All r ights reserved.