060 Phytoestrogen genistein affects susceptibility to alopecia areata in C3H/HeJ mice

K.J. McElwee1, S. Niiyama1, E. Wenzel1, P. Freyschmidt-Paul1, J.P. Sundberg2, R. Hoffmann1 Philipp University, Marburg1; The Jackson Laboratory, Bar Harbor, ME, USA2.

Alopecia areata (AA) is a complex, multi-factorial disease where genes and the environment may affect susceptibility and severity. We considered dietary soy oil content and soy derived phyto-estrogen, genistein, as potential modifying agents for C3H/HeJ mouse AA. Prior to the experiment, all mice received a standard commercial diet of 1% soy oil (4% total fat). Normal haired C3H/HeJ mice were grafted with AA affected skin, a method previously shown to successfully induce AA. Grafted mice were given one of three diets. Two groups of twenty eight mice received a 1% or 5% (7.5% total fat) soy oil diet. Eleven mice received a diet with 20% soy oil (23% total fat) formulated by the animal diet manufacturer using the 1% soy oil diet as a base and additional soy oil from the same source. In a separate study, mice on a 1% soy oil diet were injected with 1mg genistein three times per week for 10 weeks or received the drug vehicle control. Mice were monitored for at least 20 weeks after skin grafting and then necropsied. Of mice on 1%, 5%, and 20% soy oil diets, 20 of 28 mice (71%), 11 of 28 mice (39%), and 2 of 11 mice (18%) developed AA respectively. Four of 10 mice injected with genistein and 9 of 10 controls developed AA. Mice with AA had hair follicle inflammation consistent with observations for spontaneous mouse AA, but no significant association was observed between the extent of hair loss and diet or genistein injection. Mice that failed to develop AA typically regrew white hair from their skin grafts with no associated inflammation. Soy oil and derivatives have previously been reported to modify rodent inflammatory conditions. Hypothetically, soy oil compounds may act on C3H/HeJ mice through modulating estrogen-dependent mechanisms and/or inflammatory response activity to modify AA susceptibility.