Recently, we have shown that roasted peanuts have a higher level of IgE bin
ding (i.e., potentially more allergenic) than raw peanuts. We hypothesized
that this increase in IgE binding of roasted peanuts is due to an increased
levels of protein-bound end products or adducts such as advanced glycation
end products (AGE), N-(carboxymethyl)lysine (CML), malondialdehyde (MDA),
and 4-hydroxynonenal (HNE). To support our hypothesis, we produced polyclon
al antibodies (IgG) to each of these adducts, determined their levels in ra
w and roasted peanuts, and examined their ability to bind to IgE from a poo
led serum of patients with clinically important peanut allergy. Results sho
wed that AGE, CML, MDA, and HNE adducts were all present in raw and roasted
peanuts. Roasted peanuts exhibited a higher level of AGE and MDA adducts t
han raw peanuts. IgE was partially inhibited in a competitive ELISA by anti
bodies to AGE but not by antibodies to CML, MDA, or HNE. This indicates tha
t IgE has an affinity for peanut AGE adducts. Roasted peanuts exhibited a h
igher level of IgE binding, which was correlated with a higher level of AGE
adducts. We concluded that there is an association between AGE adducts and
increased IgE binding (i.e., allergenicity) of roasted peanuts.