BACKGROUND: Recent studies have reported that endocrine-disrupting compound (EDC) exposure is related to food sensitization. Bisphenol A diglycidyl ether (BADGE) is one of the most widespread EDCs and its biological effects are considered to be greater on children than on adults. This study investigated the relationship between serum BADGE-specific immunoglobulin G (IgG) concentrations and food sensitization in young children by measuring food-specific IgE levels. METHODS: In total, 98 young children (59 boys and 39 girls; median age: 7 months; 25th and 75th percentile ages: 6 and 8 months, respectively) were enrolled. Blood samples were collected twice from all children (median sampling interval: 6 months; 25th and 75th percentile: 5 and 7 months). Food sensitization was evaluated based on food-specific IgE titers (egg white, milk, and wheat), which were determined using the capsulated hydrophilic carrier polymer-radioallergosorbent test. Furthermore, a dot-blotting assay for BADGE-specific IgG and quantitative reverse-transcriptase PCR for IL-6, IL-8, IL-10, and COX-2 mRNA expression were conducted. RESULTS: BADGE-specific IgG was detected in 20% of study subjects. A significant association was observed between the presence of BADGE-specific IgG and elevated wheat-specific IgE levels (OR = 3.56; 95% CI 1.13-11.2; P = 0.031). This relationship was particularly strong in girls (OR = 9.46; 95% CI 1.01-89.0; P = 0.049). A slight but non-significant association was noted between the presence of BADGE-specific IgG and elevated milk-specific IgE levels (OR = 2.77; 95% CI 0.93-8.22; P = 0.067). The expression of IL-6 mRNA among children with BADGE-specific IgG tended to increase, along with wheat-specific IgE levels. CONCLUSION: BADGE exposure might enhance food sensitization in early childhood. Therefore, this should be strictly regulated, especially in younger children.

Several studies have shown that docosahexaenoic acid (DHA) attenuates epileptic seizures; however, the molecular mechanism by which it achieves this effect is still largely unknown. DHA stimulates the retinoid X receptor, which reportedly regulates the expression of cytochrome P450 aromatase (P450arom). This study aimed to clarify how DHA suppresses seizures, focusing on the regulation of 17β-estradiol synthesis in the brain. Dietary supplementation with DHA increased not only the expression of P450arom, but also 17β-estradiol in the cerebral cortex. While DHA did not affect the duration or scores of the seizures induced by pentylenetetrazole, DHA significantly prolonged the seizure latency. A P450arom inhibitor, letrozole, reduced 17β-estradiol levels and completely suppressed the elongation of seizure latency elicited by DHA. These results suggest that DHA delays the onset of seizures by promoting the synthesis of 17β-estradiol in the brain. DHA upregulated the expression of anti-oxidative enzymes in the cerebral cortex. The oxidation in the cerebral cortex induced by pentylenetetrazole was significantly attenuated by DHA, and letrozole completely inhibited this suppressive action. Thus, the anti-oxidative effects of 17β-estradiol may be involved in the prevention of seizures mediated by DHA. This study revealed that 17β-estradiol in the brain mediated the physiological actions of DHA.