Bisphenol A (BPA) is used in various areas of daily life as a major component of plastic products. However, it is also known as a strong endocrine disruptor that affects the human immune system. Studies have indicated that BPA possibly exacerbates allergic diseases such as atopic dermatitis and asthma. The main aim of this study was to elucidate whether BPA is directly involved in the exacerbation of allergic inflammation. Initially, in vivo experiments with mouse models of allergic inflammation induced by Th2 type hapten toluene-2, 4-diisocyanate (TDI) was performed. Mice were subjected to oral administration of BPA 48, 24, and 4 h before challenge with TDI. Dermal challenge of TDI onto the ear auricle was performed for the allergic dermatitis model, and intratracheal challenge of TDI was performed for the allergic airway inflammation model. In the allergic dermatitis model, ear-swelling response was significantly downregulated by high doses of BPA. The opposite reaction was observed in the allergic airway inflammation model, including significant exacerbation of red coloration in the lung, local cytokine levels, and total IgE levels in serum by BPA administration. To confirm the in vivo results, in vitro experiments with human epidermal keratinocytes (HEKs) and bronchial epithelial (BEAS-2B) cells were carried out. Significant enhancement of cytokine release from BEAS-2B cells but not HEKs in the BPA-treated group supported the in vivo observations. Our results imply that exposure to BPA directly exacerbates allergic airway inflammation but not allergic dermatitis.
To determine the potential effects of pesticides on aquatic organisms inhabiting a realistic environment, we explored the characteristics and mechanisms of chemical tolerance in Scapholeberis kingi. We established a chemical-tolerant population via continuous exposure to pirimicarb, an acetylcholinesterase (AChE) inhibitor, and examined the effects of pirimicarb concentration on the intrinsic growth rates (r) of tolerant cladocerans. We also explored the association between r and feeding rate and tested the involvement of antioxidant enzymes [peroxidase (PO) and superoxide dismutase] and AChE in pirimicarb sensitivity. S. kingi was continuously exposed to sublethal pirimicarb concentrations (0, 2.5, 5, and 10 µg/L) for 15 generations and changes (half maximal effective concentration at 48 h, 48 h-EC 50 ) in chemical sensitivity were investigated. In the F14 generation, the sensitivity of the 10 µg/L group was three times lower than that of the control group, suggesting the acquisition of chemical tolerance. Moreover, r was signi cantly and negatively correlated with 48 h-EC 50 , suggesting a tness cost for tolerance. Surprisingly, there was no signi cant correlation between r and feeding rate. Our generalized linear model indicated that elevated PO activity may be related to chemical tolerance. Therefore, oxidative stress regulation may be involved in the acquisition of chemical tolerance in cladocerans. These ndings will help elucidate the characteristics and mechanisms of chemical tolerance in aquatic organisms inhabiting a realistic environment.
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