Radiocesium dynamics in the aquatic ecosystem of Lake Onuma on Mt. Akagi following the Fukushima Dai-ichi Nuclear Power Plant accident.

Understanding ecosystem dynamics of radionuclides is necessary to ensure effective management for food safety. The Fukushima Dai-ichi Nuclear Power Plant (FDNPP) accident on March 11, 2011 released large amounts of radiocesium (Cs and Cs) and contaminated the environment across eastern Japan. In this study, we aimed to elucidate the temporal dynamics of Cs in the aquatic ecosystem of Lake Onuma on Mt.

Fractionation of radiocesium in soil, sediments, and aquatic organisms in Lake Onuma of Mt. Akagi, Gunma Prefecture using sequential extraction.

The Fukushima Daiichi Nuclear Power Plant (FDNPP) accident has resulted in the contamination of the environment in Gunma Prefecture with radioisotope cesium (radio-Cs, Cs and Cs). Concentrations of radio-Cs >500Bqkg were found in wakasagi (Hypomesus nipponensis) in Lake Onuma at the top of Mount (Mt.) Akagi in August 2011.

NF-κB activation via MyD88-dependent Toll-like receptor signaling is inhibited by trichothecene mycotoxin deoxynivalenol.

Macrophages induce the innate immunity by recognizing pathogens through Toll-like receptors (TLRs), which sense pathogen-associated molecular patterns. Myeloid differentiation factor 88 (MyD88), which is an essential adaptor molecule for most TLRs, mediates the induction of inflammatory cytokines through nuclear factor κB (NF-κB). Trichothecene mycotoxin deoxynivalenol (DON) shows immunotoxic effects by interrupting inflammatory mediators produced by activated macrophages.

Inhibitory effect of citrinin on lipopolisaccharide-induced nitric oxide production by mouse macrophage cells.

The present study evaluated the immunotoxicity of citrinin (CIT), a mycotoxin produced by several Aspergillus, Penicillium, and Monascus species. Because nitric oxide (NO), a pro-inflammatory mediator, plays an important role in the protection from pathogens, we addressed the effect of CIT on NO production by a mouse macrophage-like cell line RAW264 activated with lipopolysaccharide (LPS). LPS-induced NO release from RAW264 cells was inhibited by CIT.