Uptake, translocation, and metabolism of thiamethoxam in soil by leek plants.

Thiamethoxam (TMX) is commonly applied on leek plants by root irrigation. It might be taken up by leek plants and thus has lasting dietary risk. In this study, the uptake, translocation, and metabolism of TMX in leek plants were investigated. The results obtained from both the hydroponic and soil experiments indicated that TMX could be easily translocated upward and accumulated in leek shoots after being absorbed by roots. The total absorbed TMX amount (Mtotal) in leek plants from the tested soils varied greatly with its adsorption governed by soil characteristics. Interestingly, Mtotal was closely correlated with the concentration of TMX in in situ pore water, indicating that TMX in in situ pore water could be a useful approach to predict uptake of this chemical by leek plants from various soils. Profoundly, clothianidin (CLO) was detected with concentration of 0.07-1.54 mg/kg in roots and 0.27-4.12 mg/kg in shoots at 14 d, respectively, suggesting that TMX is easily converted into CLO in leek plants. The results showed that TMX used in soil is easily absorbed by leek and accumulated in edible parts accompanying with formation of CLO.

Administration of exogenous 1,25(OH)2D3 normalizes overactivation of the central renin-angiotensin system in 1α(OH)ase knockout mice.

Previously, we reported that active vitamin D deficiency in mice causes secondary hypertension and cardiac dysfunction, but the underlying mechanism remains largely unknown. To clarify whether exogenous active vitamin D rescues hypertension by normalizing the altered central renin-angiotensin system (RAS) via an antioxidative stress mechanism, 1-alpha-hydroxylase [1α(OH)ase] knockout mice [1α(OH)ase(-/-)] and their wild-type littermates were fed a normal diet alone or with 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], or a high-calcium, high-phosphorus "rescue" diet with or without antioxidant N-acetyl-l-cysteine (NAC) supplementation for 4 weeks. Compared with their wild-type littermates, 1α(OH)ase(-/-)mice had high mean arterial pressure, increased levels of renin, angiotensin II (Ang II), and Ang II type 1 receptor, and increased malondialdehyde levels, but decreased anti-peroxiredoxin I and IV proteins and the antioxidative genes glutathione reductase (Gsr) and glutathione peroxidase 4 (Gpx4) in the brain samples. Except Ang II type 1 receptor, these pathophysiological changes were rescued by exogenous 1,25(OH)2D3 or NAC plus rescue diet, but not by rescue diet alone. We conclude that 1,25(OH)2D3 normalizes the altered central RAS in 1α(OH)ase(-/-)mice, at least partially, through a central antioxidative mechanism.