1,3,6-Tri-O-methylarthothelin

1,3-Dichloro-2-propanol (1,3-DCP), as a food pollutant, exists in a variety of foods. Studies have shown that it has nephrotoxicity. In the study, we found that 1,3-DCP caused renal injury with necroptosis in C57BL/6J mice. The mechanism of 1,3-DCP-caused nephrotoxicity was further explored in NRK-52E cells in vitro. We found that 1,3-DCP caused cell necroptosis with the increase in lactate dehydrogenase (LDH) levels and the expressions of RIPK3 and MLKL. But pretreatment with a ROS inhibitor N-acetyl-l-cysteine (NAC), a RIPK3 inhibitor GSK'872, or RIPK3 gene silencing alleviated 1,3-DCP-induced cell necroptosis. The data indicated that 1,3-DCP induced necroptosis through the ROS/RIPK3/MLKL pathway in NRK-52E cells. In further mechanistic studies, we explored how 1,3-DCP induced ROS production. We found that 1,3-DCP inhibited the expressions of nuclear and cytoplasmic Nrf2. But pretreatment with an Nrf2 activator dimethyl fumarate (DMF) up-regulated the expressions of nuclear and cytoplasmic Nrf2 and down-regulated ROS levels and RIPK3 and MLKL expressions. We also examined the effects of mitophagy on 1,3-DCP-induced ROS. The data manifested that 1,3-DCP suppressed mitophagy in NRK-52E cells by decreasing LC3-II, Pink1, and Parkin levels, increasing p62 levels, and decreasing colocalization of LC3 and Mito-Tracker Red. Pretreatment with an autophagy activator rapamycin (Rapa) decreased 1,3-DCP-induced ROS. Taken together, our data identified that 1,3-DCP caused renal necroptosis through the ROS/RIPK3/MLKL pathway.

The title compounds, 6-cyclo-propyl-1,3-diphenylfulvene, C21H18, [systematic name: 5-(cyclo-propyl-methyl-idene)-1,3-di-phen-yl-cyclo-penta-1,3-diene], 1, and 6-(2,3-di-meth-oxy-naphth-yl)-1,3-diphenylfulvene, C30H24O2, {systematic name: 5-[(3,4-di-meth-oxy-naphthalen-2-yl)methyl-idene]-1,3-di-phenyl-cyclo-penta-1,3-di-ene}, 2, were prepared from 1,3-di-phenyl-cyclo-penta-diene, pyrrolidine, and the corresponding aldehydes in an ethano-lic solution. Each structure crystallizes with one mol-ecule per asymmetric unit and exhibits the alternating short and long bond lengths typical of fulvenes. A network of C-H⋯C ring inter-actions as well as C-H⋯O inter-actions is observed, resulting in the compact packing found in each structure.

1,3-xylan is present in the cell walls of some red and green algae and is an important organic carbon in the ocean. However, information on its bacterial degradation is quite limited. Here, after enrichment with 1,3-xylan, the diversity of bacteria recovered from marine algae collected in Hainan, China, was analyzed with both the 16S rRNA gene amplicon sequencing and the culture-dependent method. Bacteria recovered were affiliated with more than 19 families mainly in phyla Proteobacteria and Bacteroidetes, suggesting a high bacterial diversity. Moreover, 12 strains with high 1,3-xylanase-secreting ability from genera Vibrio, Neiella, Alteromonas, and Gilvimarinus were isolated from the enrichment culture. The extracellular 1,3-xylanases secreted by Vibrio sp. EA2, Neiella sp. GA3, Alteromonas sp. CA13-2, and Gilvimarinus sp. HA3-2, which were taken as representatives due to their efficient utilization of 1,3-xylan for growth, were further characterized. The extracellular 1,3-xylanases secreted by these strains showed the highest activity at pH 6.0-7.0 and 30-40°C in 0-0.5M NaCl, exhibiting thermo-unstable and alkali-resistant characters. Their degradation products on 1,3-xylan were mainly 1,3-xylobiose and 1,3-xylotriose. This study reveals the diversity of marine bacteria involved in the degradation and utilization of 1,3-xylan, helpful in our understanding of the recycling of 1,3-xylan driven by bacteria in the ocean and the discovery of novel 1,3-xylanases.