Transformation and fate of non-reactive phosphorus (NRP) in enhanced biological phosphorus removal process with sidestream phosphorus recovery.

Recovery of phosphorus (P) from wastewater can help establish a new P cycle. However, there are many P forms in wastewater, not always in reactive forms, which are the most suitable for direct recovery. The enhanced biological phosphorus removal process with sidestream phosphorus recovery (EBPR-SPR) is an effective way to remove and recover P resources in wastewater, but there is a lack of research on the transformation and fate of non-reactive phosphorus (NRP) in it. This study selected four model NRP to investigate their transformation and fate in an EBPR-SPR process. The transformation of NRP in pure water and activated sludge under anaerobic and aerobic conditions were compared. The effects of Ca/P ratio and pH on NRP recovery were studied, and the recovery products of NRP were characterized. It was found that NRP containing phosphoanhydride and phosphoester bonds were more easily hydrolyzed to reactive P (RP) than that containing PC bonds. NRP will be adsorbed and accumulated by activated sludge, and activated sludge will accelerate the conversion of NRP to RP. Tripolyphosphate can form complex precipitation with Ca2+. When multiform P co-existed, Ca2+ preferably complexed with polyphosphate, which harmed RP recovery. The conversion of NRP should be strengthened to recover more P in wastewater. The effect of NRP should be considered when recovering P from wastewater.

Aspirin suppresses neuronal apoptosis, reduces tissue inflammation, and restrains astrocyte activation by activating the Nrf2/HO-1 signaling pathway.

The nuclear factor E2-related factor 2 (Nrf2)/antioxidant response element signaling pathway plays a substantial role in preventing oxidative stress-related diseases. Aspirin has been shown to exert several pharmacological effects by inducing the expression of the heme oxygenase-1 (HO-1) protein. However, the effects of aspirin on spinal cord injury (SCI) have rarely been studied. Therefore, we sought to investigate the neuroprotective effects of aspirin after SCI. We employed a spinal cord contusion model in Sprague-Dawley rats, and aspirin was administered intraperitoneally for 7 days. Nissl staining showed that the aspirin treatment significantly reduced the loss of motor neurons after SCI compared with vehicle-treated animals. The expression of Nrf2, quinine oxidoreductase 1, and HO-1 proteins was increased in aspirin-treated animals after SCI compared with the vehicle group. In addition, aspirin simultaneously decreased the expression of inflammation-related proteins, such as tumor necrosis factor-α and interleukin-6 after SCI. Moreover, the ratio of apoptotic neurons in the anterior horn and the levels of the apoptosis-related proteins caspase-3, cleaved caspase-3, and Bax were significantly decreased in the aspirin group compared with the vehicle group. Immunofluorescence staining was used to detect the colocalization of NeuN and HO-1, and the results showed that aspirin significantly increased expression of the HO-1 protein in neurons. In addition, western blots and immunofluorescence staining showed aspirin restrained astrocyte activation. In conclusion, aspirin induces neuroprotective effects by inhibiting astrocyte activation and apoptosis after SCI through the activation of the Nrf2/HO-1 signaling pathway.