Biochar alleviating heavy metals phytotoxicity in sludge-amended soil varies with plant adaptability.

Recycling sewage sludge (SS) to soil potentially causes soil heavy metal (HM) pollution and plant phytotoxicity. Biochar plays an important role in alleviating HM phytotoxicity, and responses vary with the feedstocks and usage of biochar. However, the effect of plant adaptability on biochar-mediated alleviation is poorly understood. Here, SS-derived biochar (SB) and rice straw-derived biochar (RB) applied at rates of 1.5% and 3% (W/W, SB1.5, SB3, RB1.5, and RB3) were used to improve the properties of soil amended with SS at 50% (W/W). Alleviation of phytotoxicity by biochar was further analyzed with SS-sensitive plant Monstera deliciosa and SS-resistant plant Ruellia simplex. Results revealed that both SB and RB significantly decreased the soil's bulk density and increased water retention. They also changed soil organic matter content and HMs fractionation. The addition of SB or RB alleviated the SS phytotoxicity, and they significantly promoted the growth and the root morphology and physiological index of M. deliciosa. But for R. simplex, these significant changes only synchronously occurred in SB3 treatment. The alleviation in M. deliciosa was more prominent and more closely connected with soil property changes than in R. simplex. Also, more soil property predictors were observed to play an important role in M. deliciosa growth than in R. simplex growth. These results indicated that biochar alleviating HMs phytotoxicity in SS-amended soil is associated with the changes of soil property. Moreover, the alleviation varies more prominently with plant adaptability than with biochar feedstocks and usage.

Ursolic acid promotes cancer cell death by inducing Atg5-dependent autophagy.

Ursolic acid (UA) has been reported to possess anticancer activities. Although some of the anticancer activities of UA have been explained by its apoptosis-inducing properties, the mechanisms underlying its anticancer actions are largely unknown. We have found that UA-activated autophagy induced cytotoxicity and reduced tumor growth of cervical cancer cells TC-1 in a concentration-dependent manner. UA did not induce apoptosis of TC-1 cells in vitro as determined by annexin V/propidium iodide staining, DNA fragmentation, and Western blot analysis of the apoptosis-related proteins. We found that UA increased punctate staining of light chain 3 (LC3), which is an autophagy marker. LC3II, the processed form of LC3I which is formed during the formation of double membranes, was induced by UA treatment. These results were further confirmed by transmission electron microscopy. Wortmannin, an inhibitor of autophagy, and a small interfering RNA (siRNA) for autophagy-related genes (Atg5) reduced LC3II and simultaneously increased the survival of TC-1 cells treated with UA. We also found that LC3II was significantly reduced and that survival was increased in Atg5-/- mouse embryonic fibroblast (MEF) cells compared to Atg5+/+ MEF cells under UA treatment. However, silencing BECN1 by siRNA affected neither the expression of LC3II nor the survival of TC-1 cells under UA treatment. These results suggest that autophagy is a major mechanism by which UA kills TC-1 cells. It is Atg5 rather than BECN1 that plays a crucial role in UA-induced autophagic cell death in TC-1 cells. The activation of autophagy by UA may become a potential cancer therapeutic strategy complementing the apoptosis-based therapies. Furthermore, regulation of Atg5 may improve the efficacy of UA in cancer treatment.