Intensive crop rotation is one of the main causes of the continued depletion in soil potassium (K) content in the Yangtze River basin (YRB). However, recent studies have shown that soil K content is increasing in the YRB. Therefore, in this study, experimental and statistical data were collected to evaluate the soil K changes caused by K fertilizer application and straw return across the YRB. The results showed that soil available K increased, on average, by 21.7% across the YRB as a result of balanced K fertilization and an increasing proportion of straw return. From 1990 to 2019, K fertilizer input has increased from 10.1% to 24.1%, respectively. Meanwhile, from 2003 to 2011, the proportion of straw return increased by 32.8%. Considering these changes, we evaluated the effect of K fertilizer application and straw return on the soil K status. Overall, crop yield and soil available K increased by 9.9%, 7.3%, 16.3%, and 42.5%, 23.8%, and 66.4%, respectively, with K fertilization, straw return, and the concurrent use of both practices. Further, a synergistic increase in indigenous K input and soil available K alleviated the soil K negative balance and reduced the soil K fixation rate. In general, balanced K fertilization and an increasing proportion of straw return are the most vital measures for realizing the sustainable development of soil K across the YRB. The results of this research will provide useful information for sustainable K management and incentive policymaking.
Hypoxic conditions are a typical extrinsic factor for the modification of trophoblast biological functions, including cell proliferation, migration, and invasion. Hypoxia-induced reactive oxygen species (ROS) accumulation causes chronic trophoblast injury and contributes to preeclampsia (PE). Glutathione-S-transferase P (GSTP1) is a main regulator of ROS. However, it is still unknown whether GSTP1 is involved in ROS regulation under hypoxic conditions. Here, we investigated the expression level of GSTP1 in first-trimester villi placentas compared with full-term placentas and the effect of hypoxic conditions on GSTP1. GSTP1 expression in first-trimester villi placentas was much higher than that in full-term placentas. After hypoxia exposure, GSTP1 was significantly upregulated in JEG3 cells, a trophoblast-like cell line. Hypoxic-induced GSTP1 scavenged ROS accumulated by hypoxia exposure, potentially by promoting GST activity. The inhibitory effects of hypoxia exposure on cell proliferation, migration, and invasion induced by hypoxia exposure were obviously reversed by overexpression of GSTP1. Hypoxia-induced cell apoptosis was also reversed by GSTP1 overexpression, indicating the protective effects of GSTP1 against ROS-induced cell injury. Moreover, overexpressed GSTP1 markedly promoted the cell proliferation, migration, invasion, and colony formation abilities in JEG3 cells, demonstrating that GSP1 also exerts promoting effects under normoxic conditions. These data show that hypoxia-induced GSTP1 expression facilitates trophoblast cell proliferation, migration, and invasion and exerts protective effects under hypoxic conditions, which may play an important role during the increase in PE.
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