Flooding duration affects the temperature sensitivity of soil extracellular enzyme activities in a lakeshore wetland in Poyang Lake, China.

Extracellular enzymes play central roles in the biogeochemical cycles in wetland ecosystems. Their activities are strongly impacted by hydrothermal conditions. Under the ongoing global change, many studies reported the individual effects of flooding and warming on extracellular enzyme activities, however, few researches investigated their interactive effects. Therefore, the current study aims to determine the responses of extracellular enzyme activities to warming in wetland soils under divergent flooding regimes. We investigated the temperature sensitivity of seven extracellular enzymes related to carbon (α-glucosidase, AG; ß-glucosidase, BG; cellobiohydrolase, CBH; ß-xylosidase, XYL), nitrogen (ß-N-acetyl -glucosaminidase, NAG; leucine aminopeptidase, LAP), and phosphorus (Phosphatase, PHOS) cycling along the flooding duration gradient in a lakeshore wetland of Poyang Lake, China. The Q10 value, calculated using a temperature gradient (10, 15, 20, 25, and 30 °C), was adopted to represent the temperature sensitivity. The average Q10 values of AG, BG, CBH, XYL, NAG, LAP, and PHOS in the lakeshore wetland were 2.75 ± 0.76, 2.91 ± 0.69, 3.34 ± 0.75, 3.01 ± 0.69, 3.02 ± 1.11, 2.21 ± 0.39, and 3.33 ± 0.72, respectively. The Q10 values of all the seven soil extracellular enzymes significantly and positively correlated with flooding duration. The Q10 values of NAG, AG and BG were more sensitive to the changes in flooding duration than other enzymes. The Q10 values of the carbon, nitrogen, and phosphorus-related enzymes were mainly determined by flooding duration, pH, clay, and substrate quality. Flooding duration was the most dominant driver for the Q10 of BG, XYL, NAG, LAP, and PHOS. In contrast, the Q10 values of AG and CBH were primarily affected by pH and clay content, respectively. This study indicated that flooding regime was a key factor regulating soil biogeochemical processes of wetland ecosystems under global warming.

Neohesperidin induces cellular apoptosis in human breast adenocarcinoma MDA-MB-231 cells via activating the Bcl-2/Bax-mediated signaling pathway.

Neohesperidin, a flavonoid compound found in high amounts in Poncirus trifoliata, has free radical scavenging activity. For the first time, our study indicated that neohesperidin also induces cell apoptosis in human breast adenocarcinoma MDA-MB-231 cells, which was possibly mediated by regulating the P53/Bcl-2/Bax pathway. MDA-MB-231 cells were subjected to treatment with neohesperidin. MTT and Trypan blue exclusion assays were applied to assess the cell viability. The morphological changes of cells were observed using an inverted microscope, and cell apoptosis was detected by flow cytometric analysis. Immunoblot analysis was conducted to evaluate the protein expressions of apoptosis-related genes, including P53, Bcl-2 and Bax. Our results indicated that the proliferation of MDA-MB-231 cells was inhibited by the treatment with neohesperidin in a time- and dose-dependent manner. The IC50 values of neohesperidin at 24 and 48 h were 47.4 +/- 2.6 microM and 32.5 +/- 1.8 microM, respectively. The expressions of P53 and Bax in the neohesperidin-treated cells were significantly up-regulated, while that of Bcl-2 was down-regulated. Our study suggested that neohesperidin could induce apoptosis of MDA-MB-231 cells, a process which was associated with the activation of the Bcl-2/Bax-mediated signaling pathway.