Spatial and temporal variations in algal phosphorus in Taihu Lake

Phosphorus circulation in Taihu Lake has attracted extensive attention, but the contribution of Microcystis to phosphorus circulation in this area is unknown. In this study, the phosphorus concentrations in algal samples collected from the lake in 2015–2016 were determined in the laboratory. From the concentration data, the total quantity of algal phosphorus was calculated and the seasonal variations in algal phosphorus were examined. The results indicated that the intracellular phosphorus content of Microcystis in Taihu varied from 0.044 to 0.130 pg/cell and tended to be high in spring and low in summer. The total amount of algal phosphorus in Taihu Lake ranged between 7.78 and 97.32 t over the study period. Algal phosphorus only accounted for between 1.5 and 18.5% of the phosphorus stock in the water. Because Microcystis accumulated downwind, there was a tendency for the total phosphorus concentrations to be low in the east of the lake and high in the west of the lake. This new information about the spatial and temporal distribution of algal phosphorus contributes to our understanding of how phosphorus in Microcystis contributes to phosphorus circulation in Taihu Lake.

MO340THE EFFECT OF NA+/PI COTRANSPORTER IN TENOFOVIR INDUCED NEPHROTOXITY BY REGULATING INTRACELLULAR PHOSPHORUS BALANCE AND MITOCHONDRIAL FUNCTION

Background and Aims Tenofovir disoproxil fumarate (TDF), a reverse transcriptase inhibitor used to treat virus infections, could cause proximal tubular (PT) dysfunctions and eGFR decline with mitochondria damages. PDZ domain containing 1 (PDZK1), PDZK1-interacting protein 1 (PDZK1IP1), and Na+/H+ exchanger regulatory factor 1 (NHERF1) are scaffold proteins or membrane-associated proteins that influence the localization and function of membrane proteins. We tried to investigate the changes of both proximal tubular transporters and membrane-associated proteins in TDF induced nephrotoxic model. Method C57/BL6 mice (n = 8) were gavaged daily with 10mg/kg/d, 50mg/kg/d of TDF for 8 weeks. The human renal tubular epithelial cells (HK-2) were grown and received 24 to 72 h exposure to 0–128 µM TDF or vehicle. Results Chronic TDF administration to mice and HK-2 cells resulted in PT damages including swollen and exfoliated tubular epithelial cells, brush border cilia lodging and dissolving, and serum creatinine elevation (P<0.05, mean 10.23±2.683 vs. 27.18±18.41) compared to the control group. The Na+/Pi cotransporter (Npt) and sodium-glucose cotransporter type 2 (SGLT-2) were decreased in the kidneys of TDF treated mice and HK-2 cells. The intracellular phosphorus concentrations decreased with the increase of TDF concentration and the extension of TDF treatment time, which were in line with down-regulated Npt expressions. Mitochondrial morphological changes were seen in TDF treated mice and HK-2 cells by electron microscope, including unclear boundaries, damaged membrane structures, disappeared mitochondrial cristae, and fragmented mitochondria or abnormal giant mitochondria in PT cells. The expression of cytochrome b was reduced by 52.0% (P<0.0001), indicating the damages of mitochondrial respiratory chain. ATP levels which reflected mitochondrial functions were also decreased after TDF treatment in HK-2 cells with a time- and dose-dependent relationship. Conclusion TDF may down-regulate Npt expression, leading to decreased intracellular phosphorus concentrations, mitochondrial dysfunctions, and finally kidney injury.

Potential interaction of inflammatory hyperemia and hyperphosphatemia in tumorigenesis

The present article proposes that the association of inflammation with cancer is potentially mediated by the interaction of inflammatory hyperemia and hyperphosphatemia. Hyperemia increases blood flow rate and blood volume, and hyperphosphatemia is caused by elevated serum levels of dysregulated inorganic phosphate. It is hypothesized that the interaction of inflammatory hyperemia and hyperphosphatemia circulates increased amounts of inorganic phosphate to the tumor microenvironment, where increased uptake of inorganic phosphate through sodium-phosphate cotransporters is sequestered in cells. Elevated levels of intracellular phosphorus increase biosynthesis of ribosomal RNA, leading to increased protein synthesis that supports tumor growth. The present article also proposes that the interaction of inflammatory hyperemia and hyperphosphatemia may help explain a chemopreventive mechanism associated with NSAIDs.