Phosphorus biogeochemistry regulated by carbonates in soil.

Phosphates are the dominant phosphorus (P) source on Earth. The phosphates govern available P in soil, or even the complete ecosystem. The common deficiency of available P in carbonate-enriched soils suggests the tight correlation between P and C biogeochemistry, although the two elements have diverse abundance in soil. The influences of carbonates on P cycle were reviewed in this study, via both abiotic and biotic pathways. The abiotic processes at geochemical scale include element release, transport, sorption, desorption, weathering, precipitation, etc. The sorption of P on carbonate and buffering ability of carbonates were particularly addressed. Biotic factors are ascribed to various microorganisms in soil. As the most active P pool in soil, microorganisms prefer to consume abundant P, and then accumulate it in their biomass. Carbonates, however, are usually utilized by microorganisms after conversion to organic C. Meanwhile, extracellular precipitation of Ca-P phases significantly regulates the transportation of P in/out the cells. Moreover, they boost and complexify both carbonates and P turnover in soil via bioweathering and biomineralization, i.e., the intense interactions between biosphere and lithosphere. Based on this review, we proposed that carbonates may negatively affect P supply in soil system. This comprehensive review regarding the regulation by carbonates on P biogeochemistry would shed a light on predicting long-term P availability influenced by C biogeochemistry.

Evaluating the survival of Aspergillus niger in a highly polluted red soil with addition of Phosphogypsum and bioorganic fertilizer.

Phosphate-solubilizing fungi (PSF) can enhance P release from phosphate minerals to immobilize heavy metals. However, this promotion substantially depends on their survival in highly polluted soils. The aim of this study was to investigate the survival of PSF after addition of phosphogypsum (PG) and bioorganic fertilizer (BF) in the soil with coexistence of multiple heavy metals, e.g., Pb, As, Cd, Sb, etc. Addition of typical PSF (Aspergillus niger) did not promote the formation of pyromorphite (the most stable form of Pb), possibly due to the buffering effect of the soil (the secreted oxalic acid was neutralized) and limited P supply. Meanwhile, despite that A. niger has high tolerance to heavy metal stress, its survival was significantly declined due to the deficiency of available P. It was also shown that PG, as the major by-product in phoschemical industry, still has relatively high available P compared with common natural soils. PG addition dramatically increased available P (up to 93.87 mg/kg) and the subsequent fungal growth. However, sole PG did not promote the formation of pyromorphite, probably as the abundant Fe2+ and Mn2+ prevented the contact between PO43- and Pb2+ in the soil system. The enhanced soil respiration after addition of BF and PG confirmed the promoted microbial activity (elevated to 3465.58 µg C kg h-1). This study showed PG's potential as P source for both microbial growth and heavy metal remediation in soil system. A combination of PG, A. niger, and BF can hence achieve long-term bioremediation of heavy metals.

Extract of Fructus Cannabis Ameliorates Learning and Memory Impairment Induced by D-Galactose in an Aging Rats Model.

Hempseed (Cannabis sativa L.) has been used as a health food and folk medicine in China for centuries. In the present study, we sought to define the underlying mechanism by which the extract of Fructus Cannabis (EFC) protects against memory impairment induced by D-galactose in rats. To accelerate aging and induce memory impairment in rats, D-galactose (400 mg/kg) was injected intraperitoneally once daily for 14 weeks. EFC (200 and 400 mg/kg) was simultaneously administered intragastrically once daily in an attempt to slow the aging process. We found that EFC significantly increased the activity of superoxide dismutase, while lowering levels of malondialdehyde in the hippocampus. Moreover, EFC dramatically elevated the organ indices of some organs, including the heart, the liver, the thymus, and the spleen. In addition, EFC improved the behavioral performance of rats treated with D-galactose in the Morris water maze. Furthermore, EFC inhibited the activation of astrocytes and remarkably attenuated phosphorylated tau and suppressed the expression of presenilin 1 in the brain of D-galactose-treated rats. These findings suggested that EFC exhibits beneficial effects on the cognition of aging rats probably by enhancing antioxidant capacity and anti-neuroinflammation, improving immune function, and modulating tau phosphorylation and presenilin expression.

[The effect of hyperbaric oxygen on acute pancreatitis through downregulating hypoxia-inducible factor.].

OBJECTIVE: To observe the therapeutic effect of hyperbaric oxygen (HBO) on acute pancreatitis (AP) by downregulating hypoxia-inducible factor (HIF). METHODS: Forty Wistar rats were randomly divided into 4 groups (n = 10): sham group, AP group, normo-oxygen group (NP) and HBO group. At 4 hours after taurocholate-induced AP, the rats of NP group and HBO group were respectively treated with oxygen or HBO for 90 min. Several parameters were measured to evaluate oxygen stress after treatment including oxygen saturation (SaO2), partial pressure of oxygen (PO2), pH, and serum LDH. Pancreatic tissues were subjected to histopathological analysis, immunostained, and homogenized for Western blotted analysis of HIF-1alpha and VEGF, and measuring myeloperoxidase activity. The serum TNF-alpha and pancreatic histopathological scores were evaluated the severity of AP. RESULTS: It was proved by immunohistochemisty that HIF in acinar cell and polymorphonuclear leukocytes (PMNs) was activated and transferred from cytoplasm into nucleus in AP group, NP group, and HBO group, following upregulation of VEGF. HBO therapy elevated blood SaO2 (99.6% +/- 0.7% vs. 87.7% +/- 1.8% or 91.2% +/- 2.5%, P < 0.05) and PaO2 [(369.1 +/- 67.6) mm Hg (1 mm Hg = 0.133 kPa) vs. (86.6 +/- 5.6) mm Hg or (99.9 +/- 4.0) mm Hg, P < 0.05]. HBO therapy attenuated the severity of AP through inhibiting AP-induced upregulation of HIF-1alpha and VEGF, as evidenced by reducing histopathological scores (12.40 +/- 1.21 vs. 16.45 +/- 1.10 or 16.38 +/- 1.10, P < 0.05), dry/wet weight ratio of pancreatic tissues, and myeloperoxidase activity. CONCLUSIONS: HIF-1alpha plays a key role in the pathogenesis of AP. HBO therapy attenuates the severity of AP through downregulating the expression of HIF-1alpha.

Determination of biotin by high-performance liquid chromatography in infant formula, medical nutritional products, and vitamin premixes.

A solid-phase extraction sample preparation procedure was developed for use with a high-performance liquid chromatography (HPLC) method for biotin analysis. The HPLC method used a reversed-phase C18 column; chromatography run time was 8.5 min. After eluting from the column, biotin went through postcolumn reaction to form a conjugate with streptavidin-fluorescein isothiocyanate, which was then detected by a fluorescence detector. This method was tested with infant formula, medical nutritional products, and vitamin premix samples.

Quantitative analysis of 23-hydroxybetulinic acid in mouse plasma using electrospray liquid chromatography/mass spectrometry.

23-Hydroxybetulinic acid is a newly isolated derivative of betulinic acid. The agent exhibits potential anti-tumor activity and functions in this regard via apoptosis. In support of pharmacokinetic and toxicological evaluations, a new assay based on liquid chromatography/mass spectrometry (LC/MS) was developed for the quantitative analysis of 23-hydroxybetulinic acid. Sample preparation consisted of extraction of the plasma by the addition of methylene chloride followed by centrifugation. Aliquots of the supernatant were analyzed using an isocratic reversed-phase high-performance liquid chromatography (HPLC) system coupled to a negative ion electrospray mass spectrometer. Molecules of 23-hydroxybetulinic acid and the internal standard limonin were detected using selected ion monitoring at m/z 471 and 469, respectively. The limit of detection of 23-hydroxybetulinic acid was 0.05 pg (0.11 fmol) injected on-column (10 pg/mL, 5 microL injection volume), and the limit of quantitation was 10 pg (21.19 fmol, 2 ng/mL, 5 muL injection volume). 23-Hydroxybetulinic acid was stable in plasma samples at -20 degrees C for at least 3 weeks. The intra-day and inter-day coefficients of variation of the assay were 3.0 and 4.8%, respectively. The utility of the assay was demonstrated by measuring 23-hydroxybetulinicacid in mouse plasma following intragastric administration (IG) in vivo. Pharmacokinetic parameters were calculated using the 3P97 pharmacokinetic software package. A two-compartment, first-order model was selected for pharmacokinetic modeling. The result showed that after IG of 200 mg/kg 23-hydroxybetulinic acid, the plasma concentrations reached peaks at 2 h with C(max) of 3.1 microg/mL. The 200 mg/kg 23-hydroxybetulinic acid suspension IG doses were found to have long elimination half-lives of 25.6 h and low bioavailability of 2.3%. No interference was noted due to endogenous substances. These analytical methods should be of value in future studies related to the development and characterization of 23-hydroxybetulinic acid.