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The goal of this study was to investigate the possible protective effects of sitagliptin against dyslipidemia-related kidney injury in apolipoprotein E knockout (apoE-/-) mice. Eight-week-old male apoE-/- mice were randomized to receive either a high fat diet (HFD, apoE-/- group) or HFD mixed with sitagliptin (sita + apoE-/- group) for 16 weeks. A control group of age- and gender-matched C57BL/6J mice were fed a HFD. The apoE-/- group exhibited increases in body weight and serum lipid levels in addition to high-density lipoprotein, and increases in 24-h urinary 8-hydroxy-2-deoxyguanosine and albuminuria excretion. Decreased insulin sensitivity was also observed in the apoE-/- group. These mice additionally contained enlargements of the glomerular mesangial matrix area, lipid deposition area, and renal interstitium collagen area. The apoE-/- group also demonstrated down-regulation of phosphorylated AMP-activated protein kinase (AMPK), increases in renal mRNA expression of transforming growth factor-beta 1 (TGF-β1) and fibronectin (FN), and increased protein expression of Akt, TGF-β1, FN and p38/ERK mitogen-activated protein kinase (MAPK). Sitagliptin treatment successfully ameliorated all the deleterious effects of dyslipidemia tested. To our knowledge, this is the first time that sitagliptin has been shown to reverse the renal dysfunction and structural damage induced by dyslipidemia in apoE-/- mice. Our results suggest that the renoprotective mechanism of sitagliptin may be due to a reduction in Akt levels, a restoration of AMPK activity, and inhibition of TGF-β1, FN, and p38/ERK MAPK signaling pathways.

This study provides a new understanding on sources of P, which may serve as a foundation for further exploration of anthropogenic effects on P input. Estimation of net anthropogenic phosphorus input (NAPI) was based on an inventory of phosphorus (P) fertilizer use, consumption of human food and animal feed, seeding phosphorus and non-food phosphorus net flux. Across Mainland China, NAPI had an upward trend from 1981 to 2009, which reflects development trend of the population and economic. NAPI for years 1981, 1990, 2000 and 2009 are 190 kg P km(-2)yr(-1) (1.8 kg P per person yr(-1)), 295 kg P km(-2) yr(-1) (2.5 kg P per person yr(-1)), 415 kg P km(-2) yr(-1) (3.1 kg P per person yr(-1)) and 465 kg P km(-2) yr(-1) (3.4 kg P per person yr(-1)), respectively. On a geographical basis, NAPI per unit area is lower in northwest Mainland China than in southeast Mainland China with the largest NAPI of 3101 kg P km(-2) yr(-1) in Shanghai, while NAPI per person is in reverse with the largest NAPI 7.7 kg P per person yr(-1) in Tibet. P input of fertilizer is the largest source of NAPI, accounting for 57.35-83.73% (109-390 kg P km(-2) yr(-1)) of the total NAPI, followed by non-food P and P in human food and animal feed. Year 2000 was a critical point where P changed almost from net input to output. Grain production rate per unit mass of fertilizer showed an obvious downward trend. The primary factor in relation to the change in NAPI is total population., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Occurrence of polycyclic aromatic hydrocarbons (PAHs) during the coking process has been widely recognized. The formation of polychlorinated naphthalenes (PCNs) from PAHs during some thermal related processes has been confirmed in many studies. Thus, the coking process is assumed to be a potential source of PCNs. However, intensive investigations on PCN emissions during the coking process are lacking. In order to evaluate PCN emissions from the coking process, an intensive study comprising 11 typical coke plants was undertaken. PCNs were qualified and quantified by isotope dilution HRGC/HRMS techniques. The concentrations of PCNs in stack gas samples collected from the investigated coke plants were in the range of 1.6-91.8 ng Nm(-3) (0.08-4.23 pg TEQ Nm(-3)). The emission factors of PCNs were found to be in the range of 0.77-1.24 ng TEQ per ton of coke production. The estimated annual toxic emissions of PCNs from the global coking industry vary from 430 to 692 mg TEQs. Characteristics of the PCN profiles were dominated by the lower chlorinated homologues, with mono-CN being the most abundant homologue. According to the PCN distribution and correlations of PCN homologues, it was speculated that chlorination is possibly the dominant pathway of PCN formation during the coking process.

The coking process is considered to be a potential source of unintentionally produced persistent organic pollutants (UP-POPs). However, intensive studies on the emission of UP-POPs from the coking industry are still very scarce. Emission of polychlorinated dibenzo-p-dioxins/dibenzofurans (PCDD/Fs), dioxin-like polychlorinated biphenyls (dl-PCBs), hexachlorobenzene (HxCBz), and pentachlorobenzene (PeCBz) covered under the Stockholm Convention were investigated for the coking process in this study. Stack gases from some typical coke plants in China were collected and analyzed to estimate the emission of UP-POPs from the coking industry. Emission factors of 28.9 ng WHO-TEQ tonne(-1) for PCDD/Fs, 1.7 ng WHO-TEQ tonne(-1) for dl-PCBs, 596 ng tonne(-1) for HxCBz, and 680 ng tonne(-1) for PeCBz were derived based on the investigated data. The annual emissions from the global coking industry were estimated to be 15.8 g WHO-TEQ for PCDD/Fs, 0.93 g WHO-TEQ for dl-PCBs, 333 g for HxCBz, and 379 g for PeCBz, respectively (reference year 2007). According to the distribution of PCDD/Fs, we argued for the de novo synthesis to be the major pathway of PCDD/F formation. With regard to the characteristics of dl-PCBs, the most abundant congener was CB-118, and the most dominant contributor to the total WHO-TEQ of dl-PCBs was CB-126.

Arsenic is highly toxic and therefore represents a potential threat to the environment and human health. The mobility and fixation of arsenic in natural environment is significantly affected by co-occurring dissolved natural organic acids, which are widely present in soils and sediments due to the decomposition of natural organic matters and the metabolism of plant roots and microorganisms. It was reported recently that at lower pH, citrate decreased arsenate adsorption on metal oxides as the result of competitive adsorption. This study examined the relationship between citrate-promoted goethite dissolution and citrate-suppressed arsenate adsorption in the equilibrated goethite-arsenate-citrate systems with different contact orders. The results indicated that there is obvious correlation between the suppression of arsenate adsorption and dissolution of goethite. Arsenate adsorption and goethite dissolution in the presence of citrate (1.0mM), oxalate (1.5mM) and acetate (3.0mM) were compared. The results showed that arsenate adsorption was most significantly inhibited by citrate among the three organic acids. Although oxalate dissolved goethite more significantly, it inhibited arsenate adsorption much less than citrate. Hence it is proposed that the competition for binding sites rather than citrate-promoted goethite dissolution played a key role in the reduction of arsenate adsorption by citrate at lower pH.

The fate of arsenic in natural environments is influenced by adsorption onto metal (hydr)oxides. The extent of arsenic adsorption is strongly affected by coexisting dissolved natural organic acids. Recently, some studies reported that there existed competitive adsorption between arsenate and citrate on goethite. Humic acid is known to interact strongly with arsenate by forming complexes in aqueous solution, hence it is necessary to undertake a comprehensive study of the adsorption of arsenate/citrate onto goethite in the presence of one another. The results showed that at the arsenate concentrations used in this study (0.006-0.27 mmol/L), citrate decreased arsenate adsorption at acidic pH but no effect was observed at alkaline pH. In comparison, citrate adsorption was inhibited at acidic pH, but enhanced at alkaline pH by arsenate. This was probably due to the formation of complex between arsenate and citrate like the case of arsenate with humic acid. These results implied that the mechanism of the adsorption of arsenate and citrate onto goethite in the presence of one another involved not only competition for binding sites, but the cooperation between the two species at the water-goethite interface as well.

The minor bioactive saponins of the total saponin from the leaves of Panax notoginseng (Burk.) F. H. Chen. were separated and purified by column chromatographies on silica gel and thin layer gel. Four compounds were identified as: ginsenoside C-K (I) [20 (S) -protopanaxadiol 20-O-beta-D-glucopyranoside], ginsenoside-Rh1 (II) [20 (S) -protopanaxatriol-6-O-beta-D-glucopyranoside], ginsenoside-Mc (III) [20 (S)-protopanaxadiol 20-O-alpha-L-arabinofuranosyl (1 --> 6) -D-glucopyranoside] and notoginsenoside-Fe (IV) [20(S) -protopanaxadiol-3-O-beta-D-glucopyranosido-20-O-alpha-L-arabinofuranosyl(1 --> 6)-beta-D-glucopyranoside]. Compound I was isolated from the leaves of Panax notoginseng for the first time.