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Abstract: Concentrations of degradation products of nonylphenol polyethoxylates (NPEOs) were analyzed in river water samples in order to determine the distribution characteristic of these alkylphenolic compounds in 18 major rivers of Taiwan. The degradation products of NPEOs were detected in all river samples, with the dicarboxylates alkylphenolic degradation products (CAPEC) being detected most frequently and at the highest concentrations. Concentrations of NP and NP1EO in rivers ranged from n.d. to 5.1μgl−1 and n.d. to 0.5μgl−1, respectively. The total concentrations of shortened carboxylates (i.e., NP1EC+NP2EC+NP3EC) and dicarboxylates alkylphenolic degradation products (CAP1EC+CAP2EC) ranged from n.d. to 63.6μgl−1 and n.d. to 94.6μgl−1, respectively. Concentrations of NP2EC, NP3EC and all CAPEC residues were determined semi-quantitatively by comparing with the internal standard. Significantly higher concentrations of CAPEC residues were detected in the river waters as compared to those of NP, NP1EO and NPEC degradation products and the average proportions of these compounds in the samples of the rivers were as follows: NP+NP1EO was 5±2.5%, total NPEC was 25±12%, and total CAPEC was 70±12%. The high concentration ratios of CAPEC/NPEC illustrate that aerobic biodegradation plays a main route in the fate of NPEO in the rivers of Taiwan. [Copyright &y& Elsevier]

Camptothecin (CPT) has been used for colorectal cancer therapy. At low concentration of 10 − 9 M, CPT modulates endothelial nitric oxide production following the phosphorylation of LKB1 Ser431, AMPK-α Thr172, eNOS Ser633 and Ser1177. Elevated nitric oxide (NO) was observed by FA-OMe fluorescent probe. 726 S-nitrosoproteins were identified by iTRAQ quantitative proteomics. IPA analysis indicated that ERK/MAPK was closely linked in the signaling network. Further studies showed that CPT phosphorylated p38 MAPK Thr180/Tyr182 and dephosphorylated Tau Ser199/202. CPT also suppressed the TNF-α-induced expression of the inflammasome and cyclooxygenase 2. All this suggests that in addition to the original character of CPT in attenuating the binding of topoisomerase I and DNA in cancer cells, the role of CPT in triggering NO production and the subsequent S-nitrosylated signaling including anti-inflammatory effects in endothelial cells are proposed here. CPT, therefore, provides a potential application addition in preventing vascular disorders. [ABSTRACT FROM AUTHOR]

Background: Hydrogen sulfide (H 2 S) is one of the endogenous gaseous molecules promoting the production of nitric oxide (NO) which has cardioprotective functions. However, the role of the H 2 S-mediated protein S-nitrosoproteome and its subsequent physiological response remains unclear., Methods: Endothelial cells EAhy 926 were treated with 50 μM of H 2 S for 2 hours. The NO bound S-nitrosoproteins were purified by a biotin-switch and then digested by trypsin. Resulting peptides from control and H 2 S treatment were separately labeled by isobaric tag for relative and absolute quantitation 114/115, quantified by liquid chromatography tandem-mass spectrometry and analyzed by ingenuity pathway analysis (IPA) software. The microP software was applied to analyze the morphological changes of mitochondria., Results: With the treatment of H 2 S, 416 S-nitrosylated proteins were identified. IPA analysis showed that these proteins were involved in five signaling pathways. The NO-bound cysteine residues and the S-nitrosylation levels (115/114) were shown for ten S-nitrosoproteins. Western blot further verified the S-nitrosylation of thioredoxin-dependant peroxide reductase, cytochrome c oxidase and cytochrome b-c1 complex that are involved in the mitochondrial signaling pathway. H 2 O 2 -induced mitochondrial swelling can be reduced by the pretreatment of H 2 S., Conclusions: The H 2 S-mediated endothelial S-nitrosoproteome has been confirmed. In the present study, we have proposed the cardioprotective role of H 2 S via maintaining mitochondrial homeostasis.

Plastic products are wildly used in human life. Di(2-ethylhexyl)phthalate (DEHP) is an essential additive in plastic manufacturing and is used as plasticizer for many products including plastic food packaging. DEHP is a teratogenic compound and can cause potent reproductive toxicity. DEHP can also cause liver damage, peroxisome proliferation, and carcinogenesis. DEHP is also strongly associated with peptic ulcers and gastric cancer; however, the underlying effect and mechanism of DEHP on the gastrointestinal tract are not entirely clear. The oral infection route of H. pylori parallels the major ingestion route of DEHP into the human body. Therefore, we wanted to study the effect of DEHP and H. pylori exposure on the human gastric epithelial cell line, AGS (gastric adenocarcinoma). The viability of the AGS cell line was significantly lower in 80  μ M-DEHP and H. pylori (MOI = 100 : 1) coexposure than DEHP or H. pylori alone. DEHP and H. pylori coexposure also induced caspase-3 activation, and increased Bax/Bcl-2 ratio and DNA fragmentation in AGS cells. These results indicate that DEHP can enhance H. pylori cytotoxicity and induce gastric epithelial cell apoptosis. Therefore, it is possible that DEHP and H. pylori coexposure might enhance the disruption of the gastric mucosa integrity and potentially promote the pathogenesis of gastric carcinogenesis.