Okra (Abelmoschus esculentus (L.) Moench), a healthy vegetable, is widely spread in tropical and subtropical areas. Previous studies have proven that okra pods possess anti-fatigue activity, and the aim of this research is to clarify the anti-fatigue constituents. To achieve this, we divided okra pods (OPD) into seeds (OSD) and skins (OSK), and compared the contents of total polysaccharides, total polyphenols, total flavonoids, isoquercitrin, and quercetin-3-O-gentiobiose and the antioxidant activity in vitro and anti-fatigue activity in vivo between OSD and OSK. The contents of total polyphenols and total polysaccharides were 29.5% and 14.8% in OSD and 1.25% and 43.1% in OSK, respectively. Total flavonoids, isoquercitrin and quercetin-3-O-gentiobiose (5.35%, 2.067% and 2.741%, respectively) were only detected in OSD. Antioxidant assays, including 1-diphenyl-2-picrylhydrazyl (DPPH) scavenging, ferric reducing antioxidant power (FRAP) and reducing power test, and weight-loaded swimming test showed OSD possessed significant antioxidant and anti-fatigue effects. Moreover, biochemical determination revealed that that anti-fatigue activity of OSD is caused by reducing the levels of blood lactic acid (BLA) and urea nitrogen (BUN), enhancing hepatic glycogen storage and promoting antioxidant ability by lowering malondialdehyde (MDA) level and increasing superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) levels. These results proved okra seeds were the anti-fatigue part of okra pods and polyphenols and flavonoids were active constituents.

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Recent findings suggest that oxidative stress caused by pyrethroid pesticides could be closely involved in the neurotoxicity. tert-Butylhydroquinone ( tBHQ) is a known inducer of Nrf2-mediated transcription, and treatment of cells with tBHQ can confer protection against H 2O 2 and 6-hydroxydopamine (6-OHDA). In this study, we investigated the neuroprotective effect of tBHQ against deltamethrin (DM)-induced oxidative stress using rat PC12 adrenal pheochromocytoma cells. The pretreatment of PC12 cells with tBHQ significantly reduced DM-induced generation of reactive oxygen species (ROS) and increased intracellular ionized calcium ([Ca (2+)] i). We also observed that DM or tBHQ induced the expression of NF-E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1), a Nrf2-regulated gene. In addition, the Nrf2 antioxidant responsive element (ARE) pathways activated by tBHQ caused a partial inhibition of the DM-induced Nrf2 and HO-1 expression. Altogether, our data clearly indicate that an activation of Nrf2/ARE pathways in PC12 cells by tBHQ treatment protects cells from DM-induced oxidative stress and regulates DM- mediated adaptive responses in PC12 cells via translocation of Nrf2.

Here, we report for the first time a waterborne outbreak of Shigella sonnei in China in 2015. Eleven multidrug-resistant (MDR) S. sonnei isolates were recovered, showing high resistance to azithromycin and third-generation cephalosporins in particular, due to an mph(A)-and bla CTX-M-14 -harboring IncB/O/K/Z group transmissible plasmid of 104,285 kb in size. Our study highlights the potential prevalence of the MDR outbreak of S. sonnei in China and its further dissemination worldwide with the development of globalization.

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In the present study, the cytotoxic effects and toxicological mechanism of six polybrominated diphenyl ethers (PBDEs) metabolites (3-OH-BDE47, 3-MeO-BDE47, 5-OH-BDE47, 5-MeO-BDE47, 6-OH-BDE85 and 6-MeO-BDE85) on L02 cells were explored by investigating the cell viability, apoptosis, lactic dehydrogenase (LDH) leakage, and oxidative stress response. The results showed that these metabolites could inhibit cell proliferation and induce apoptosis, among which 6-OH-BDE85 had the highest efficiency. LDH leakage test also showed that 6-OH-BDE85 had the strongest ability to cause LDH release. The reactive oxygen species (ROS) levels in 6-OH-BDE85- and 3-OH-BDE47-treated groups were significantly elevated in a dose-dependent manner. After treatment for 24 h, four BDE47 metabolites (3-OH-BDE47, 3-MeO-BDE47, 5-OH-BDE47, and 5-MeO-BDE47) induced an increase in superoxide dismutase (SOD) activity and decrease in glutathione (GSH) level, whereas 6-OH-BDE85 led to a decrease in both SOD activity and GSH level. These effects disappeared after continued culturing for another 24 h. In conclusion, these PBDE metabolites, especially 6-OH-BDE85, showed cytotoxicity on L02 cells, which was at least partially related to the oxidative stress level.

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