Dissolved organic phosphorus promotes Cyclotella growth and adaptability in eutrophic tropical estuaries.

Dissolved organic phosphorus (DOP) is an important nutrient for phytoplankton growth in oligotrophic oceans. However, little is known about the impact of DOP on phytoplankton growth in eutrophic waters. In the present study, we conducted field monitoring as well as in situ and laboratory experiments in the Pearl River estuary (PRE). Field observations showed an increase in the nitrogen-to-phosphorus ratio and DOP in recent years in the PRE. The phytoplankton community was dominated by nanophytoplankton Cyclotella in the upper and middle estuary, with high concentrations of DOP and light limitation during the ebb stage of the spring to neap tide in summer. The relative abundance of Cyclotella in natural waters was higher after enrichment with estuarine water with a background of 0.40-0.46 µM DOP, even when dissolved inorganic phosphorus was sufficient (0.55-0.76 µM). In addition, the relative abundance of Cyclotella in natural waters was higher after enrichment with phosphoesters. Laboratory culture results also confirmed that phosphoesters can enhance the growth rate of Cyclotella cryptica. Our study highlights that Cyclotella can become the dominant species in estuaries with increased levels of phosphoesters and low and fluctuating light adaptability and under the joint effect of dynamic processes such as upwelling and tides. Our results provide new insights into the role of Cyclotella in biogeochemical cycles affected by DOP utilization and potential applications in relieving the hypoxia of tropical eutrophic estuaries.IMPORTANCEThis study provides evidence that Cyclotella can become the dominant species in estuaries with increased levels of phosphoesters and low and fluctuating light adaptability and under the joint effect of dynamic processes such as upwelling and tides. Our study provides new insights into the role of Cyclotella in biogeochemical cycles affected by dissolved organic phosphorus utilization, especially affected by anthropogenic inputs and climate change. Potential applications include relieving the hypoxia of tropical eutrophic estuaries.

The acute exposure of tetrachloro-p-benzoquinone (a.k.a. chloranil) triggers inflammation and neurological dysfunction via Toll-like receptor 4 signaling: The protective role of melatonin preconditioning.

This study is aimed to investigate the inflammation and neurological dysfunction induced by tetrachloro-p-benzoquinone (TCBQ) through Toll-like receptor 4 (TLR4) signaling. We also investigated the protective role of melatonin as an antioxidant and anti-inflammatory agent. In vitro model was established by rat pheochromocytoma PC12 cells, meanwhile, TLR4 wild-type (C57BL/6) and knockout mice (C57BL/10ScNJ TLR4-/-) were used as in vivo model. In vitro study showed TCBQ exposure enhanced the expression of TLR4, myeloid differentiation factor 88 (MyD88) at both transcriptional and post-transcriptional levels. By contrast, melatonin decreased TLR4 and MyD88 expressions. Moreover, our result indicated that melatonin disrupted the formation of TLR4/MyD88/MD2/CD14 complex. In addition, melatonin terminated TCBQ-mediated phosphorylation of c-Jun N-terminal kinase (JNK), p38, and extracellular regulated protein kinase (ERK) signaling and hampered its downstream pro-inflammatory cytokine releases. In vivo result also indicated TLR4 deficiency partially protected against TCBQ-induced morphological and neuropathological changes in mice brain, suggested the role of TLR4. In conclusion, melatonin modulates TCBQ-mediated inflammatory genes through TLR4/MyD88-dependent signaling pathway. Our current study, to the best of our knowledge, is the first time show melatonin not only disrupt the binding of TLR4 and MyD88, but also restricted the formation of TLR4/MD2/CD14 complex, suggesting that melatonin supplementary may represent a valuable therapeutic strategy for inflammatory neurological dysfunction.

Bazhen decoction protects against acetaminophen induced acute liver injury by inhibiting oxidative stress, inflammation and apoptosis in mice.

Bazhen decoction is a widely used traditional Chinese medicinal decoction, but the scientific validation of its therapeutic potential is lacking. The objective of this study was to investigate corresponding anti-oxidative, anti-inflammatory and anti-apoptosis activities of Bazhen decoction, using acetaminophen-treated mice as a model system. A total of 48 mice were divided into four groups. Group I, negative control, treated with vehicle only. Group II, fed with 500 mg/kg/day Bazhen decoction for 10 continuous days. Group III, received a single dose of 900 mg/kg acetaminophen. Group IV, fed with 500 mg/kg/day Bazhen decoction for 10 continuous days and a single dose of 900 mg/kg acetaminophen 30 min before last Bazhen decoction administration. Bazhen decoction administration significantly decrease acetaminophen-induced serum ALT, AST, ALP, LDH, TNF-α, IL-1ß, ROS, TBARS and protein carbonyl group levels, as well as GSH depletion and loss of MMP. Bazhen decoction restore SOD, CAT, GR and GPx activities and depress the expression of pro-inflammatory factors, such as iNOS, COX-2, TNF-α, NF-κB, IL-1ß and IL-6, respectively. Moreover, Bazhen decoction down-regulate acetaminophen-induced Bax/Bcl-2 ratio, caspase 3, caspase 8 and caspase 9. These results suggest the anti-oxidative, anti-inflammatory and anti-apoptosis properties of Bazhen decoction towards acetaminophen-induced liver injury in mice.

Role of α-lipoic acid in LPS/d-GalN induced fulminant hepatic failure in mice: studies on oxidative stress, inflammation and apoptosis.

This study investigated the protective effect of α-lipoic acid (LA) on lipopolysaccharide (LPS)/d-galactosamine (d-GalN)-induced fulminant hepatic failure in mice. First, we found that LA markedly reduced LPS/d-GalN-induced increases in serum ALT and AST activities, which were supplemented with histopathological examination, suggested that LA has a protective effect on this model of hepatic damage. Livers challenged with LPS/d-GalN exhibited extensive areas of vacuolization with the disappearance of nuclei and the loss of hepatic architecture. On the contrary, these pathological alterations were ameliorated by LA treatment. Next, we found that ROS and TBARS levels were increased in LPS/d-GalN treated liver homogenates, which were attenuated by LA administration. Consistently, decreases in hepatic CAT and GPx activities were observed in LPS/d-GalN group and were significantly restored by LA administration. Moreover, pretreatment with LA markedly reduced LPS/d-GalN-induced iNOS, COX-2, TNF-α, NF-κB, IL-1ß and IL-6 expressions. Furthermore, our data showed that TUNEL-positive cells increased in LPS/d-GalN-treated mice liver which was counteracted by LA administration. LPS/d-GalN induced apoptosis of hepatocytes, as estimated by caspase 3, caspase 8 and caspase 9 activations. Also, the increasing of Bax and the decreasing of Bcl-2 expressions also supported LPS/d-GalN induced apoptosis. Interestingly, LA marked relieved these apoptotic features. Taking together, our results indicated that LA plays an important role on LPS/d-GalN-induced fulminant hepatic failure through its antioxidant, anti-inflammatory and anti-apoptotic activities.

Selenium supplementation shows protective effects against patulin-induced brain damage in mice via increases in GSH-related enzyme activity and expression.

AIMS: This study was designed to investigate the protective effects of selenium supplementation on patulin-induced neurotoxicity. MAIN METHODS: Mice were subjected to patulin for 8 weeks. Sodium selenite (Na2SeO3) and selenium-methionine (Se-Met) were supplemented with the diet, and we investigated the effects of selenium on patulin-induced neurotoxicity. The animals were randomly divided into 4 groups containing 6-8 mice each. The first group was used as a control, and only physiological saline (0.9%) was injected. The second group was treated with patulin (1mg/kg) intraperitoneally. The third group was treated with patulin (1mg/kg) along with a dietary supplementation of Na2SeO3 (0.2mg Se/kg of diet). The fourth group was treated with patulin (1mg/kg) plus Se-Met (0.2mg Se/kg of diet). KEY FINDINGS: Patulin treatment increased oxidative damage in the brain, as evidenced by a decrease in non-protein thiol and total thiol groups, along with significant increases in GSSG, reactive oxygen species, thiobarbituric acid reactive substances and protein carbonyl levels. Moreover, the activities of glutathione peroxidase (GPx) and glutathione reductase were inhibited with patulin treatment. Selenium supplementation significantly ameliorated these biological parameter changes. In addition, selenium treatments significantly increased the mRNA levels of GPx-1, GPx-4 and thioredoxin reductase. SIGNIFICANCE: Our data show that selenium supplementation increases the activity and expression of glutathione-related enzymes and offers significant protection against brain damage induced by patulin.

Hepatotoxicity and genotoxicity of patulin in mice, and its modulation by green tea polyphenols administration.

Patulin (PAT) is a mycotoxin produced by certain species of Penicillium, Aspergillus, and Byssochlamys. Previous studies demonstrated its cytotoxic, genotoxic, and mutagenic effects in different cell lines. However, there is little information available concerning its toxic behavior in vivo. In the present study, we investigated PAT-induced hepatotoxicity and genotoxicity in mice. We also investigated the antioxidant and anti-genotoxicity efficiency of green tea polyphenols (GTP) against PAT-induced toxicity. We found that PAT-treatment induced serum alanine transaminase (ALT) and aspartate transaminase (AST) activities significantly. PAT-induced lipid peroxidation was confirmed with the elevation of thiobarbituric acid-reactive substances (TBARS). Moreover, the increasing of reactive oxygen species (ROS) and decreasing of GSH level implied its oxidative damage mechanism. In bone marrow cell, PAT was found to induce micronucleus and chromosomal aberration formation. In addition, our result suggested that GTP administration has dose-dependent antioxidative and antigenotoxic effect in against PAT-induced hepatotoxicity and genotoxicity.