The regulation of rhizosphere bacterial community structure and metabolism by plants in municipal solid waste landfills is a key to enhancing the biodegradation of chlorobenzene (CB). In this study, we employed biodiversity and metabolomics methods to systematically analyze the mechanisms of different plant species in regulating the rhizosphere bacterial community structure and metabolic features and then improved the methane (CH₄) oxidation and CB degradation capacity. The results showed that the rhizosphere soil of Rumex acetosa exhibited the highest CH₄ oxidation and CB degradation capacity of 0.08 g/(kg·h) and 1.72×10^-6 g/(L·h), respectively, followed by the rhizosphere soil of Amaranthus spinosus L., with the rhizosphere soil of Broussonetia papyrifera showing the weakest activity. Rumex acetosa promoted the colonization of Methylocaldum in the rhizosphere, and the small-molecule organic amine, such as triethylamine and N-methyl-aniline, secreted from the roots of this plant enhanced the tricarboxylic acid cycle and nicotinamide metabolism, thereby increasing microbial activity and improving CH₄ and CB degradation efficiency. Conversely, cinnamic acid and its derivatives secreted by Broussonetia papyrifera acted as autotoxins, inhibiting microbial activity and exacerbating the negative effects of salt stress on key microbes such as methanotrophs. This study probed into the mechanisms of typical plants growing in landfill cover soil in regulating bacterial ecological functions, offering theoretical support and practical guidance for the plant-microbe joint control of landfill gas pollution.
Biodegradation, Environmental ; Rhizosphere ; Soil Microbiology ; Waste Disposal Facilities ; Chlorobenzenes/metabolism* ; Bacteria/metabolism* ; Soil Pollutants/metabolism* ; Methane/metabolism* ; Plant Roots/microbiology* ; Amaranthus/microbiology* ; Soil

Chlorobenzene contaminants (CBs) pose a threat to the eco-environment, and functional strains hold considerable potential for the remediation of CB-contaminated sites. To deeply explore the application potential of functional bacteria in the in-situ bioremediation of CBs, this study focused on the biodegradation characteristics and degradation kinetics of CB and 1, 2-dichlorobenzene (1, 2-DCB) in soil by the isolated strain Serratia marcescens TF-1. Additionally, an in-situ remediation trial was conducted with this strain at a chemical industrial site. Batch serum bottle experiments showed that the degradation rate of CB at the concentrations ranging from 20 to 200 mg/L by TF-1 was 0.22-0.66 mol/(g_cell·h), following the Haldane model, with the optimal concentration at 23.12 mg/L. The results from simulated soil degradation experiments indicated that the combined use of TF-1 and sodium succinate (SS) significantly enhanced the degradation of CBs, with the maximum degradation rate of CB reaching 0.104 d^-1 and a half-life of 6.66 d. For 1, 2-DCB, the maximum degradation rate constant was 0.068 7 d^-1, with a half-life of 10.087 d. The in-situ remediation results at the chemically contaminated site demonstrated that the introduction of bacterial inoculant and SS significantly improved the removal of CBs, achieving the removal rates of 84.2%-100% after 10 d. CB, 1, 4-dichlorobenzene (1, 4-DCB), and benzo[a]pyrene were completely removed. Microbial diversity analysis revealed that the in-situ remediation facilitated the colonization of TF-1 and the enrichment of indigenous nitrogen-fixing Azoarcus, which may have played a key role in the degradation process. This study provides a theoretical basis and practical experience for the in situ bioremediation of CBs-contaminated sites.
Chlorobenzenes/isolation & purification* ; Biodegradation, Environmental ; Soil Pollutants/isolation & purification* ; Serratia marcescens/metabolism* ; Industrial Waste ; Soil Microbiology

OBJECTIVETo evaluate the effect of white rot fungus Phanerochaete chrysosporium on removal of gaseous chlorobenzene.

METHODSFungal mycelium mixed with a liquid medium was placed into airtight bottles. A certain amount of chlorobenzene was injected into the headspace of the bottles under different conditions. At a certain interval, the concentrations in the headspace were analyzed to evaluate the degradation of chlorobenzene by P. chrysosporium.

RESULTSThe degradation effects of P. chrysosporium on chlorobenzene under different conditions were investigated. The difference in the optimum temperature for the growth of the fungi and chlorobenzene degradation was observed. The data indicated that a lower temperature (28 degrees C) would promote the degradation of chlorobenzene than the optimum temperature for the growth of the fungi (37 degrees C). A low nitrogen source concentration (30 mg N/L) had a better effect on degrading chlorobenzene than a high nitrogen source concentration (higher than 100 mg N/L). A high initial concentration (over 1100 mg/m3) of chlorobenzene showed an inhibiting effect on degradation by P. chrysosporium. A maximum removal efficiency of 95% was achieved at the initial concentration of 550 mg/m3.

CONCLUSIONP. chrysosporium has a rather good ability to remove gaseous chlorobenzene. A low nitrogen source concentration and a low temperature promote the removal of chlorobenzene by P. chrysosporium. However, a high initial chlorobenzene concentration can inhibit chlorobenzene degradation.

Air Pollutants ; metabolism ; Biodegradation, Environmental ; Chlorobenzenes ; metabolism ; Culture Media ; chemistry ; Microbiological Techniques ; Nitrogen ; pharmacology ; Phanerochaete ; drug effects ; growth & development ; metabolism ; Temperature ; Time Factors

OBJECTIVETo evaluate the antiproliferative activity of 3-(2-chlorophenyl)-1-(2-hydroxy-4, 6-dimethoxy-3-((ethyl(methyl) amino) methyl) phenyl) prop-2-en-1-one (DMF) against human androgen-independent prostate cancer PC3 cells in vitro and its underlying mechanisms.

METHODSThe cytotoxic effect of DMF on PC3 cells was measured by MTT assay. Induction of apoptosis was assessed by propidium iodide staining and flow cytometric analysis. Changes of mitochondrial membrane potential (DeltaPsim) were detected by JC-1 staining. The levels of apoptosis related proteins were analyzed by Western blot.

RESULTSDMF exhibited high efficiency on cell growth inhibition in PC3 cells with an IC50 value of (9.5 +/- 0.2)micromol/L. Flow cytometric analysis indicated that DMF could induce apoptosis in PC3 cells. A significant decrease of mitochondrial membrane potential was observed in PC3 cells treated with DMF, which was in a time- and dose-dependent manner. The results of Western blot indicated that DMF induced the activation of caspase-3, increased the ratio of Bax/Bcl-2 and downregulated the expression of phosphate-p38.

CONCLUSIONDMF is a potential compound against PC3 cells and the mitochondrial pathway might be involved in DMF-induced apoptosis in PC3 cells.

Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Blotting, Western ; Caspase 3 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Chlorobenzenes ; pharmacology ; Dose-Response Relationship, Drug ; Enzyme Activation ; drug effects ; Flavonoids ; pharmacology ; Flow Cytometry ; Growth Inhibitors ; pharmacology ; Humans ; Male ; Membrane Potential, Mitochondrial ; drug effects ; Piperidines ; pharmacology ; Prostatic Neoplasms ; metabolism ; pathology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; bcl-2-Associated X Protein ; metabolism ; p38 Mitogen-Activated Protein Kinases ; metabolism

OBJECTIVETo evaluate the antiandrogenic effect of heterocyclic fungicide dimethachlon and its mechanism.

METHODSA combination of in vivo and in vitro assays was selected. Hershberger assay was used to determine the antiandrogenic potential of dimethachlon in vivo. Six-week-old castrated male SD rats were administrated once daily for 7 days with testosterone propionate (TP, 100 micro g/d, sc) plus gavage doses of dimethachlon (50, 100 or 200 mg x kg(-1) x d(-1)), or procymidone (150 or 300 mg x kg(-1) x d(-1), positive control), or iprodione (100 mg x kg(-1) x d(-1), positive control), or flutamide (50 mg x kg(-1) x d(-1), positive control). Transcriptional activation assay in vitro was employed to determine the mechanism of antiandrogenic activity of dimethachlon. Human hepatoma liver cells HepG2 were transiently cotransfected with human androgen receptor (AR) expression plasmid and AR-dependent luciferase report plasmid. Transfected cells were exposed to various concentrations of dimethachlon or flutamide with or without dihydrotestosterone to induce the expression of luciferase gene.

RESULTSIn Hershberger assay, dimethachlon, as well as other known antiandrogens, caused decrease in weight of androgen dependent organs or tissues. In 200 mg/kg group, the weight of seminal vesicle, ventral prostate, dorsolateral prostate, Cowper's gland, and levator ani plus bulbocavernosus muscles decreased by 57.8%, 44.8%, 43.9%, 30.1%, and 34.1% respectively, but did not decrease in the vehicle control group. The order of their antiandrogenic potencies was: flutamide > procymidone > dimethachlon > iprodione. In transcriptional activation assay, dimethachlon could inhibit dihydrotestosterone-dependent AR activity in transfected HepG2 cells in dose-effect relationship. The inhibiting potency of dimethachlon was about 1/100 of that of flutamide.

CONCLUSIONDimethachlon has antiandrogenic effect, and acts as an AR antagonist. Its antiandrogenic potency is lower than flutamide and procymidone, but higher than iprodione.

Aminoimidazole Carboxamide ; analogs & derivatives ; pharmacology ; toxicity ; Androgen Antagonists ; pharmacology ; toxicity ; Androgens ; blood ; metabolism ; Animals ; Body Weight ; drug effects ; Bridged Bicyclo Compounds ; pharmacology ; toxicity ; Cell Line, Tumor ; Chlorobenzenes ; pharmacology ; toxicity ; Dose-Response Relationship, Drug ; Flutamide ; pharmacology ; toxicity ; Fungicides, Industrial ; pharmacology ; toxicity ; Humans ; Hydantoins ; Luciferases ; genetics ; metabolism ; Male ; Pesticides ; pharmacology ; toxicity ; Plasmids ; genetics ; Rats ; Rats, Sprague-Dawley ; Receptors, Androgen ; drug effects ; genetics ; metabolism ; Succinimides ; pharmacology ; toxicity ; Transfection