ABSTRACT
This study aims to understand the influence of nitrogen accumulation, fungal endophyte, yield, nitrogen use efficiency, and grain nutritional quality parameters on the yield of quinoa in some areas of China. The endophytic microbial community in plants plays a crucial role in plant growth, development, and health, especially in quinoa plants under different nitrogen fertilizer levels. The results from the present study indicated that appropriate nitrogen application significantly enhanced the nitrogen accumulation and yield of quinoa grains during maturity, increasing by 34.54-42.18% and 14.59-30.71%, respectively. Concurrently, protein content, amylose, total starch, ash, and fat content also increased, with respective growth rates of 1.15-18.18%, 30.74-42.53%, 6.40-12.40%, 1.94-21.94%, and 5.32-22.22%. Our constructed interaction network of bacterial and fungal communities revealed that bacteria outnumbered fungi significantly, and most of them exhibited synergistic interactions. The moderate increase in N150 was beneficial for increasing quinoa yield, achieving nitrogen use efficiency (NUE) of over 20%. The N210 was increased, and both the yield and NUE significantly decreased. This study provides novel insights into the impact of nitrogen fertilizer on quinoa growth and microbial communities, which are crucial for achieving agricultural sustainable development.
ABSTRACT
An efficient asymmetric hydroesterfication of diarylmethyl carbinols is developed for the first time with a Pd-WingPhos catalyst, resulting in a series of chiral 4-aryl-3,4-dihydrocoumarins in excellent enantioselectivities and good yields. The method features mild reaction conditions, a broad substrate scope, use of easily accessible starting materials, and low palladium loadings. A plausible stereochemical model is also proposed with the Pd-WingPhos catalyst. This method has enabled a 4-step asymmetric synthesis of (R)-tolterodine from readily available starting materials.
ABSTRACT
As a maternal and developmental toxicant, cadmium (Cd) possesses weak penetrability through the placental barrier. However, the underlying mechanism remains unclear. To gain insight into the protein molecules associated with Cd toxicity in placenta and explore their roles in Cd transportation, a reproductive animal experiment was carried out using Sprague-Dawley rats. We performed proteomic analysis of the placenta by Difference Gel Electrophoresis (DIGE) combined with Matrix-Assisted Laser Desorption/Ionization Time-of-Flight Tandem Mass Spectroscopy (MALDI-TOF/TOF MS). The DIGE assay identified 15 protein spots that were differentially expressed with a greater than 1.5-fold change in placenta of Cd-treated rats compared to the control rats. Based on the expression patterns and biological functions of the proteins, we selected the ABCG2 and ABCB4 transporter proteins for further analysis. Western blot analysis showed that Cd exposure could down-regulate the expression of ABCG2 and ABCB4 in the placenta. There was a negative dose-response relationship between Cd exposure and the expression of ABCG2 or ABCB4 protein. These results indicated that down-regulation of ABCG2 and ABCB4 transporters may regulate Cd across through placenta and thus affect the in vivo toxic effect of Cd to fetus.
Subject(s)
ATP Binding Cassette Transporter, Subfamily B/biosynthesis , ATP Binding Cassette Transporter, Subfamily G, Member 2/biosynthesis , Cadmium/toxicity , Placenta/drug effects , Placenta/metabolism , Animals , Down-Regulation , Female , Male , Placenta/pathology , Pregnancy , Proteomics/methods , Rats , Rats, Sprague-Dawley , ATP-Binding Cassette Sub-Family B Member 4ABSTRACT
Trichloroethylene induced hypersensitivity syndrome is dose-independent and potentially life threatening disease, which has become one of the serious occupational health issues and requires intensive treatment. To discover the genetic risk factors and evaluate the performance of risk prediction model for the disease, we conducted genomewide association study and replication study with total of 174 cases and 1761 trichloroethylene-tolerant controls. Fifty seven SNPs that exceeded the threshold for genome-wide significance (P < 5 × 10(-8)) were screened to relate with the disease, among which two independent SNPs were identified, that is rs2857281 at MICA (odds ratio, 11.92; P meta = 1.33 × 10(-37)) and rs2523557 between HLA-B and MICA (odds ratio, 7.33; P meta = 8.79 × 10(-35)). The genetic risk score with these two SNPs explains at least 20.9% of the disease variance and up to 32.5-fold variation in inter-individual risk. Combining of two SNPs as predictors for the disease would have accuracy of 80.73%, the area under receiver operator characteristic curves (AUC) scores was 0.82 with sensitivity of 74% and specificity of 85%, which was considered to have excellent discrimination for the disease, and could be considered for translational application for screening employees before exposure.
Subject(s)
Anesthetics, Inhalation/adverse effects , Drug Hypersensitivity Syndrome/etiology , Genetic Predisposition to Disease , Trichloroethylene/adverse effects , Case-Control Studies , Genome-Wide Association Study , Histocompatibility Antigens/genetics , Humans , Polymorphism, Single Nucleotide , Prognosis , ROC Curve , Risk FactorsSubject(s)
Spermatozoa/drug effects , Testis/drug effects , Triazines/toxicity , Animals , Male , Organ Size , Rats , Rats, Sprague-Dawley , Spermatozoa/growth & developmentABSTRACT
OBJECTIVES: The aim of this study was to explore the involved pathophysiological processes and develop biomarkers of trichloroethylene-induced hypersensitivity dermatitis (THD). METHODS: We examined the impact of THD on the serum proteome in 8 male patients by comparing the serum samples between acute and healed stages. Sample pooling and immunodepletion were applied for sample preparation. Two-dimensional gel electrophoresis coupled with matrix-assisted laser-desorption ionization time-of-flight mass spectrometry (MALDI-TOF-TOF/MS) was utilized to identify and quantitate differentially expressed proteins. Changes in selected proteins were further confirmed by an ELISA assay. RESULTS: A total of 41 spots were quantitated with significant alteration (p<0.05; fold-change≥± 3.0) in the serum between the acute and healed stages. Of these proteins, 26 proteins were identified by MALDI-TOF-TOF/MS. The identified proteins could be categorized into diverse functional classes, e.g., immunity and defense response, vitamin and lipid transport, fatty acid biosynthesis, actin binding, proteolysis and glycolysis. The ELISA assay confirmed the relative upregulation of calprotectin (S100A8/A9) and downregulation of retinol binding protein (RBP4) in the serum of the acute stage. The alteration of calprotectin and RBP4 was found to be specific to THD rather than trichloroethylene exposure. CONCLUSIONS: The pathophysiological processes underlying THD may involve elevated inflammatory responses and oxidative stress, inhibition of vitamin transport, depression of fatty acid biosynthesis, loss of extracellular actin scavenger, increase in oxygen transport, dysfunction in lipid transport, proteolysis and glycolysis. The combination of higher calprotectin and lower RBP4 levels in the serum could be used as potential biomarkers of THD.
Subject(s)
Dermatitis/etiology , Hypersensitivity/etiology , Leukocyte L1 Antigen Complex/biosynthesis , Occupational Exposure/adverse effects , Retinol-Binding Proteins, Cellular/biosynthesis , Trichloroethylene/toxicity , Adolescent , Adult , Air Pollutants, Occupational/toxicity , Dermatitis/immunology , Dermatitis/metabolism , Electrophoresis, Gel, Two-Dimensional , Enzyme-Linked Immunosorbent Assay , Humans , Hypersensitivity/immunology , Hypersensitivity/metabolism , Inhalation Exposure , Male , Middle Aged , Proteome/analysis , Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization , Young AdultABSTRACT
OBJECTIVE: To observe the urinary S-phenylmercapturic acid (S-PMA) variation in the benzene dynamic exposed rat models and benzene exposed workers, and study the feasibility of use of urinary S-PMA as the biomarker in benzene exposed. METHODS: In an animal model study, forty-eight adult Wistar rats were randomly divided into 4 groups: the control group, low-dose group, middle-dose group and high-dose group. The exposed groups were dynamically exposed for 28 days (4 periods) by benzene and the concentration was monitored. The urine was immediately collected after every exposure period and detected by the liquid chromatographic/mass spectrometry methods. In a cohort study, eighty benzene exposed workers in a ship-yard in Guangzhou were selected as the exposed subjects while forty healthy officers in the same shipyard who were not occupationally exposed to benzene were treated as the control. The urine was collected after work shift. The urinary S-PMA and the benzene in the workplace was treated as the rat model. RESULTS: In the animal model study, the urinary S-PMA increased along with the environment benzene in every period and had significantly difference in the different exposed groups (P < 0.01 or P < 0.05), but did not change along with the exposed time course (P > 0.05). In the cohort study, the urinary S-PMA in the high-dose group [(27.2 +/- 7.9)microg/L] was significantly higher than the low-dose group [(13.6 +/- 3.4)microg/L] (P < 0.01). Otherwise, the background of urinary S-PMA was lower than 5microg/L in both workers and rat models. CONCLUSION: The urinary S-PMA can be proposed as a sensitive biomarker of occupational benzene exposure.
Subject(s)
Acetylcysteine/analogs & derivatives , Benzene/toxicity , Environmental Exposure/adverse effects , Acetylcysteine/urine , Adult , Animals , Benzene/administration & dosage , Female , Humans , Male , Middle Aged , Rats , Rats, Wistar , Young AdultABSTRACT
OBJECTIVE: To establish the association between genetic polymorphisms of HLA-DMA and HLA-DMB and risk of developing trichloroethylene-induced medicamentosa-like dermatitis (TIMLD). METHODS: Sixty-one cases were medically confirmed to have been affected with TIMLD and 60 controls were selected from exposed workers who were free from TIMLD. The TIMLD cases and controls were similar in terms of age, sex, and duration of exposure. DNA was extracted both from the TIMLD cases and controls, HLA-DMA and HLA-DMB loci were amplified by using Touchdown PCR, and the alleles and genotypes were confirmed by restriction fragment length polymorphism (RFLP) and direct sequencing. Finally, the frequencies of HLA-DMA and HLA-DMB variants were compared between the two groups. RESULTS: The results showed that the frequency of HLA-DMA*0101 and HLA-DMB*0103 alleles was significantly increased in TIMLD patients than in controls (71.3% vs. 55.0% for HLA-DMA*0101; P<0.05) (11.5% vs. 3.3% for HLA-DMB*0103; P<0.05). In addition, the frequency of HLA-DMA*0102-*0102 homozygous genotype was also significantly higher in the controls than in the patients (25.0% vs. 8.2%, P<0.05), whereas the frequency of heterozygous HLA-DMB *0101-*0102 genotype was lower in the patients in comparison with the controls. Conclusion The polymorphisms of HLA-DM may be associated with the susceptibility to TIMLD.
Subject(s)
Dermatitis, Contact/genetics , Genetic Predisposition to Disease , HLA-D Antigens/genetics , Polymorphism, Genetic , Trichloroethylene/toxicity , Alleles , Humans , Polymorphism, Restriction Fragment LengthABSTRACT
OBJECTIVES: To study the contact allergenic activities of trichloroethylene (TCE) and its three metabolites trichloroacetic acid, trichloroethanol and chloral hydrate. METHODS: A modified guinea pig maximization test (GPMT) was adopted. The skin sensitization (edema and erythema) was observed in trichloroethylene, trichloroacetic acid, trichloroethanol, chloral hydrate and 2,4-dinitrochlorobenzene. RESULTS: The allergenic rate of TCE, trichloroacetic acid and 2,4-dinitrochlorobenzene was 71.4%, 58.3% and 100.0% respectively, and that of trichloroethanol and chloral hydrate was 0%. The mean response score of TCE, trichloroacetic acid and 2,4-dinitrochlorobenzene was 2.3, 1.1, 6.0 respectively. The histopathological analysis also showed an induction of allergenic transformation in guinea pig skin by both TCE and trichloroacetic acid. CONCLUSION: TCE appears to be a strong allergen while trichloroacetic acid a moderate one. On the other hand, both trichloroethanol and chloral hydrate are weak sensitization potentials. Immunologic reaction induced by TCE might be postulated as the pathological process of this illness. Consequently, it is suggested that in the mechanism of Occupational Dermatitis Medicamentose-Like (ODML) induced by TCE, the chemical itself might be the main cause of allergy. As one of its metabolic products, trichloroacetic acid might be a subordinate factor.
Subject(s)
Allergens/toxicity , Dermatitis, Allergic Contact/immunology , Ethylene Chlorohydrin/analogs & derivatives , Skin/drug effects , Trichloroethylene/toxicity , Animals , Chloral Hydrate/toxicity , Dermatitis, Allergic Contact/etiology , Dermatitis, Irritant/etiology , Dermatitis, Irritant/immunology , Ethylene Chlorohydrin/toxicity , Guinea Pigs , Skin/immunology , Toxicity Tests , Trichloroacetic Acid/toxicity , Trichloroethylene/metabolismABSTRACT
OBJECTIVES: To determine the possible relationship between plasma potassium concentration and severity of acute trimethyltin chloride (TMT) poisoning and to assess the mechanism of TMT induced hypokalemia. METHODS: SD rats were treated with various dosages of TMT (i.p.). All the indices were measured and analysed for determining their possible relations with plasma K+. RESULTS: With increase of dosage, the plasma K+ level dropped rapidly, and deaths appeared more quickly. The LD50 of TMT (i.p.) was 14.7 mg/kgbw. In the low dosage group (10 mg/kgbw), the plasma K+ level dropped slowly with the lowest dosage on day 6 (4.85 mmol/L). It rose again on day 11 (5.06 mmol/L), and recovered on day 28. The poisoning signs corresponded with decline of the span of K+ level. The plasma Na+ level dropped half an hour after TMT treatment, but recovered 24 h later. In the high dosage group (46.4 mg/kgbw), the levels of plasma K+ and Na+ fell rapidly within half an hour (P < 0.05), the intracellular potassium concentration of RBC did not decrease obviously (P > 0.05), the activities of Na(+)-K(+)-ATPase and Mg(2+)-ATPase in RBC membrane were depressed remarkably (P < 0.01, P < 0.05, respectively), the plasma aldosterone concentrations rose as high as tenfold (P < 0.01), the arterial blood pH fell from 7.434 to 7.258 (P < 0.01), pCO2 was raised from 29.62 to 45.33 mmHg (P < 0.01). In the 24 h urine test, when rats were treated with TMT (21.5 mg/kgbw, i.p.), urine volume, urinary potassium, sodium and chloride increased significantly in comparison with those in the controls (P < 0.01). CONCLUSION: TMT could induce hypokalemia in SD rats. The available evidence suggests that TMT can induce acute renal leakage of potassium. At the same time, a significant rise of plasma aldosterone may play an important role in promoting potassium leakage from kidney to result in severe hypokalemia with inhaling acid-base abnormalities produced, which aggravate the poisoning symptoms. In the end the rats would die of respiratory failure.
Subject(s)
Hypokalemia/chemically induced , Trimethyltin Compounds/poisoning , Animals , Female , Hypokalemia/veterinary , Injections, Intraperitoneal , Kidney Diseases/chemically induced , Kidney Diseases/veterinary , Lethal Dose 50 , Male , Rats , Rats, Sprague-Dawley , Severity of Illness Index , Trimethyltin Compounds/pharmacologyABSTRACT
OBJECTIVE: To observe the effect of fluoroacetamide on cardiomyocytes of rat and the antidotal effect of acetamide. METHODS: 4 groups of SD rats were treated with various dosages of fluoroacetamid(p.o.) and 2 groups of them were treated with acetamide(i.p.). The changes of cardiomyocytes and serum AST, LDH, CK, CK-MB and HBDH were measured at different intervals after poisoning. RESULTS: In the group treated with fluoroacetamid 8 mg/kg. bw, serum AST[(589.58 +/- 821.72) U/L], CK[(916.78 +/- 343.55) U/L], HBDH[(504.47 +/- 148.88) U/L] raised obviously compared with control[(187.70 +/- 46.87), (755.65 +/- 498.90), (347.25 +/- 228.40) U/L respectively] (P < 0.01), and the pathological findings such as degeneration, liquefactive necrosis and filtration of inflammatory cells in cardiac muscles were observed 24 hours later, while all the male dead within 3 days. In the group treated with fluoroacetamid 4 mg/kg. bw, serum LDH and HBDH rose significantly compared with control(P < 0.01) 5 day later. On the day of 10, myocardial enzymes restored in all experiment groups with some interstitial fibroblastic proliferation. The pathological changes were reduced in the group treated with acetamide synchronously (100 mg/kg. bw). CONCLUSION: Acute intoxication of fluoroacetamide could damage cardiomyocytes while acetamide could reduce the injury of them, but the injury was reversible. The levels of serum myocardial enzymes could be a usable index for early diagnosis.