Paraquat mediates BV-2 microglia activation by raising intracellular ROS and inhibiting Akt1 phosphorylation.

Microglia is the innate immune cell in central nervous system (CNS) and plays an important role in neuroinflammation. Microglia mediated neuroinflammation is the key factor affecting the development of neurodegenerative diseases. Although there was evidence that paraquat (PQ) could induce inflammatory response, its mechanism was not clear.

Birth outcome measures and prenatal exposure to 4-tert-octylphenol.

Exposure to 4-tert-octylphenol (tOP) has been linked with adverse health outcomes in animals and humans, while epidemiological studies about associations between prenatal exposure to tOP and fetal growth are extremely limited. We measured urinary tOP concentrations in 1100 pregnant women before their delivery, and examined whether tOP levels were associated with birth outcomes, including weight, length, head circumference and ponderal index at birth. tOP could be detected in all samples, and the median uncorrected and creatinine-corrected tOP concentrations were 0.

Assessment of chlorpyrifos exposure and absorbed daily doses among infants living in an agricultural area of the Province of Jiangsu, China.

Purpose: Chlorpyrifos (CPF) is one of the most widely used organophosphorous pesticides in China. However, few reports on CPF pesticide exposure and body burden of infants at 2 years of age in China are available. The aim of this study was to assess the exposure level and the absorbed daily dose (ADD) of CPF among infants from an agricultural area of Jiangsu, China, and determine whether the infants' estimated dose exceeds the recommended reference dose (RfD) and the population adjusted dose (PAD) set by U.

[Paraquat involves differentiation of human neural stem cells via Notch signaling].

Objective: To investigate effects of paraquat on the mRNA expression of key elements of Notch signaling (Notch1, Jagged1 and DTX1) during differentiation process of human neural stem cells (hNSCs).

Methods: hNSCs exposed to PQ at the concentrations 0.10, 1.

[Determination of1-bromopropane in the workplace air by GC-FID].

Objective: To establish a method for determination 1-bromopropane (1-BP) in workplace air by gas chromatography-flame ionization detector (GC-FID).

Method: 1-bromopropane in workplace air was collected with activated charcoal tube, then desorbed by carbon disulfide and determined by GC-FID. 1-bromopropane was quantitatively measured using retention time and peak area.

[Effects of pyrrolidine dithiocarbamate on expressions of α-smooth muscle actin, integrin α5 and fibronectin in acute paraquat poisoned rats].

Objective: To observe the expressions of α-SMA, integrin α5 and fibronectin (Fn) in acute paraquat poisoned rats and the effect of PDTC. To investigate the mechanism of paraquat-induced pulmonary fibrosis.

Methods: Sprague-Dawley rats were randomly divided into three experimental groups: Control group (6 rats), PQ group (36 rats) and PQ+PDTC group (36 rats).

[Intervention of pyrrolidine dithiocarbamate on expressions of connective tissue growth factor, type I collagen, and type III collage in acute paraquat poisoned rats].

Objective: To observe the changes in the expression of connective tissue growth factor (CTGF), type I collagen (Col I), and type III collagen (Col III) among the rats with acute paraquat (PQ) poisoning and the intervention effect of pyrrolidine dithiocarbamate (PDTC) on their expression, and to investigate the mechanism of PQ-induced pulmonary fibrosis and the intervention effect of PDTC on the disease.

Methods: Sprague-Dawley rats were randomly divided into control group (n = 6), PQ group (n = 36), and PQ + PDTC group (n = 36). The PQ group and PQ + PDTC group were given a single dose of saline-diluted PQ (80 mg/kg) by gavage; 2 h later, the PQ + PDTC group was intraperitoneally injected with a single dose of PDTC (100 mg/kg), and the PQ group was intraperitoneally injected with the same amount of saline.

[Involvement of excitatory amino acid system in astrocytes activation caused by dimethoate].

Objective: To study the involvement of excitatory amino acid system in astrocytes activation caused by dimethoate.

Methods: Pure-cultured astrocytes were gained by three passages from primary cultured rat nerve cells, then treated with 10(-6),10(-5),10(-4) mol/L dimethoate for 48 h, 50 micromol/L and 100 micromol/L MK801, a NMDA receptor blocker, was used to intervene the effects induced by 10(-4) mol/L dimethoate. HPLC-FLD was utilized to measure the concentrations of excitatory amino acid (EAA), RT-PCR was used to detect the expression levels of NR2B, GLT-1, GLAST, GFAP and S100beta mRNA, and immunofluorescence staining method was applied to measure the expression levels of GFAP and S100beta proteins.

[Effects of controlling specific dangerous pesticides on prevention of acute pesticide poisoning in rural area].

Objective: To investigate the effects of controlling the specific dangerous pesticides on prevention of acute pesticide poisoning in rural area.

Methods: The data of reported cases of pesticide poisoning were analyzed to find out the specific dangerous pesticide in acute pesticide poisoning. Then the occurrence of occupational pesticide poisoning and fatality of non-occupational pesticide poisoning were estimated under the hypothesis of removing the specific dangerous pesticides.

[Role of connective tissue growth factor and α-smooth muscle actin in pulmonary fibrosis among acute paraquat poisoned rats].

Objective: to observe the expression of the connective tissue growth (CTGF) and a smooth muscle actin (α-SMA) in acute paraquat (PQ) poisoned rats and investigate the mechanism of paraquat-induced pulmonary fibrosis.

Methods: sprague-Dawley rats were randomly divided into two experimental groups: control group (6 rats) and PQ group (56 rats). On the 3rd, the 7th, the 14th, the 28th and the 56th day after exposure, the expression of CTGF and α-SMA were evaluated by SABC Immunohistochemistry and Western blot; and the relationship of the expression with pathologic score, hydroxyproline were also analyzed, respectively.

[Toxic effect of neonatal exposure to 2,2',4,4',5,5'-hexa-chlorobiphenyl on spermatogenesis in rats].

Objective: To determine the long-term testicular effect after neonatal exposure to 2,2', 4,4',5,5'-hexa-chlorobiphenyl (PCB153).

Methods: On birth day (Postnatal day 0, PNDO), the Sprague-Dawley (SD) male rats were mixed together and divided into 12 pups/litter. At PND1, the rats were grouped randomly into control and treatment groups according to different litters, 24 pups/group.

[Risk assessment of renal dysfunction caused by occupational lead exposure].

Objective: To assess the risk of renal dysfunction caused by occupational lead exposure through epidemiological investigation.

Methods: The workers in a battery factory were selected as the subjects for the exposure and effect assessment. The occupational environmental monitoring data was collected and used to calculate the total external dose of lead.

[Risk assessment of nerve conduction velocity in workers exposed to lead].

Objective: To explore the dose-effect relationship between lead exposure and nerve conduction velocity, and to assess risk characteristics of nerve conduction velocity induced by lead exposure.

Methods: The external dose, internal dose (blood lead, urine lead) and the conduction velocity of peripheral nerve were examined. The benchmark dose of a population exposed to occupational lead was estimated to develop risk assessment of nerve conduction velocity in worker exposed to lead by use of BMDS (version 1.

[Effect of neonatal exposure to environmental pollutants on the DNA methylation of rat testis].

Objective: To investigate the effects of neonatal exposure of DNA methylation inhibitor, Cadmium and PCB153 on DNA methylation, apoptosis and spermatogenesis in SD rats.

Methods: Neonatal SD rats were randomly divided into 10 groups and received oral administrations of PCB153 (0.025, 0.

[Changes of cytokine and nuclear factor-kappa B in acute paraquat poisoned rats].

Objective: To observe the changes of cytokine and NF-kappaB activity in acute paraquat poisoned rats and the effect of PDTC and the mechanism of lung injury caused by paraquat poisoning.

Methods: Sprague-Dawley (SD) rats were randomly divided into three groups: Control group (6 rats), PQ group (56 rats) and PQ + PDTC group (46 rats). On the 1st, the 3rd, the 7th, the 14th, the 28th and the 56th day after treatment, the level of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta 1 (TGF-beta1) and platelet-derived growth factor (PDGF) in serum were detected; the activity of NF-kappaB in lung tissues was detected.

[Change of oxidative stress and nuclear factor-kappa B in acute paraquat poisoned rats].

Objective: To investigate the change of oxidative stress and nuclear factor-kappaB (NF-kappaB) activity in acute paraquat (PQ) poisoned rats and the effect of PDTC.

Methods: 144 SD rats were randomly divided into four experimental groups: control group (6 rats), PDTC group (36 rats), PQ group (56 rats) and PQ + PDTC group (46 rats). On the 1st, the 3rd, the 7th, the 14th, the 28th and the 56th day after treatment, the level of malondialdehyde (MDA), the activity of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT) and myeloperoxidase (MPO) in serum were detected; the content of hydroxyproline (Hyp) and the activity of NF-kappaB in lung tissues were detected; the lung pathological changes of rats were observed.

[Effect of dimethoate on primary cultured rat cortical neuron].

Objective: To investigate the effect and mechanisms of dimethoate on the primary cultured cortical neuronal cell injury.

Methods: Cortical neuronal cells were isolated and cultured in serum free medium for 6 days in vitro, and 1, 5, 10, 50 and 100 micromol/L dimethoate were added to the medium and intracellular SOD, MDA and GSH. The content of excitatory amino acid was measured after 48 hours.

[Influence of pyrrolidine dithiocarbamate (PDTC) on expression of transforming growth factor beta(1), matrix metalloproteinase-2 and tissue inhibitor-1 of metalloproteinase in rats with pulmonary damage induced by paraquat].

Objective: To investigate the influence of pyrrolidine dithiocarbamate (PDTC) on the expression of transforming growth factor beta(1) (TGF-beta(1)), matrix metalloproteinase-2 (MMP-2) and tissue inhibitor-1 of metalloproteinase (TIMP-1) in rats with pulmonary damage induced by paraquat (PQ).

Methods: Fifty-four healthy male SD rats were randomly assigned into the control group (normal saline), the PQ-treatment groups (4 groups) and the PDTC treatment groups (4 groups). Except the rats in the control group, the rats in the PQ group were gavaged only with 40 mg/kg PQ, and PDTC group with 40 mg/kg PQ plus immediate injection 120 mg/kg PDTC (i.

N'-[(E)-(5-Bromo-2-hydroxy-phen-yl)(phen-yl)methyl-idene]-4-chloro-benzo-hydrazide.

The Schiff base, C(20)H(14)BrClN(2)O(2), displays a trans conformation with respect to the C=N double bond. The aromatic rings at either end of the -C(=O)-NH-N=C- fragment are nearly parallel [dihedral angle = 3.4 (5)°].

{N'-[(E)-(5-Bromo-2-oxidophen-yl)(phen-yl)methyl-ene]benzohydrazidato}pyridine-nickel(II).

The asymmetric unit of title complex, [Ni(C(20)H(13)BrN(2)O(2))(C(5)H(5)N)], contains two independent mol-ecules. In each mol-ecule, the central Ni(II) atom has a square-planar environment, formed by the tridentate hydrazone and the monodentate pyridine ligands, with the N atoms in a trans arrangement about the Ni(II) atom.

{N'-[(E)-1-(5-Bromo-2-oxidophen-yl)ethyl-idene]-4-chloro-benzohydrazidato}pyridinenickel(II).

The title complex, [Ni(C(15)H(10)BrClN(2)O(2))(C(5)H(5)N)], displays a square-planar coordination geometry around the Ni(II) ion, formed by the tridentate hydrazone and monodentate pyridine ligands, with the N atoms in a trans arrangement about the Ni center.

N'-[(E)-(5-Bromo-2-hydroxy-phen-yl)(phen-yl)methyl-ene]benzohydrazide.

In the title compound, C(20)H(15)BrN(2)O(2), the C=N double bond displays a trans configuration. The crystal structure features an intra-molecular O-H⋯N hydrogen bond.

{N'-[(E)-(5-Bromo-2-oxidophen-yl)(phenyl)-methyl-ene]-4-chloro-benzo-hydrazidato}pyridine-nickel(II).

The asymmetric unit of title complex, [Ni(C(20)H(12)BrClN(2)O(2))(C(5)H(5)N)], contains one complex with the central Ni atom in a slightly distorted square-planar environment, formed by the tridentate hydrazone and the monodentate pyridine ligands, with N atoms in a trans arrangement about the Ni atom.

(meso-5,7,7,12,14,14-Hexamethyl-1,4,8,11-tetra-azacyclo-tetra-deca-4,11-diene)nickel(II) bis-[O,O'-bis(4-methyl-phen-yl) dithio-phosphate].

In the title compound, [Ni(C(16)H(32)N(4))](C(14)H(14)O(2)PS(2))(2) or [Ni(trans[14]dien)][S(2)P(OC(6)H(4)Me-4)(2)](2), where trans[14]dien is meso-5,7,7,12,14,14-hexa-methyl-1,4,8,11-tetra-azacyclo-tetra-deca-4,11-diene, the Ni(II) ion lies across a centre of inversion and is four-coordinated in a relatively undistorted square-planar arrangement by the four N atoms of the macrocyclic ligand trans[14]dien. The two O,O'-di(4-methyl-phen-yl)dithio-phos-phates act as counter-ions to balance the charge. Important geometric data include Ni-N = 1.