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.S. Environmental Protection Agency (EPA). METHODS: In our study, 364 infants at 2 years of age who lived in the agricultural area of Jiangsu Province (China) were enrolled into the biomonitoring study from June 2011 to January 2012. CPF exposure was estimated based on both questionnaire survey and measured results of urinary metabolite 3,5,6-trichloro-2-pyridinol (TCPy) of CPF by high-performance liquid chromatography. Furthermore, the ADD of CPF among infants was also evaluated and compared with the RfD and the PAD values issued by EPA. RESULTS: Urinary TCPy was detected in more than 70 % of the urine samples among 364 infants. The unadjusted and creatinine-adjusted geometric means in these subjects for TCPy were 1.33 µg/L and 6.73 µg/g Cre., respectively. Infants lived nearby (100 m distance) plantations or green parks present significantly higher levels of urinary TCPy than those lived far away (p = 0.045). Urinary TCPy levels were also significantly higher in infants who had frequent hand-to-mouth activities than those with less frequency (p = 0.037). Urinary TCPy concentrations in the infants at 2 years of age in Jiangsu were lower than those in the children at 2-6 years of age in the USA. The median estimated ADD of CPF in this study (0.07 µg/kg/day) was much lower than the acute and chronic RfDs (5 and 0.3 µg/kg/day, respectively) announced by EPA, but higher than the chronic PAD (cPAD) (0.03 µg/kg/day) for children. Additionally, the 75th percentile of the estimated ADD in our study was 2.5 times as much as the cPAD from EPA, even assuming only half of the TCPy amount from CPF exposure. CONCLUSIONS: Our findings revealed that infants at 2 years of age in Jiangsu of China were widely exposed to CPF pesticide. The estimated ADD probably suggested that about 25 % of the enrolled infants were at potential risk of pesticide exposure, which warned of urgency to eliminate the potential exposure risk to infants living in agricultural areas of China.

[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. The control group was given saline (1 ml/kg) by gavage and was intraperitoneally injected with the same amount of saline 2h later. At 1, 3, 7, 14, 25, and 56 days after operation, the protein expression of CTGF was evaluated by Western blot; the mRNA expression of CTGF, Col I, and Col III was analyzed by real-time quantitative PCR; the content of hydroxyproline in lung tissue was measured, and the pathological changes of lung tissue of the poisoned rats were observed. RESULTS: The protein expression of CTGF in the PQ group increased as the time went on, slowly from the 3rd to the 14th day and rapidly from the 28th to the 56th day, significantly higher than that in the control group at each time point (P < 0.05 or P < 0.01). The mRNA expression of CTGF in the PQ group began to rise markedly on the 1st day, increased rapidly from the 3rd to the 14th day, and remained at a relatively high level from the 28th to the 56th day, significantly higher than that in the control group at each time point (P < 0.01). The mRNA expression of Col I in the PQ group changed little on the 1st and 3rd day, increased slightly on the 7th day, and increased greatly from the 14th to the 56th day, significantly higher than that in the control group from the 7th to the 56th day (P < 0.05 or P < 0.01). The mRNA expression of Col III in the PQ group began to rise on the 1st day, reached the peak level on the 7th day, and then declined, significantly higher than that in the control group at each time point (P < 0.05 or P < 0.01). Masson staining showed that fibroblasts proliferated from the 14th to the 28th day, and collagen fibers increased gradually. Compared with the PQ group, the PQ + PDTC group showed significantly decreased protein expression of CTGF as well as mRNA expression of CTGF, Col I, and Col III (P < 0.05 or P < 0.01). CONCLUSION: In PQ-induced pulmonary fibrosis, the expression of CTGF keeps rising, and the collagen secretion and matrix synthesis are increased probably by upregulating the transcriptional levels of Col I and Col III; CTGF plays an important role in PQ-induced pulmonary fibrosis. PDTC can inhibit the expression of CTGF, thus reducing the lung injury in rats with PQ poisoning.

[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, 1.00, 10.00 M. Cell proliferation ability was assessed using MTT assay and mRNA expressions of Notch1, Jagged1 and DTX1 were detected by Real-time RT-PCR at 2, 4, 8, 12 d of differentiation. RESULTS: Compared with control group, NOTCH1, JAG1 mRNA expression levels exposed to PQ at the concentration of 0.10 M significantly reduced at 2, 4, 8 d and significantly went up at 12d (P < 0.01). Compared with control group, NOTCH1, JAG1 and DTX1 mRNA expression levels exposed to PQ at the concentration of 10.00 M significantly reduced at 2, 8, 12 d (P < 0.01). PQ could down-regulate Notch1, Jagged1 and DTX1 mRNA expressions at the early stage of differentiation, then up-regulate Notch1 mRNA expression, and down-regulate Notch1, Jagged1 and DTX1 mRNA expressions at the end of differentiation. CONCLUSION: Notch signaling pathway may be involved in differentiation of neural stem cell exposed to PQ.

[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). On the 1st, 3rd, the 7th, the 14th, the 28th and the 56th day after exposure, the protein expression of α smooth muscle actin (α-SMA) was evaluated by western blot. The mRNA levels of integrin α5 and fibronectin (Fn) were analyzed with real-time quantitative PCR (RT-PCR). Meanwhile, the lung pathological changes were observed and semi-quantified. RESULTS: T With the time passing, the expression of α-SMA in PQ group increased gradually compared with control group (P < 0.05 or P < 0.01). The increasing extent was gently on the 3 rd, the 7 th day. While increasing extent was rapidly from the 28 th to the 56 th day. RT-PCR showed PQ significantly increased Fn mRNA level on all time points and increased integrin α5 mRNA level from the 7 rd to 56 th day compared with control group (P < 0.05 or P < 0.01). PDTC treatment significantly deceased α-SMA, Fn, and integrin α5 levels compared with PQ group in corresponding time points (P < 0.05 or P < 0.01) Noteworthy, in PQ+PDTC group, the occurrence of pathological changes were drastically attenuated and pathologic score significantly decreased (P < 0.05 or P < 0.01). CONCLUSIONS: α-SMA, integrin α5 and fibronectin could play an important role in the development of pulmonary fibrosis caused by paraquat poisoning. PDTC, asa strong NF-κB inhibitor, may inhibit NF-κB activity and further significantly decreased expressions of α-SMA, integrin α5 and fibronectin which were important part of ECM, leading to drastically attenuated pulmonary fibrosis. However, the mechanisms of PDTC intervention still remains to be explored.

[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. RESULTS: Linear regression formula was Y = 3353.4x-10064 in a range of 2.50 ∼ 500.00 µg/ml with regression coefficient R = 0.9998. Detection limit was 0.25 µg/ml and the lowest detection concentration of 1-brmopropane in air was 0.14 mg/m(3) (at air volume 1.8L). The mean recoveries of 1-BP were between 96.8% and 102.6%, and relative standard deviation of inter and intra-assay was less than 10%. The average desorption efficiencies were between 93.2% and 104.4%. The samples in activated charcoal tube could be stably stored for 5 days at room temperature. CONCLUSION: The method could be feasible to determine 1-bromopropane in workplace air.

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. The present study investigated the mechanisms of PQ-induced inflammatory responses in BV-2 microglia cells, and tried to reveal the role of ROS/Akt1 pathway. The results showed that the cell activation markers (iNOS and CD206) of BV-2 cells were increased after PQ treatment, suggesting that BV-2 microglia were activated. PQ induced the reactive oxygen species (ROS) and inhibited the AKT1 phosphorylation in BV-2 cells. Besides, the M1 markers expression (IL-6, TNF-α and IL-1ß) were significantly increased after PQ treatment, which suggested that PQ induced the increase of M1 phenotype of BV-2 microglia. Pre-treated with NAC (ROS scavenger), the M1 phenotype was decreased while the p-Akt1 was restored compared to PQ stimulation. Furthermore, we built an Akt1(S473E)-overexpression BV-2 cell line. The Akt1 (S473E) partially attenuated the PQ induced increase in M1 phenotype, while ROS did not significantly change. These results indicated that PQ induced BV-2 microglia activation by increased ROS mediated Akt1 activation inhibition, leading to neuroinflammation.

[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. RESULTS: The expression levels of GLAST mRNA in all exposure groups were 67.8%, 68.6% and 76.2% of control level, respectively, which were significantly lower than that of control group (P < 0.05); The concentrations of EAA significantly decreased in 10(-4) mol/L dimethoate group, as compared with control group (P < 0.01); the expression levels of GFAP mRNA in 10(-4) mol/L dimethoate group, of S100beta mRNA in 10(-5) mol/L dimethoate group, of GFAP protein in 10(-4) mol/L and 10(-5) mol/L dimethoate groups and S100beta protein in 10(-4) mol/L dimethoate group were significantly higher than those in control group (P < 0.01). The expression levels of GLT-1 and GLAST mRNA in 10(-4) mol/L dimethoate plus 50 micromol/L or 100 micromol/L MK801 groups increased significantly, as compared with 10(-4) mol/L dimethoate group (P < 0.01), the expression levels of NR2B mRNA in 10(-4) mol/L dimethoate plus 50 micromol/L or 100 micromol/L MK801 groups increased significantly, as compared with control group (P < 0.05 or P < 0.01); the concentration of Glu in 10(-4) mol/L dimethoate plus 100 micromol/L MK801 group increased significantly, as compared with 10(-4) mol/L dimethoate group (P < 0.01); the expression levels of GFAP mRNA and protein in 10(-4) mol/L dimethoate plus 50 micromol/L or 100 micromol/L MK801 groups decreased significantly (P < 0.01); S100beta protein expression level in 50 micromol/L MK801 intervention group was significantly higher than thatl in control group (P < 0.01). CONCLUSION: Excitatory amino acid system involved in astrocytes activation caused by dimethoate. MK801 was useful to control astrocytes gliosis.

[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. RESULTS: The data indicated that parathion (including methyl parathion) was the specific dangerous pesticide inducing occupational pesticide poisoning. After removing the use of parathion, the hazard of pesticides which caused occupational pesticide poisoning would be significantly decreased (P < 0.01). Parathion was also the most dangerous pesticide which caused non-occupational pesticide poisoning, with its fatality up to 15.8%. If parathion was well controlled, the fatality of non-occupational pesticide poisoning would be declined from 9.4% to 7.4%. The analyses of related literatures also revealed the similar results. CONCLUSION: The occurrence of occupational pesticide poisoning and fatality of non-occupational pesticide poisoning may decrease if the most dangerous pesticides are well supervised.

[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. The lung pathological changes of rats were observed and pathological evaluation was made. RESULTS: it was similar that the expression pattern of CTGF, α-SMA detected by immunohistochemistry and Western blot. With the time passing, their expression in PQ group increased gradually compared with control group (P < 0.05 or P < 0.01). The increasing extent of CTGF, α-SMA were gentle on the 3rd, the 7th day. While their increasing extent was rapid from the 14th to the 56th day. CTGF was positively correlated with α-SMA, pathologic score and hydroxyproline respectively (r = 0.74, r = 0.87, r = 0.71, P < 0.05 or P < 0.01). Meanwhile, the histological changes such as lung fibroblast proliferation, disorganized collagen fibers were observed in PQ group. CONCLUSION: CTGF and α-SMA could play an important role in the development of pulmonary fibrosis caused by paraquat poisoning; CTGF may promote the transformation of fibroblasts to myofibroblasts and further strengthen the ability of synthesis collagen and extracellular matrix.

[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 1.3.3). The BMDL in terms of blood lead and urine lead was calculated. RESULTS: There was correlation between blood lead and urine lead. The sense nerve conduction velocity was decreased significantly in the group of lead exposure workers (P < 0.05). The BMDLs-05 for median nerve conduct velocity, ulnar nerve conduction velocity, and superficial peroneal nerve conduction velocity in terms of blood lead were 456.99, 332.36 and 468.38 microg/L respectively; the BMDLs-05 in terms of urine lead were 14.1, 9.2 and 13.6 microg/gCr respectively. CONCLUSION: The internal dose is the better index to reflect the level of lead exposure. Blood lead is identified as a specific and sensitive biomarker for sense nerve conduction velocity reduction. Ulnar nerve conduction velocity can be used as highly sensitive biomarkers to screen the high risk population of lead exposure.

[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. The relationship between external dose and internal dose of lead was analyzed. The external dose, blood lead (BPb) and urinary lead (UPb) were used as exposure biomarkers while the urinary N-acetyl-D-glucosaminidase (UNAG), and urinary albumin (UALB) were used as the effect biomarkers for the renal dysfunction caused by lead. Software of BMDS (BMDS 11311) was used to calculate BMD. RESULTS: The external and internal does of lead was positively correlated (BPb: r = 0.466, P < 0.01; UPb: r = 0.383, P < 0.01). The levels of BPb, UPb in exposure group (654.03 microg/L, 143.45 microg/g Cr) were significantly higher than those in the control group (57.12 microg/L, 7.20 microg/g Cr), so were UALB, UNAG; in addition, all of them presented significant dose-response relationship. The BPb BMD of UALB, UNAG were 607.76, 362.56 microg/L respectively and the UPb BMD of UALB, UNAG were 117.79, 78.79 microg/gCr respectively. CONCLUSION: Occupational lead exposure can cause renal dysfunction, which presents dose-response relationship; the risk assessment of renal dysfunction caused by occupational lead exposure is performed by BMD calculation of BPb and UPb.

[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. They were treated by oral gavage with PCB153 in corn oil at doses of 0, 0.025, 0.250 and 2.500 mg/kg BW-day from PNDI to PND7. The rats were sacrificed at PND8 and PND90 by anesthesia. The testes were collected and weighed for histological examination and daily sperm production at PND8 or/and PND90. The epididymidis and the epididymidis cauda also were collected and weighed for determination the sperm counts at PND90. RESULTS: The body weight of 2.500 mg/kg dose group was decreased significantly from PND3 to PND8 compared with that of control (P < 0.05). At PND8, the loose structure in seminiferous cord and the spermatogonia with enlarged volume and detached from the cord were observed in 2.500 mg/kg dose group by light microscope and electronic microscopy. With the increase of exposure doses, the testicular daily sperm production (DSP) and the sperm counts of epididymidis cauda were decreased in dose-dependent manner at PND90. The DSP in 0.250 mg/kg [30 x 10(6)/testis(g)] and 2.500 mg/kg [18 x l0(6)/testis(g)] dose groups were significantly reduced compared with that of control [36 x 10(6)/testis(g)] (P < 0.05). And there was a significant reduction in the sperm counts of epididymidis cauda in 0.250 mg/kg [42 x 10(7)/epididymidis cauda (g)] and 2.500 mg/kg [18 x 10(7)/epididymidis cauda (g)] dose groups compared with that of control [51 x 10(7)/epididymidis cauda (g)] (P < 0.05). CONCLUSIONS: The spermatogenesis of adult testis is disturbed, which causes the decrease in the testicular DSP and the sperm counts of epididymidis cauda after neonatal exposure to PCB153. The long-term damage in male reproductive function is caused by neonatal exposure to chemicals.

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-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)°]. The hydr-oxy group forms an intra-molecular hydrogen bond to the imino N 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 = 1.9135 (16) and 1.9364 (15) Å.

{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.

{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-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)-(5-Bromo-2-oxidophen-yl)(phen-yl)methyl-ene]benzohydrazidato}pyridine-copper(II).

The asymmetric unit of title complex, [Cu(C(20)H(13)BrN(2)O(2))(C(5)H(5)N)], contains two independent mol-ecules. In each mol-ecule, the central Cu(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 Cu(II) atom.

[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. RESULTS: The level of MDA and MPO in serum increased and the activity of GSH-Px, SOD, CAT in serum decreased significantly in PQ group compared with control and PDTC group (P<0.05 or P<0.01) in the corresponding sacrifice dates. There were a significant decrease of MDA and increase of GPx, SOD, CAT in PQ + PDTC group compared with PQ group (P<0.05 or P<0.01) in the corresponding sacrifice dates. The activity of NF-kappaB in lung tissue of PQ group significantly increased on the 1st, the 3rd, the 7th and 14th day compared with control and PDTC group (P<0.01). There was a significant decrease in NF-kappaB activity on the 1st, the 3 rd, the 7th day in PQ + PDTC group compared with PQ group (P<0.05 or P<0.01). The MPO activity on the 14th day was (119.56 +/- 21.23) U/L, was lower than that of PQ group (P<0.05). Meanwhile, the content of Hyp in PQ group was significantly higher than control and PDTC group on the 14th, the 28th and the 56th day (P<0.01), and its content was lower in PQ + PDTC group on the 28th and the 56th day (0.89 +/- 0.05), (0.93 +/- 0.13) microg/mg compared with PQ group (P<0.01). The histological changes such as alveolitis and fibrosis in PQ + PDTC group were slighter than those in PQ group. CONCLUSION: Oxidative stress and NF-kappaB could play an important role in lung injury of poisoned rats. PDTC may improve redox imbalance and inhibit the expression of NF-kappaB and therefore might have therapeutic effect on acute paraquat poisoning.