• Toxicological Research
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• v.13 no.4
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• pp.393-400
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• 1997

The effects of superoxide dismutase(SOD) and catalase on the toxicity of paraquat(PQ) were studied using diethyldithiocarbamate(DDC), 3-amino-1,2,4-triazole(AT) which are inhibitors of Cu, Zn-SOD and catalase in rats. Sprague Dawley rats were divide into 6 groups: control, DDC, PQ, AT, DDC+PQ, and AT+PQ group. The PQ (50 mg/kg body weight(BW); about half dose of $LD_{50}$) was administered with orally, otherwise AT(1.0g/kg BW) and DDC(1.0g/kg BW) were administered by intrperitoneal(iP) injection. The survival rate of rats in PQ+AT group was significantly decreased compared with PQ group while the difference of survival rate between DDC group and DDC+PQ group was not significant. The SOD activity after administration of DDC was decreased in liver, lung and kidney, but catalase activity was not changed. The catalase activity in liver, lung and kidney of AT treated rats was decreased, while SOD activity was not changed in this group. The effects of DDC and AT to the PQ toxicity was also observed in primary cultured rat Skin fibroblasts. The viable cells that was measured with MTT method, was decreased in AT+PQ treated group compared to PQ treated group, but the difference of cell viability between DDC treat group and DDC+PQ treated group was not observed. This result, AT potentlate PQ toxicity while DDC were not affect, suggested that the decreased catalase activity lead to elevation of hydrogen peroxide levels and PQ toxicity may be correlate with the hydrogen peroxide rather than the superoxides.

• Journal of Plant Biotechnology
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• v.41 no.2
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• pp.73-80
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• 2014

Pretreatment of chinese cabbage leaves with $100{\mu}M$ sodium nitroprusside (SNP), a nitric oxide (NO) donor, effectively improved their tolerance to subsequent $2{\mu}M$ paraquat (PQ)-induced oxidative damage. The fresh weight, and chlorophyll and protein contents in primary leaves treated with PQ alone were noticeably reduced over 24 h light incubation. However, these leaf injury symptoms were significantly alleviated with $100{\mu}M$ SNP pretreatment for 3 h prior to PQ exposure. In additions, the increase of the contents of malondialdehyde (MDA) and $H_2O_2$ due to PQ exposure were significantly inhibited by SNP pretreatment. Together with the protective effects of SNP against PQ toxicity in leaves, the changes of ascorbate-glutathione cycle enzymes activities were examined. In the PQ alone treatment, the activities of APX, DHAR, and GR after 6 h incubation were rapidly reduced and showed 19%, 50% and 39% respectively, compared with those of the control. However, the decreases in these enzyme activities were significantly inhibited by SNP pretreatment. As a result, their activities were higher than those of PQ alone treatment by 5 times, 2 times, and 1.5 times, respectively, at 6 h incubation. Thereafter, these enzymes decrease their activities gradually showing high levels than those of PQ alone. Based on the above results, it can be assumed that the activation of ascorbate-glutathione cycle by SNP pretreatment in chinese cabbage leaves exposed to PQ can prevent $H_2O_2$ accumulation, thereby leading to protection against PQ-induced oxidative stress. Also, these results indicate that NO acts as an protectant against PQ stress in the leaves of chinese cabbage.

• Biomedical Science Letters
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• v.8 no.2
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• pp.71-75
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• 2002

Paraquat (N,N'-dimethyl-4,4'-bipyrrimidinium-dichlorides (PQ): MW 186.6) has been used to killing verierty of hubside plants. For this study were use Sprague-dawely rats (190$\pm$10 gm) and injection 40 mg/kg BW of paraquat (LD$_{50}$) to 24 hrs PQ and 4 days PQ group excepte normal control. For the measurement of blood calcium Ino-phosphorus and activity of alkaline phosphatase (ALP) by HITTACH 746. In serum phosphoruse of normal control were 8.0$\pm$1.2 mg/dl and 24 hrs PQ group were 8.9$\pm$1.0 mg/dl (P<0.05) and 4 days PQ group were 8.8$\pm$0.42 gmm/dl (P<0.05). In serum phosphorus were very sensitive uptaked to 10% within only 24 hours, but 4 days of PQ were similar uptake level than 24 hrs PQ. So this 8.9 mg/dl of sem phosphorus may be thought threshold level becouse does not more encrease. In blood calcium normal of rats were measured 9.51$\pm$0.3 mg/dl and 24 hrs of PQ group were 9.9$\pm$0.51 mg/dl (uptaked 4.5%, p>0.05). This uptake cannot fined meaning mathmatic statistics but 4 days PQ groups of calcium were 10.43$\pm$0.37 gm/dl (uptaked 10%, p<0.05). That 24 hrs PQ groups of caclium dose not reacted sensitive to irritated by PQ. So, when use oxidants of PQ, the blood calcium and Ino-phosphorus were linear correlated uptake that reasone thought may be move out form hardness bone tissue to in blood it does not take feeding to hunger for 4 days. In ALP normal of rats were measured 991$\pm$106 unit/L. In 24 hrs irritated PQ rats were fall down by 629$\pm$91 unit/L (P<0.001) but in 4 days of PQ rats were 792$\pm$85 unit/L (P<0.0011) that the activity of level were mild recovered activity from 629 unit (63%) to 792 unit (80%). So, that the reasone of ALP were very sensitive activity and reverse correlated to blood calcium or phosphorus irritated by PQ.

• Korean Journal of Veterinary Research
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• v.36 no.1
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• pp.209-219
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• 1996

This study examined the effect of alcohol(AL) and/or paraquat(PQ) on serum TSH, thyroid hormones and enzyme activities, and the protective effect of selenium(SE) againse alcohol and/or paraquat-induced thyroid toxicity in guinea pigs. The experomental group consisted of control, 15% alcohol(AL), 4ppm sodium selentite(SE), 200ppm paraquat(PQ), AL+PQ, AL+SE, PQ+SE and AL+PQ+SE mixed in drinking water-fed guinea pigs for 4 weeks. The morphological changes of thyroid gland were studies on paraffin-embedded sections stained with H-E stain. Body weight losses, high serum concentration in TSH and cholesterol, and low values on triiodothyronine($T_3$), thyrozine($T_4$), free $T_4$ and alkaline phosophatase(ALP) were produced in the groups fed AL and/or PQ. We also noted that AL+PQ-fed group was marked increase in serum TSH. In AL or AL+PQ-fed groups when cpmpared to control group had increased the ratio of thyroid weight to body weight(ratio Twt/Bwt), whereas the ratio Twt/Bwt was decresed in SE or PQ-fed groups. However, the serum TSH, $T_3$,$T_4$ free $T_4$ and cholesterol values, and the ratio Twt/Bwt were reversed in groups given the combination of SE, compared with AL and/or Pq-fed groups, also ALP values were reversed in groups given the combination of SE, compared with AL or AL+PQ-fed groups. In microscope, morphological changes showed a remarkable between the AL or PQ-fed group and controls. In AL+PQ+SE-fed guinca pig, follicular colloid is high density in thyroid follicle and increased in connective tissue around the thyroid cells, and thyroidal epithelia were composed of cuboidal or columnar epithelium. The indicated that the morphological changes of thyroid were direct action in the thyroid cell. The results of this study confirmed that the toxic effect of AL or PQ on thyroid occur independently of changes in liver function, and that SE confers marked protection against AL or PQ-induced thyroid toxicity.

• Journal of Environmental Science International
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• v.20 no.12
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• pp.1509-1519
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• 2011

The protective effect of nitric oxide (NO) on the antioxidant system under paraquat(PQ) stress was investigated in leaves of 8-week-old lettuce (Lactuca sativa L.) plants. PQ stress caused a decrease of leaf growth including leaf length, width and weight. Application of NO donor, sodium nitroprusside (SNP), significantly alleviated PQ stress induced growth suppression. SNP permitted the survival of more green leaf tissue preventing chlorophyll content reduction and of higher quantum yield for photosystem II than in non-treated controls under PQ exposure, suggesting that NO has protective effect on chloroplast membrane in lettuce leaves. Flavonoids and anthocyanin were significantly accumulated in the leaves upon PQ exposure. However, the rapid increase of these compounds was alleviated in the SNP treated leaves. PQ treatment resulted in lipid peroxidation and induced accumulation of hydrogen peroxide ($H_2O_2$) in the leaves, while SNP prevented PQ induced increase in malondialdehyde (MDA) and $H_2O_2$. These results demonstrate that SNP serves as an antioxidant agent able to scavenge $H_2O_2$ to protect plant cells from oxidative damage. The activities of two antioxidant enzymes that scavenge reactive oxygen species, superoxide dismutase (SOD) and catalase (CAT) in lettuce leaves in the presence of NO donor under PQ stress were higher than those under PQ stress alone. Application of 2-(4-carboxyphenyl)-4, 4, 5, 5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO), a specific NO scavenger, to the lettuce leaves arrested SNP mediated protective effect on leaf growth, photosynthetic pigment and antioxidant systems. However, PTIO had little effect on lettuce leaves under PQ stress compared with that of PQ stress alone. The obtained data suggest that the damage caused by PQ stress is in part due to increased generation of active oxygen by maintaining increased antioxidant enzyme activities and SNP protects plants from oxidative stress. From these results it is suggested that NO might act as a signal in activating active oxygen scavenging system that protects plants from oxidative damage induced by PQ stress and thus confer PQ tolerance.

• Biomolecules & Therapeutics
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• v.23 no.5
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• pp.407-413
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• 2015

Paraquat dichloride (N,N-dimethyl-4-4'-bipiridinium, PQ) is an extremely toxic chemical that is widely used in herbicides. PQ generates reactive oxygen species (ROS) and causes multiple organ failure. In particular, PQ has been reported to be an immunotoxic agrochemical compound. PQ was shown to decrease the number of macrophages in rats and suppress monocyte phagocytic activity in mice. However, the effect of PQ on macrophage cell viability remains unclear. In this study, we evaluated the cytotoxic effect of PQ on the mouse macrophage cell line, RAW264.7 and its possible mechanism of action. RAW264.7 cells were treated with PQ (0, 75, and $150{\mu}M$), and cellular apoptosis, mitochondrial membrane potential (MMP), and intracellular ROS levels were determined. Morphological changes to the cell nucleus and cellular apoptosis were also evaluated by DAPI and Annexin V staining, respectively. In this study, PQ induced apoptotic cell death by dose-dependently decreasing MMP. Additionally, PQ increased the cleaved form of caspase-3, an apoptotic marker. In conclusion, PQ induces apoptosis in RAW264.7 cells through a ROS-mediated mitochondrial pathway. Thus, our study improves our knowledge of PQ-induced toxicity, and may give us a greater understanding of how PQ affects the immune system.

• YAKHAK HOEJI
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• v.43 no.6
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• pp.809-817
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• 1999

The effect of 2-(4-cyanophenyl)amino-1,4-naphthalenedione-3-pyridinium perchlorate (PQ5) on pla-telet aggregation and its action mechanisms were investigated with rat platelet. PQ5 inhibited the platelet aggregation induced by collagen ($6{\;}{\mu\textrm{g}}/ml$), thrombin (0.4 U/ml) and A23187 ($3{\mu}M$) in concentration-dependent manner with $IC_{50}$ values of 5.50, 25.89 and $37.12{\;}{\mu}M$, respectively. PQ5 also significantly reduced the thromboxane $A_2$ (TXA2) formation in a concentration dependent manner. The collagen-induced arachidonic acid (AA) release in [-3H]-AA incorporated platelet, an indication of the phospholipase $A_2$ activity, was decreased by PQ5 pretreatment PQ5 significantly inhibited the activity of thormboxane synthase only at high concentration ($100{\mu}M$), but did not affect the cyclooxygenase activity at all. Collagen-induced ATP release was significantly reduced by PQ5. Calcium-induced platelet aggregation experiment suggests that the elevation of intracellular free $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) by collagen stimulation is decreased by the pretreatment of PQ5, which is due to the inhibition of calcium release from intracellular store and influx from outside of the cell. PQ5 did not showed the effect of anticoagulation as prothrombin time (PT) or activated partial thromboplastin time (APTT). Form these results, it is suggested that PQ5 exerts its antiplatelet activity through the inhibition of the intracellular $Ca^{2+}$ mobilization and the decrease of the $TXA_2$ synthesis.

• Journal of agricultural medicine and community health
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• v.36 no.4
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• pp.218-226
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• 2011

Objectives: Paraquat (PQ) is a widely used ionic pesticide that is fatal when ingested accidentally or for suicidal purposes. It is thought that chronic exposure of PQ is related with the development of Parkinson's disease, but epidemiological studies have not yet confirmed that theory. This study attempted to estimate the possibility of environmental PQ exposure through soil and water. Materials and Methods: We analyzed the amount of decomposed PQ solution in wet soil after exposure to ultraviolet light. An artificial rainfall condition was simulated over soil sprayed with PQ to measure the amount of eluted PQ. In addition, PQ was diluted in water from three differently rated rivers and the changes in PQ concentration were measured after ultraviolet exposure over one month. High performance liquid chromatography/ultra violet detection was used to analyze the concentrations of PQ. Results: In the method we used, the recovery rate of PQ showed a precision rate less than 5%, an accuracy greater than 88%, and the calibration equation was y=5538.8x-440.01($R^2$=0.9985). There were no significant differences in the concentrations of PQ obtained from the three specimens over a 1-week period. From the PQ-sprayed soil, the artificial rainfall conditions showed no PQ elution over a 1-month period, and there was no significant differences in PQ concentrations according to ultraviolet exposure among the three samples. Conclusions: PQ remains well adsorbed naturally in soil. However, it may still exist in an integrated state for a long time in the hydrosphere, so the possibility of PQ exposure through drinking water cannot be disqualified.

• Journal of the Korean Chemical Society
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• v.38 no.1
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• pp.74-79
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• 1994

The participation of superoxide in initiating tissue damage derived from xenobiotics is best illustrated by paraquat intoxication. In the present study, the roles of superoxide dismutase and catalase on paraquat-induced cell injury were investigated using primary cultured rat skin fibroblast. The degree of cell injury was assassed by the conversion of reduced MTT to a blue formazan. Paraquat produced concentration-and time-related cell injury in cultured rat skin fibroblast. Paraquat induced-cell injury was aggravated by pretreatment of aminotriazol (AT: 10 mM), an catalase inhibitor, and attenuated by addition of catalase (100∼500 unit/ml). However, the effects of diethyldithiocarbamate (DDC : 10 mM), copper- and zinc-containing superoxide dismutase (Cu, Zn-SOD) inhibitor, and Cu, Zn-SOD on paraquat-induced injury were not significant. These results suggest that hydrogen peroxide might be more responsible factor than superoxide in the pathogenesis of paraquat-induced cell injury.

• Journal of Ginseng Research
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• v.44 no.5
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• pp.680-689
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• 2020

Background: Peptides have diverse and important physiological roles in plants and are ideal markers for species identification. It is unclear whether there are specific peptides in Panax quinquefolius L. (PQ). The aims of this study were to identify Quinetides, a series of diverse posttranslational modified native peptides of the ribonuclease-like storage protein (ginseng major protein), from PQ to explore novel peptide markers and develop a new method to distinguish PQ from Panax ginseng. Methods: We used different fragmentation modes in the LTQ Orbitrap analysis to identify the enriched Quinetide targets of PQ, and we discovered Quinetide markers of PQ and P. ginseng using ultrahigh-performance liquid chromatography-quadrupole time-of-flight mass spectrometry analysis. These "peptide markers" were validated by simultaneously monitoring Rf and F11 as standard ginsenosides. Results: We discovered 100 Quinetides of PQ with various post-translational modifications (PTMs), including a series of glycopeptides, all of which originated from the protein ginseng major protein. We effectively distinguished PQ from P. ginseng using new "peptide markers." Four unique peptides (Quinetides TP6 and TP7 as markers of PQ and Quinetides TP8 and TP9 as markers of P. ginseng) and their associated glycosylation products were discovered in PQ and P. ginseng. Conclusion: We provide specific information on PQ peptides and propose the clinical application of peptide markers to distinguish PQ from P. ginseng.