• Radiation Oncology Journal
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• v.13 no.4
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• pp.321-330
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• 1995

Purpose : To evaluate whether the early pulmonary irradiation can prevent or decrease the pulmonary damage and contribute to improve ultimate survival in paraquat lung. Materials and Methods : From Jun. 1987 to Aug. 1993, thirty patients with paraquat poisoning were evaluated. Fourteen of these patients were received pulmonary irradiation(RT). All of the patients were managed with aggressive supportive treatment such as gastric lavage, forced diuresis, antioxidant agents and antifibrosis agents. Ingested amounts of paraquat were estimated into three groups(A : minimal 50cc). Pulmonary irradiation was started within 24 hours after admission(from day 1 to day 11 after ingestion of paraquat). Both whole lungs were irradiated with AP/PA parallel opposing fields using Co-60 teletherapy machine. A total of 10Gy(2Gy/fr. x 5days) was delivered without correction of lung density. Results : In group A, all patients were alive regardless of pulmonary irradiation and in group C, all of the patients were died due to multi-organ failure, especially pulmonary fibrosis regardless of pulmonary irradiation. However, in group B, six of 7 patients($86{\%}$) with no RT were died due to respiratory failure, but 4 of 8 patients with RT were alive and 4 of 5 patients who were received pulmonary irradiation within 4 days after ingestion of paraquat were all alive though radiological pulmonary change. One patient who refused RT after 2Gy died due to pulmonary fibrosis. All 3 patients who were received pulmonary irradiation after 4 days after ingestion were died due to pulmonary fibrosis in spite of recovery from renal and hepatic toxicity Conclusion : It is difficult to find out the effect of pulmonary irradiation on the course of the paraquat lung because the precise plasma and urine paraquat concentration were not available between control and irradiation groups. But early pulmonary irradiation within 4 days after paraquat poisoning with aggresive supportive treatment appears to decrease Pulmonary toxicity and contribute survival in patients with mouthful ingestion of paraquat who are destined to have reversible renal and hepatic damage but irreversible pulmonary toxicity.

• Korean Journal of Veterinary Research
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• v.34 no.2
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• pp.339-347
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• 1994

This study was carried out to investigate the pathological changes with paraquat(1.1'-dimethyl-4.4'-dipyrildiylium dichloride) administered by intraperitoneally, orally, skin applied in mice, rats and rabbits. Results were obtained as follows; In 2 days after paraquat administration clinical signs anorexia, depression, tachypnea, and tachycardia, respiratory failure, coma and death were observed in mice, rats and rabbits. Compared toxicity of paraquat with mouse were observed toward to paraquat that resistance was strong than rats and rabbits. Also, mortality of skin application were found the low than intraperitoneal and high than oral administration. In the case of gross observation were appear lips moisture in orally administered rats and rabbits by skin application. Lung of all laboratory animals were observed congestion and haemorrhage, swelling or atrophy. In the case of microscopic findings were severe congestion and haemorrhage, interstitial pneumonia of lung. Congestion and haemorrhage of liver, congestion and haemorrhage, renal tubule epithelium necrosis of kidney were observed in mice, rats and rabbits. Skin application group of mice, rats and rabbits showed infiltration of inflammatory cells and folliculitis of epidermis and dermis. Also, in oral administration group showed congestion and haemorrhage, tachment, necrosis of alimentary tract mucosa.

• Journal of environmental and Sanitary engineering
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• v.14 no.2
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• pp.8-17
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• 1999

This research employed a senescence-accelerated mouse(SAM) to explore the possibility that differences exist among the major antioxidatns, lipid peroxidation in terms of ability to protect such animal treatment PQ, SAM-R/1 and SAM-P/8 were administered with PQ(200ppm/Kg) orally. The toxicity of PQ on SAM was determined as a bioassays of SOD, catalase and lipid peroxidation in the mouse liver. The data show that the SOD activity was induced by paraqwuat terement in both SAM-R/1 and SAM-P/8. The degree of lipid peroxidation was increased with PQ treatment. This means that SOD rather than catalase may protect against oxygen radical toxicity. Finally, over data lead to the toxicity of PQ and its function may efect to the antioxidants including SOD, catalase and lipid peroxidation in both SAM-R/1 and SAM-P/8 .

• Journal of Microbiology and Biotechnology
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• v.24 no.5
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• pp.605-613
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• 2014

We have previously shown that paraquat (PQ)-induced oxidative stress causes dramatic damage in various human cell lines. Naringenin (NG) is an active flavanone, which has been reported to have beneficial bioactivities, including antioxidative, anti-inflammatory, and antitumorigenic activities, with a relatively low toxicity to normal cells. In this study, we intended to assess the cytoprotective effect of NG against PQ-induced toxicity in the human bronchial epithelial BEAS-2B cell line. Co-treatment with NG in PQ-treated BEAS-2B cells can reduce PQ-induced cellular toxicity. NG can also decrease the generation of intracellular ROS caused by PQ treatment. We also observed that treatment with NG in PQ-exposed BEAS-2B cells can significantly induce the expression of antioxidant-related genes, including GPX2, GPX3, GPX5, and GPX7. NG co-treatment can also activate the NRF2 transcription factor and promote its nuclear translocation. In addition, NG co-treatment can induce the expression of NRF2-downstream target genes such as that of heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1). A small interfering RNA study revealed that the knockdown of NRF2 can abrogate NG-mediated protection of the cells from PQ-induced cellular toxicity. We propose that NG effectively alleviates PQ-induced cytotoxicity in human bronchial epithelial BEAS-2B cells through the NRF2-regulated antioxidant defense pathway, and NG might be a good therapeutic candidate molecule in oxidative stress-related diseases.

• Korean Journal of Environmental Agriculture
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• v.20 no.3
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• pp.155-161
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• 2001

This study was carried out to investigate cytotoxicity of paraquat or bentazone on NIH 3T3 fibroblasts, toxicity of paraquat or bentazone, and compensatory effects of 3-Methylcholanthrene(3-MC) on the rat liver. In order to MTT assay, the $5.0{\times}10^4$ cell/mL of NIH 3T3 fibroblast in each well of 24 multidish were cultured. After 24 hours, the cells were treated with solution of paraquat or bentazone(1, 25, 50, 100 ${\mu}M$ respectively). After the NIH 3T3 fibroblast of all groups were cultured in same condition for 48 hours. MTT assay were performed to evaluate the cytotoxicity of cell organelles. Paraquat or bentazone $MTT_{50}$ were 1668.97 ${\mu}M$ and 1506.97 ${\mu}M$, respectively. These $IC_{50}$ of paraquat or bentazone were decided low cytotoxicity by Borenfreund. In order to observe the toxicity and compensatory effects of paraquat or bentazone on the rat liver, Sprague-Dawley male rats were used as experimental animals and divided into paraquat or bentazone only treated group and simultaneous application group of paraquat or bentazone and 3-MC. At 30 min and 1, 3, 6, 12, 24, 48 and 96 hrs interval after each treatment, the animals were sacrificed by decapitation and liver were immediately removed, immersed in fixatives, and processed with routine method for light microscopic study. Paraffin sections were stained with H-E, PAM and Best Carmine. Under the light microscope, degenerative changes of hepatic lobules were frequently observed in portal area from 3 hrs after paraquat or bentazone treatment. All hepatic cells were induced degenerative change at 12 hrs and more severe degenerative change at 48 hrs after paraquat or bentazone treatment. Especially, hepatic cells of bentazone only treated group were distinctly showed pyknotic. Glycogen granules were increased in portal area at 3 hrs, all hepatic cells at 12 hrs and remarkably increased at 48 hrs after paraquat or bentazone treated group. But hepatic cells of bentazone only treated group were regeneration at 48 hrs from portal area and glycogen granules of hepatic cells of paraquat or bentazone and 3-MC combination treated group showed in central area only at 48 hrs. The results indicate that 3-MC may be decrease paraquat or bentazone cytotoxicity on the rat liver.

• The Korean Journal of Emergency Medical Services
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• v.10 no.1
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• pp.51-60
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• 2006

Background: The toxicity of paraquat has been known to be caused by oxygen free radicals which leads to the lipid peroxidation and multiple organ failure. High dose vitamin C has been known to be a effective antioxidant activities against the paraquat intoxication. This study was designed to evaluate the effect of regular injection of high dose vitamin C on liver damage in paraquat poisoned rat model. Method: Fifty five rats of Sprague-Dawley strain were divided into three groups: control group, only intraperitoneally injected saline; paraquat group, single dose intraperitoneally injected paraquat(24.5%, 40 mg/kg) and every 8 hours injected saline; paraquat and vitamin C group, single dose intraperitoneally injected paraquat(24.5%, 40 mg/kg) and every 8 hours injected vitamin C(72 mg/kg). Rats were sacrificed on the 12 hours, 1st day, 2nd day, 4th day, 7th day after injection and liver tissue was obtained. H&E(Hematoxylin & Eosin) stain and Masson's trichrome stain for collagen fiber detection were undertaken. The results were observed using the microscope. Results: 1. There were no differences between control and experimental group at the 12hours after regular injection of high dose vitamin C. 2. There were significantly decreased liver damage in experimental group in the 1st day after regular injection of high dose vitamin C. 3. There were significantly increased recovery of liver damage with time in experimental group after regular injection of high dose vitamin C. Conclusion: These results suggest that regular injection of high dose vitamin C is effective in decreasing liver damage in paraquat intoxication.

• Journal of Life Science
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• v.18 no.1
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• pp.129-135
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• 2008

Paraquat (1,1-dimethyl 4,4' -dipyridium dichloride; PQ) is a kind of herbicide. Terminalia chebulae (TC) has been used as a medicine in China and in Korea for treating illnesses such as diarrhea, collapsed anus, spasmodic, diphtheria, asthma etc.. This study was to examin new physiological activities of methanol extract of TC (TCM) on the toxicity of PQ. It was observed biochemical effects on the toxicity of PQ in kidney and lung tissues after treatment orally administered 100, 200, 300 mg/kg of TCM daily for two weeks. In the experiment related to the toxicity of PQ, we got following results: renal and pulmonary lipid peroxide contents, activities of aminopyrine N-demethylase, aldehyde oxidase and xanthine oxidase were significantly increased in control group as compared with normal group, in the treatment of TCM the values were decreased as compared with control group. Activities of superoxide dismutase, catalase and glutathione peroxidase which are free radical scavenging enzymes were also increased in control group as compared with normal goup, but were decreased in TCM group as compared with control group. Collagen content and glucose-6-phosphatase activity in lung tissue were increased in control group as compared with normal, but was decreased in TCM group as compared with control group. From these results, we concluded that TCM can playa role as an effective agent to decrease toxicity of PQ.

• The Korean Journal of Pesticide Science
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• v.9 no.1
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• pp.88-96
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• 2005

Paraquat-resistant biotype of Conyza canadensis (L.) Cronq. was determined by chlorophyll loss and random amplified polymorphic DNA (RAPD) analysis and the resistant mechanism was investigated with respect to absorption, translocation, and binding constant. RAPD analysis for paraquat resistant (R) and susceptible (S) biotypes found in a pear orchard revealed that the biotypes possessed remote genetic relationship. Chlorophyll loss, as an indication of paraquat toxicity, of S biotype was 7.8-fold greater than that of R biotype. There were no differences in contents of epicuticular wax and cuticle and amounts of [14C]paraquat penetrating the cuticle between the two biotypes. Little translocation of the herbicide out of the treated leaf was observed in either biotype. Binding constants of paraquat to the cell wall and thylakoid membrane were 7.4-fold and 16.9-fold, respectively, higher in R biotype than in S biotype. The results suggest that the resistance mechanism of C. canadensis biotype is due partly to high binding affinity of paraquat to the cell wall and thylakoid membrane.

• Proceedings of the Zoological Society Korea Conference
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• 2000.10a
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• pp.217.2-217
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• 2000

No Abstract, See Full Text

• Proceedings of the Korean Society of Life Science Conference
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• 2007.10a
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• pp.75.2-75.2
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• 2007

See Full Text