Resistance to paraquat (1,1'-dimethyl-4,4'-bipyridilium ion) has developed in 12 species of 8 genera to which paraquat has been applied 6 to 10 times per year for 5 or more years. In recent years, tolerance to paraquat has been found in Rehmannia glutinosa (Gaertn.) Liboch. ex Fisch. & Mey. which has never been applied with any herbicides involving paraquat. In this review, we differentiate the terms, resistance and tolerance, on the basis of the paraquat-exposure history. Five hypotheses have been evaluated in several species as potential mechanisms of paraquat resistance and/or tolerance. In a species, the mode of action may be due to 1) reduced quantities of paraquat absorbed through the leaf surface, 2) detoxification of paraquat caused by the enhanced paraquat-metabolic activity, 3) rapid sequestration reducing level of paraquat at the site of action in chloroplast, 4) alteration of site of action in photosystem I resulting in interruption of electron transport to paraquat, and 5) rapid enzymatic detoxification of superoxide and other toxic forms of oxygen.
Journal of The Korean Society of Clinical Toxicology
/
v.7
no.1
/
pp.1-9
/
2009
Purpose: Paraquat, a globally used herbicide, is highly toxic to human beings. Hence, we reviewed some cases of paraquat poisoning in Korea. Methods: We analyzed the clinical and laboratory findings of 50 patients poisoned with paraquat retrospectively. The patients were admitted to the department of internal medicine in the Eumseong KeumWang hospital from January 2008 to December 2008. Results: Among 50 cases of paraquat poisoning, 28 cases were male. Twenty-four cases (48%) were over 60 years old. Fourty-nine patients ingested paraquat on purpose as suicidal attempts, while 1 patient underwent accidental ingestion. Seven patients swallowed less than one mouthful of paraquat, of which 4 patients survived. Eleven patients swallowed two mouthfuls of paraquat, of which 8 patients survived. Thirty-two patients swallowed over three mouthfuls of paraquat and they all died. Thirty-one patients with leukocytosis died. Twenty-one patients with metabolic acidosis died. Increased levels of blood amylase and glucose were related to high mortality, and increased level of blood creatinine was related to severe mortality. Hemoperfusions were accomplished in 27 patients of paraquat poisoning, of which 12 patients survived. Conclusion: Paraquat is a highly toxic herbicide. When patients arrive at the hospital, laboratory findings, urine paraquat concentrations, arrival time, and the amount of paraquat consumed must be considered for treatment plan.
Organic ligands in the environments are expected to play an important role in regulating the biotoxicity and fate of pesticides. Influences of dissolved humic and fulvic acids on the phytotoxicity of Paraquat were investigated using a bioassay with hydroponically grown rye as indicator species. Levels of Paraquat in water culture media were ranged from 0 to $12_{{\mu}M}$ and those of humic or fulvic acid were 1.0mM as a soluble carbon. Media were prepared in a factorial combination with pHs of 4.5, 6.5 and 8.5, Standard curves of necrosis days, fresh weight, and growth rates, as Phytotoxicity Indices, versus Paraquat concentrations were employed to evaluate the effects of organic ligands on phytotoxicity of paraquat. Organic ligand itself had little effect on rye growth, but Paraquat showed a high degree of toxicity. Paraquat started to show an intensive injury to rye at $0.4{\sim}0.6{{\mu}M}$ and upper critical phytotoxic concentration was estimated to be 11.0${{\mu}M}$ In the presence of organic ligands, times required to cause necrosis due to Paraquat were delayed upto 40%. Fresh weights and growth rates were upto 20% higher in treatments of organic ligands plus Paraquat than that of Paraquat alone. Results demonstrated that complexation of organic ligand with Paraquat reduced the bioabailability of Paraquat to rye.
To elucidate the fatal blood concentration of paraquat (Gramoxone), a contact herbicide, we investigated blood concentration of paraquat in 91 cases of paraquat intoxication. The blood paraquat concentration of 91 cases due to ingestion of paraquat was 0.9 $\mu$g/ml-1023.5$\mu$g/ml and has been subdivided according to survival time. 48 of 91 cases were identified survival time. In 34 of 48 cases died within a day after ingestion of paraquat, blood paraquat concentration was ranged from 2.3-636.61$\mu$g/ml, and in 12 of 48 cases died 1-4 days after ingestion of paraquat, blood paraquat concentration was ranged from 0.9- 25.1 $\mu$g/ml.
The fourth leaves (younger leaves) amongst extended 4-upper leaves in 18 squash cultivar were the highest tolerance to the paraquat application, followed by third, the second, and the first leaves (older leaves). The forth leaves in Joongangaehobak showed more than three times higher tolerance to the paraquat application than did the first leaves. When the combining of water extract from the fourth leaves with paraquat were applied to the leaves and stems of maize, the paraquat phytotoxicity in maize was reduced compared to the paraquat application alone. Therefore, this study continued to investigate if the phytotoxicity inhibitor exist in the fourth leaves. The water extract in the fourth leaves were isolated by silica gel column chromatography, Sephadex LH-20 column chromatography, TLC, and HPLC, and the substance in the extract was speculated as a malic acid by identifying through NMR. The mixture malic acid and paraquat were applied to the maize to verify the application effect of malic acid on paraquat toxicity. The 100 ${\mu}M$ of paraquat application alone showed 62% of paraquat toxicity to the corn leaves, while the combined application of 100 ${\mu}M$ paraquat with malic acid at 0.1, 0.3, 0.5, and 1.0% did not show the symptom.
This study was undertaken to investigate paraquat-induced pulmonary injuries and effects of colchicine on pulmonary fibrosis by paraquat. Fifteen Sprague-Dawley rats were intraperitoneally injected 10 mg/kg of paraquat and repeatedly with 2 days interval. Another 15 rats were injected paraquat as same manner and simultaneously injected 10 mg/kg of colchicine in a week. Five rats in each group were sacrificed 1, 2, and 4 weeks after initial injections, and lungs extracted were observed by light and electron microscopes. On light microscopy, there was mild infiltration of neutrophils, macrophages, and lymphocytes in alveolar spaces and walls at 1 week after paraquat injection. The cellularity of alveolar wall was increased with time. However, the cellularity was not so prominent in paraquat and colchicine simultaneously injected group. On electron microscopy, there was marked swelling or excoriation of type I epithelial cells and alveolar capillary endothelium with infiltration of neutrophils, macrophages and monocytes, and lymphocytes in alveolar walls. Such findings were persisted with time. In addition, fibroblastic proliferation and deposition of collagen fibers were prominent at 4 weeks after paraquat injection. Fibrosis also occurred at 4 weeks after paraquat and colchicine simultaneous injection. It was not proninent than that of paraquat injected group. According to the above result, it would be concluded that the type I pneumocytes and alveolar capillary endothelial cells are most vulnerable on paraquat poisoning, and that the colchicine is effective on inhibition of paraquat-induced pulmonary fibrosis.
Park, Sang-chul;Kang, Hyung-sub;Lee, Ho-il;Kim, Jin-sang
Korean Journal of Veterinary Research
/
v.36
no.2
/
pp.313-325
/
1996
Experiments were undertaken to examine the ability of selenium to protect against alcohol and/or paraquat-induced hepatotoxicity and to examine the additive effect between alcohol and paraquat. Protective effect against hepatotoxic functions was measured in serum from alcohol(15% v/v), paraquat(200ppm), alcohol and paraquat, and combination of sodium selenite(4ppm) in drinking water-fed guinea pigs ad libitum for 4 weeks. A total of 68 healthy 7-weeks-old male animals were assigned at random to 8 treatment groups(9~13 animals/group). Body and liver weight losses, and high serum concentrations in aspartate aminotransferase(AST), alanine aminotransferase(ALT, in only paraquat group), $\gamma$-glutamyltranspeptidase($\gamma$-GTP), cholesterol(Cho), creatinine, blood urea nitrogen(BUN), total bilirubin(TB), direct bilirubin(DB), total protein(TP), albumin and globulin as well as low values in alkaline phosphatase(ALP) and glucose were produced in a groups of alcohol or paraquat-fed. These values were not potentiated in a group given the combination of alcohol plus paraquat. Morphological changes in the liver were also observed in the alcohol or paraquat-fed group. Lipid droplet and cell swelling in the hepatocytes were observed in alcohol-fed guinea pig, especially Mallory's hyaline arounded hepatic vein. In the paraquat-fed guinea pig, lipid droplet, pyknosis and karyolysis were observed. When alcohol or paraquat was combined with selenium-fed, hyperplasia of Kupffer cell in liver were observed. However, the mean ALT, $\gamma$-GTP, Cho, BUN, TB, TP, albumin and globulin values were lower in groups given the combination of alcohol and/or paraquat plus selenium, compared with groups given alcohol and/or paraquat. Also, the ratio of liver weight to body weight and ALP values(exception of paraquat plus selenium group) were increased by selenium. These results suggest that an adequate selenium confers marked protection against alcohol and paraquat-induced hepatotoxicity.
Background: Paraquat, a widely used herbicide, is extremely toxic, causing multiple organ failure in humans. Paraquat especially leads to irreversible progressive pulmonary fibrosis, which is related to oxygen free radicals. However, its biochemical mechanism is not clear. Natural mechanisms that prevent damage from oxygen free radicals include changes in glutathione level, G6PDH, superoxide dismutase(SOD), catalase, and glutathione peroxidase. The authors think catalase is closely related to paraquat toxicity in the lungs Method: The effects of 3-amino-1,2,4-triazole(aminotriazole), a catalase inhibitor, on mice administered with paraquat were investigated. We studied the effects of aminotriazole on the survival of mice administered with paraquat, by comparing life spans between the group to which paraquat had been administered and the group to which a combination of paraquat and aminotriazole had been administered. We measured glutathion level, glucose 6-phosphate dehydrogenase(G6PDH), superoxide dismutase(SOD), catalase, and glutathione peroxidase(GPx) in the lung tissue of 4 groups of mice: the control group, group A(aminotriazole injected), group B(paraquat administered), group C(paraquat and aminotriazole administered). Results: The mortality of mice administered with paraquat which were treated with aminotriazole was significantly increased compared with those of mice not treated with aminotriazole. Glutathione level in group B was decreased by 20%, a significant decrease compared with the control group. However, this level was not changed by the administration of aminotriazole(group C). The activity of G6PDH in all groups was not significantly changed compared with the control group. The activities of SOD, catalase, and glutathione peroxidase(GPx) in the lung tissue were significantly decreased by paraquat administration(group B); catalase showed the largest decrease. Catalase and GPX were significantly decreased by aminotriazole treatment in mice administered with paraquat but change in SOD activity was not significant(group C). Conclusion: Decrease in catalase activity by paraquat suggests that paraquat toxicity in the lungs is closely related to catalase activity. Paraquat toxicity in mice is enhanced by aminotriazole administration, and its result is related to the decrease of catalase activity rather than glutathione level in the lungs. Production of hydroxyl radicals, the most reactive oxygen metabolite, is accelerated due to increased hydrogen peroxide by catalase inhibition and the lung damage probably results from nonspecific tissue injury of hydroxyl radicals.
Background : Acute pulmonary injury by paraquat are caused by multiple mechanisms including direct injury with oxygen free radicals and several mediators released from inflammatory cells. In order to clarify whether vitamin E could reduce tissue damages induced by intraperitoneal administration of paraquat and to investigate the pathogenetic mechanisms of paraquat-induced pulmonary injury, vitamin E as a free radical scavenger was administered. Method : Rats were divided into three groups (group 1 : control, group 2 : paraquat treated group, group 3 : paraquat and vitamin E treated group). Animals were sacrificed on day 1, day 2, day 3, and day 8 after the administration of saline, paraquat, or paraquat/vitamin E. Results : Treatment with vitamin E decreased the death rate of rats treated with paraquat. Comparing with control group ($1.37{\times}10^6/ml$), mean total cell counts recovered from the lavage fluid from animals treated with paraquat($1.65{\times}10^6/ml$) were increased(p=0.06). Magnitudes of increment of the total cell counts on the Day 8 in the vitamin E treated group were smaller than those of the animals treated with paraquat alone. The neutrophils began to appear in significant amounts in the lavage fluid on Day 8 after the administration of paraquat(37.0+12.7%). A significant decreasing neutrophil concentration at Day 8 was observed in the paraquat/vitamin E treated group(20.6+13.4%). Histologically the degree of pulmonary fibrosis was most prominent in the paraquat treated group while diffuse alveolar damage was continuously observed in the paraquat/vitamin E treated group and extensive interstitial lymphocytic infiltration was seen in the paraquat/vitamin E treated group. The paraquat/vitamin E treated group showed the less histologic changes. Conclusion : In this study vitamin E acting as a scavenger of neutrophil-derived free radicals and suppressant of lipid peroxidation, seemed to be the effective antioxidant in the inhibition of paraquat-induced pulmonary injury.
Gil Hyo Wook;Yang Jong Oh;Lee Eun Young;Hong Sae Yong
Journal of The Korean Society of Clinical Toxicology
/
v.2
no.1
/
pp.45-48
/
2004
Paraquat, a widely used herbicide, is extremely toxic, causing multiple organ failure in human. Many treatment modality has been used, but now paraquat is very fatal drug. Elimination rate of plasma paraquat seems to be a factor for the survival rate. So early diagnosis and early treatment are very important. Plasma paraquat concentration could be measured by radioimmunoassay. But it is impossible that the test was done at Emergency room and the result was checked immediately. There was relation between plasma paraquat concentrations and urine paraquat concentration. Because of its simplicity and low cost, urine paraquat concentration test is complementary to the plasma concentration measurement. If the patient has psychotic problem or unconscious mental state, and is observed unexplained dyspnea and oral ulcer, urine paraquat test is very important to rule out acute paraquat intoxication. We experienced a patient who was presented as unexplained acute renal failure initially and was diagnosed as paraquat intoxication later.
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