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Toxicology
Published in Anthony FT Brown, Michael D Cadogan, Emergency Medicine, 2020
Anthony FT Brown, Michael D Cadogan
Paraquat is a highly toxic herbicide. Significant oral ingestion is associated with fulminant multi-organ failure. If patients survive this, they develop progressive pulmonary fibrosis, and may die 4–6 weeks later from hypoxaemia.
Purification and Primary Culture of Type II Pneumocytes and Their Application in the Study of Pulmonary Metabolism
Published in Joan Gil, Models of Lung Disease, 2020
Skillrud and Martin (1984) studied the direct effect of paraquat on isolated type II cells. Paraquat, a widely used herbicide, causes severe, often fatal, lung damage. In vivo studies suggest that the alveolar epithelial cells (types I and II) are specific targets of paraquat toxicity. This study used 51Cr-labeled type II cells to demonstrate that paraquat (10−5M) resulted in type II cell injury in vitro, independent of interacting immune effector agents. With 51Cr release expressed as the cytotoxic index (CI), type II cell injury was found to accelerate with increasing paraquat concentrations (10−5M, 10−4M, and 103M, resulting in a CI of 12.5 ± 2.2, 22.8 ± 1.8, and 35.1 ± 1.9, respectively). Paraquat-induced cytotoxicity (10−4M, with a CI of 22.8 ± 1.8) was effectively reduced by catalase, 1,000 U/ml (CI 8.0 ± 3.2, ρ <0.001), superoxide dismutase, 300 U/ml (CI 17.4 ± 1.7, ρ <0.05), and alpha-tocopherol 10 /¿g/ml (CI 17.8 + 1.6, ρ <0.05). Paraquat toxicity (10 3M) was potentiated in the presence of 95 % 02 with an increase in CI from 31.1 ± 1.7 to 36.4 ± 2.3 (p <0.05). Paraquat-induced type II cell injury was noted as early as 4 hr after incubation by electron microscopy, which showed swelling of mitochondrial cristae and dispersion of nuclear chromatin. Thus, this in vitro model indicates that paraquat-induced type II cell injury can be quantitated, confirmed by morphological ultrastructural changes, significantly reduced by antioxidants, and potentiated by hyperoxia.
Possible Participation of Acetylcholine in Free-Radical Processes (Redox Reactions) in Living Cells
Published in Akula Ramakrishna, Victoria V. Roshchina, Neurotransmitters in Plants, 2018
Nevertheless, remarkable data were found for molecular mechanisms of paraquat action. Paraquat is commonly employed in agriculture as an herbicide (Lock and Wilks, 2010). Paraquat as a quaternary nitrogen compound is very soluble in water and a little in most organic solvents. It is stable in neutral and acidic media but easily hydrolyzed in alkaline media. In vivo paraquat is undergoing a one-electron reduction (Bus and Gibson, 1984; Clejan and Cederbaum, 1989; Day et al., 1999). An important consequence of this reaction is the formation of monocation free radicals (Figure 12.1).
Pesticide use, agricultural outputs, and pesticide poisoning deaths in Japan
Published in Clinical Toxicology, 2022
Michael Eddleston, Hiroshi Nagami, Chien-Yu Lin, Mark L. Davis, Shu-Sen Chang
A wide variety of therapies and treatments have been studied in the last several decades for paraquat poisoning, but none have been effective in decreasing case fatality [41,42]. ICU techniques have improved over the last 50 years. However, this is unlikely to explain the reduction in deaths for either paraquat or OP insecticides. For paraquat, few patients are admitted to intensive care, due to futility. For OP insecticides, many of the most toxic pesticides kill patients soon after ingestion, before admission to hospital. The outcome for paraquat poisoning continues to be dependent on the paraquat ion dose absorbed and blood concentration [43,44]. In the absence of any effective antidote, paraquat’s LD50 of about 50 mg/kg in humans [34,45] indicates that it should be categorized as a WHO Hazard Class Ib highly hazardous pesticide [25,46].
The early impact of paraquat ban on suicide in Taiwan
Published in Clinical Toxicology, 2022
Shu-Sen Chang, Chien-Yu Lin, Ming-Been Lee, Lih-Jong Shen, David Gunnell, Michael Eddleston
Paraquat, a commonly used herbicide, is amongst the pesticides most frequently involved in suicides. Paraquat is highly lethal when ingested [3], with an estimated case fatality of 55% in Taiwan [4]. Restricting access to paraquat may effectively prevent suicide from paraquat poisoning and reduce pesticide suicide rates [5], as few pesticides are as toxic as paraquat [3] and therefore even a shift to other pesticides in acts of self-poisoning is unlikely to result in higher case fatality. In Taiwan, a nationwide (first-stage) ban on the import and production of paraquat was implemented from February 2018, followed by a complete (second-stage) ban on its sale and use from February 2020. However, some have argued for a reversal of the policy and lifting the ban, citing the possibility of a shift to use other pesticides or methods for suicide that could lead to no effect of the ban on suicide [6]. Therefore, there is an urgent need to evaluate the ban’s early effect on reducing deaths. We assessed the impact of the first-stage paraquat ban (i.e., ban on import and production) on suicide in Taiwan. We hypothesised that the impact on pesticide suicides would be most marked in rural areas, males, and the elderly (aged 65+ years), which were previously shown to have the largest burden of pesticide suicides in Taiwan [7,8].
Clinical outcome of paraquat poisoning during pregnancy
Published in Clinical Toxicology, 2019
Satariya Trakulsrichai, Bootsakorn Paisanrodjanarat, Charuwan Sriapha, Achara Tongpoo, Umaporn Udomsubpayakul, Winai Wananukul
Paraquat uptake was observed in lung slices of mature rats; it occurred primarily in pneumocyte type II cells, and active transport into fetal rat lung slices was noted on day 20 of gestation [9]. In humans, the terminal saccular stage, at which alveolar epithelial cells are more clearly differentiated into mature type I and type II pneumocytes, begins at 24 weeks and continues to the late fetal period [10]. Accordingly, if exposure to paraquat occurs sufficiently early, relative to the maturation of type II pneumocytes, pulmonary toxicity in the fetus might not be severe [4]. This is supported by a prior case report of paraquat poisoning in a woman of 28 weeks GA, who developed typical symptoms and signs of poisoning and finally died. However, sections of fetal lungs, kidneys, pancreas, liver, and spleen showed no abnormalities in that case [11]. Furthermore, other reports revealed that patients with GA of 10 weeks [12], 20 weeks [13], and 27 weeks [14] survived; their children were later delivered and were normal at the ages of 4, 3, and 5 years [12–14].