Percutaneous Paraquat Intoxication

Athanaselis, Sotiris; Qammaz, Samir; Alevisopoulos, G.; Koutselinis, A.

doi:10.3109/15569528309088518

Cited by 24 publications

(7 citation statements)

References 3 publications

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“…Control of sarcoplasmic reticulum (SR) Ca 2+ release is voltage driven in skeletal muscle, however, L-type Ca 2+ current is the primary trigger for SR Ca 2+ release in cardiac muscle. While additional experimental work is needed to further clarify the exact mechanisms underlying the observed contractile decrement in cardiac and skeletal muscles, our findings corroborate previously published clinical studies which have described PAR-induced lesions in skeletal muscle [36], [37] and the heart [38]. Moreover, two cases of suicide from oral ingestion of PAR have been reported [39].…”

Section: Discussionsupporting

confidence: 89%

Vitamin E Ameliorates the Decremental Effect of Paraquat on Cardiomyocyte Contractility in Rats

et al. 2013

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BackgroundExposure to pesticides and industrial toxins are implicated in cardiovascular disease. Paraquat (PAR) is a toxic chemical widely used as an herbicide in developing countries and described as a major suicide agent. The hypothesis tested here is that PAR induced myocardial dysfunction may be attributed to altered mechanisms of Ca2+ transport which are in turn possibly linked to oxidative stress. The mechanisms of PAR induced myocardial dysfunction and the impact of antioxidant protection was investigated in rat ventricular myocytes.MethodologyForty adult male Wistar rats were divided into 4 groups receiving the following daily intraperitoneal injections for 3 weeks: Group 1 PAR (10 mg/kg), Control Group 2 saline, Group 3 vitamin E (100 mg/kg) and Group 4 PAR (10 mg/kg) and vitamin E (100 mg/kg). Ventricular action potentials were measured in isolated perfused heart, shortening and intracellular Ca2+ in electrically stimulated ventricular myocytes by video edge detection and fluorescence photometry techniques, and superoxide dismutase (SOD) and catalase (CAT) levels in heart tissue.Principal FindingsSpontaneous heart rate, resting cell length, time to peak (TPK) and time to half (THALF) relaxation of myocyte shortening were unaltered. Amplitude of shortening was significantly reduced in PAR treated rats (4.99±0.26%) and was normalized by vitamin E (7.46±0.44%) compared to controls (7.87±0.52%). PAR significantly increased myocytes resting intracellular Ca2+ whilst TPK and THALF decay and amplitude of the Ca2+ transient were unaltered. The fura-2–cell length trajectory during the relaxation of the twitch contraction was significantly altered in myocytes from PAR treated rats compared to controls suggesting altered myofilament sensitivity to Ca2+ as it was normalized by vitamin E treatment. A significant increase in SOD and CAT activities was observed in both PAR and vitamin E plus PAR groups.ConclusionsPAR exposure compromised rats heart function and ameliorated by vitamin E treatment.

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Section: Discussionsupporting

confidence: 89%

Vitamin E Ameliorates the Decremental Effect of Paraquat on Cardiomyocyte Contractility in Rats

et al. 2013

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“…The higher concentration of PQ in lung tissue could be predicted due to its accumulation against a concentration gradient through the polyamine uptake system . The concentration of PQ in blood is usually much lower than that in lung tissue or might not even be detected in the late phase of poisoning following PQ ingestion . In this case, the patient died 24 days after first exposure to PQ.…”

Section: Resultsmentioning

confidence: 91%

Homicidal Paraquat Poisoning

Fan

Jin

et al. 2018

Journal of Forensic Sciences

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Paraquat poisoning usually results from suicide, occupational, or accidental exposure. Herein, we report a rare fatal case of homicidal paraquat poisoning. A 58‐year‐old man was poisoned by taking paraquat‐mixed medicine and wearing paraquat‐soaked underwear. In the absence of a history of paraquat exposure, the patient was misdiagnosed with pulmonary infection and scrotal dermatitis and died of respiratory failure 24 days after the initial exposure to paraquat. Ultra‐performance liquid chromatography‐tandem mass spectrometry (UPLC‐MS/MS) was applied to detect and quantify paraquat in postmortem specimens. The concentration of paraquat in postmortem specimens from high to low is lung (0.49 μg/g), brain (0.32 μg/g), kidney (0.24 μg/g), liver (0.20 μg/g), cardiac blood (0.11 μg/mL), and stomach wall (

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“…There have been a few reports of poisoning and death from pulmonary fibrosis as a result of dermal exposure to paraquat (16), including cases which have occurred after the application of dilute paraquat according to label instructions (17,18). In the occupational setting, such cases are probably rare in developed countries, where application is commonly aerial and where workers are more likely to be well protected (19).…”

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confidence: 99%