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Year : 2020  |  Volume : 9  |  Issue : 3  |  Page : 184-185

Urine sodium dithionite test: A useful clinical test for paraquat poisoning

Department of Biochemistry, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India

Date of Submission04-Jan-2020
Date of Decision21-Jan-2020
Date of Acceptance21-Jan-2020
Date of Web Publication27-Oct-2020

Correspondence Address:
Kiranmayi S Vinapamula
Associate Professor, Department of Biochemistry, Sri Venkateswara Institute of Medical Sciences, Tirupati 517 507, Andhra Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JCSR.JCSR_1_20

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How to cite this article:
Jyothsna P, Vinapamula KS. Urine sodium dithionite test: A useful clinical test for paraquat poisoning. J Clin Sci Res 2020;9:184-5

How to cite this URL:
Jyothsna P, Vinapamula KS. Urine sodium dithionite test: A useful clinical test for paraquat poisoning. J Clin Sci Res [serial online] 2020 [cited 2022 May 21];9:184-5. Available from: https://www.jcsr.co.in/text.asp?2020/9/3/184/298948

Paraquat (N, N′-dimethyl-4,4′-dipyridylium dichloride; molecular formula C12H14 Cl2N2; molecular weight 257.2), which is also known as methyl viologen, is a nitrogen-containing toxic chemical that is widely used as a herbicide for controlling weed and grass in agriculture.[1] Paraquat acts rapidly and in a non-specific manner on plant tissues and destroys them. Paraquat was first produced commercially during the 1960s and in India, it is available as a dichloride salt under the trade names Gramoxone and Weedol. Cases of paraquat poisoning have been reported from all over the world; the first case of paraquat poisoning in India was reported by Singh et al.[2] Acute intoxication occurs most commonly due to intentional self-administration. The symptoms of paraquat poisoning depend on the amount of the toxin, its concentration and the route of exposure.[1] The possible routes of exposure include contact through skin and eyes, ingestion and inhalation. Ingestion, especially in a concentrated form, results in extensive damage to the gastrointestinal mucosa due to the corrosive nature of the compound. Paraquat intoxication causes damage to multiple organs such as lungs, liver and kidney. The major effects of acute poisoning include abdominal pain, vomiting, diarrhoea and cardiac, renal and hepatic failure. Paraquat poisoning is associated with very high mortality rates due to the high toxicity of the compound and lack of effective treatment.[3]

After its entry into the body, paraquat taken up by cells is metabolised by enzymes such as cytochrome P-450 and xanthine oxidase, resulting in the generation of paraquat mono-cation radical (PQ+). During the further oxidisation of the paraquat radical cation to its cationic form (PQ2+), there is a generation of superoxide anion and other free radicals which are highly reactive and harmful. Hence, once accumulated in tissues, the subsequent effects of paraquat poisoning are a result of the free radical-mediated damage. Paraquat toxicity affects multiple organs, however lungs are majorly involved because paraquat tends to accumulate in lungs by an active transport mechanism against concentration gradient.[3] The LD50 in human beings is about 3–5 mg/kg, which occurs with a consumption of 10–15 mL of a 20% solution.[4]

Once ingested, paraquat is rapidly distributed to organs such as liver, muscle, kidney and lung. About 90% of the absorbed paraquat is excreted unchanged in the urine within 12–24 h of ingestion.[3] This enables qualitative detection of paraquat in urine, which forms the basis for diagnosing paraquat poisoning.[4]

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The test is based on the reduction of the paraquat cation to a blue radical ion by sodium dithionite in alkaline medium. To 10 mL of urine sample, 2 ml of freshly prepared 1% sodium dithionite in 1 N sodium hydroxide is added and mixed well. The development of blue or green colour indicates the presence of paraquat in the urine sample [Figure 1]. If the urine sample turns black, it indicates the presence of very high concentration of paraquat and the test should be repeated after diluting the urine sample. The sodium dithionite test can detect paraquat up to a concentration of 1 μg/mL in a clear urine sample.[5] The test can also be performed as a quantitative test by using known concentrations of paraquat solutions and comparing the colour change in the urine sample.[5]
Figure 1: Urine sodium dithionite test showing positive result in the test sample

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Paraquat poisoning, although rare, is associated with a high fatality and may needs to be differentiated from poisoning due to organophosphorus compounds. Although measurement of paraquat concentration in blood helps in confirming the diagnosis and predicting outcomes, it does not determine the intervention.[3] Specific antidote is not available for paraquat toxicity, however early detection of poisoning helps in taking up measures of decontamination and to prevent further absorption of the poison. The urine sodium dithionite test is a simple and inexpensive test that readily detects paraquat in the urine of suspected cases and can be performed as a bedside clinical test and even at the level of primary health centres.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Dinis-Oliveira RJ, Duarte JA, Sánchez-Navarro A, Remião F, Bastos ML, Carvalho F. Paraquat poisonings: Mechanisms of lung toxicity, clinical features, and treatment. Crit Rev Toxicol 2008;38:13-71.  Back to cited text no. 1
Singh S, Bambery P, Chaudhry D, Makharia G, Kakkar N, Singh D. Fatal paraquat poisoning: Report of two cases. J Assoc Physicians India 1999;47:831-2.  Back to cited text no. 2
Gawarammana IB, Buckley NA. Medical management of paraquat ingestion. Br J Clin Pharmacol 2011;72:745-57.  Back to cited text no. 3
Ingale PW, Shelke SN, Sundharan S, Raul NM. Importance of urine sodium dithionite test in paraquat poisoning: A case study. Int J Res Med Sci 2015;3:310-11.  Back to cited text no. 4
Berry DJ, Grove J. The determination of paraquat (I, I'-dimethyl-4,4' -bipyridylium cation) in urine. Clin Chim Acta 1971;34:5-11.  Back to cited text no. 5


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