Weidel and Russo published the first description of paraquat in 1882. Its redox characteristics were identified in 1933 by Michaelis and Hill, who gave the substance the name, methyl viologen. Paraquat's herbicidal qualities were originally discussed in 1958, and it was first made commercially available in 1962. The principal form of paraquat is an aqueous solution with surface-active ingredients. A low strength granular formulation (also containing diquat) is offered in several countries. Paraquat is a non-selective, fast-acting contact herbicide1. When it
comes into touch with soil clay, it is deactivated2. In the 1960s, New Zealand and Ireland reported the first human exposure instances, which were brought on by accidental intake3. In many regions of Asia, including Bangladesh, paraquat, is one of the major causes of poisoning that results in death4. Median lethal dose (LD50) in humans, which is roughly 3-5 mg/kg, 10-15 ml of a 20% solution would be sufficient5. 
 
It is known that 90% of the paraquat in the body is eliminated within 12 to 24 hours following fast absorption (Pond, et al., 1993). Paraquat is sequestered inside the body and undergoes sluggish clearance, 
which may be caused by kidney and liver damage6. The remaining Paraquat is concentrated inside numerous cells where it undergoes redox cycling and produces reactive oxygen species. Several enzyme systems are involved in the metabolism of paraquat (NADPH-cytochrome p450 reductase; Xanthine oxidase; NADH: ubiquinone oxidoreductase and nitric oxide synthase)6.
 
Upon metabolism by these systems, a paraquat mono-cation radical (PQ+) is produced. PQ+ quickly reoxidizes to PQ2+ inside the cell, producing superoxide (O2?) in the process. In this reaction, (O2?) serves as an electron acceptor and NADPH as an electron donor. In addition, this causes the Fenton reaction, which results in the creation of the hydroxyl free radical (HO·), in the presence of iron. Peroxinitrite (ONOO-·), a very potent oxidant and nitrating intermediate, is produced when NO and O2· combine. Nitric oxide is created enzymatically from L arginine by NO synthase, and PQ also directly or indirectly stimulates this enzymatic generation of NO7.
 
Generation of highly reactive oxygen and nitrite species results in toxicity. So, damage occurs to the mitochondria in numerous cell types8, oxidation of the NADPH, which results in an increase in oxidative stress susceptibility9, generation of inflammatory cytokines as a result of NF-?B activation10. All these processes eventually result in cellular death. Toxicity is particularly severe in the lungs as paraquat is taken up against the concentration gradient in to the lung6. 
 
Pneumonitis and lung fibrosis are caused by the active concentration of paraquat in lung tissue11. Additionally, paraquat harms the liver, kidney, and gastrointestinal systems12. In humans, ARDS and pulmonary fibrosis are the leading causes of death13. 
 
There is no known specific antidote, hence the fatality rate is extremely high. Early arrival, quick decontamination, and the implementation of resuscitative procedures are essential for management. Further absorption can be reduced using Fuller's earth and activated charcoal. Contraindications apply to gastric lavage. Hemodialysis and hemoperfusion have a low chance of altering the clinical trajectory. 
 
Weak evidence supports the use of immunosuppression with dexamethasone, cyclophosphamide, and methylprednisolone. It might be advantageous to employ antioxidants like acetylcysteine and salicylate to scavenge free radical6. 
 
This study was carried out with an aim to observe tongue   ulcer,   nausea,   vomiting,   abdominal  pain, 
 
diarrhoea and upper GI ulcer in endoscopy to determine their association with paraquat ingestion specially at higher doses (≥ 10 ml of 20% solution).