ArticlePloS one2019
Protective mechanism of 1-methylhydantoin against lung injury induced by paraquat poisoning.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 22 citations in OpenAlex.
- Pharmacogenomics and Pharmacometabolomics in Precision Tramadol Prescribing for Enhanced Pain Management: Evidence from QBB and EMR Data.Pharmaceuticals (Basel, Switzerland) · 2025Article
- The Link Between Paraquat and Demyelination: A Review of Current Evidence.Antioxidants (Basel, Switzerland) · 2024Review
- Baicalin and lung diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Effects of early repeated hemoperfusion combined with hemodialysis on the prognosis of patients with paraquat poisoning.American journal of translational research · 2023Article
- Synthesis and Anti-Inflammatory Activity of 1-Methylhydantoin Cinnamoyl Imides.Molecules (Basel, Switzerland) · 2022Article
- Article
- Paraquat Induces Lung InjuryFrontiers in pharmacology · 2022Article
- Changes on proteomic and metabolomic profile in serum of mice induced by chronic exposure to tramadol.Scientific reports · 2021Article
- HGF-Modified Dental Pulp Stem Cells Mitigate the Inflammatory and Fibrotic Responses in Paraquat-Induced Acute Respiratory Distress Syndrome.Stem cells international · 2021Article
- Comparison of Pancreatic Damage in Rats for Two Methods of Paraquat Administration.Frontiers in pharmacology · 2021Article
- Tetrandrine attenuates hyperoxia-induced lung injury in newborn rats via NF-κB p65 and ERK1/2 pathway inhibition.Annals of translational medicine · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paraquat (PQ), one of the most widely used herbicides worldwide, causes severe toxic effects in humans and animals. 1-methylhydantoin (MH) is an active ingredient of Ranae Oviductus, which has broad pharmacological activities, e.g., eliminating reactive oxygen species and inhibiting inflammation. This study investigated the effects of MH on lung injury induced by PQ. A PQ poisoning model was established by intragastric infusion of PQ (25 mg/kg), and the control group was simultaneously gavaged with the same dose of saline. The MH group was intraperitoneally injected with 100 mg/kg once per day after intragastric infusion of PQ (25 mg/kg) for five consecutive days. All animals were sacrificed on the sixth day, and the lung tissues were dissected for metabolomics analysis. The lactate dehydrogenase (LDH) activity, superoxide dismutase (SOD) activity, TNF-α and malondialdehyde (MDA) content were determined according to the instructions of the detection kit. Compared with that in the control group, the content of LDH, TNF-α and MDA in the lung tissue of the PQ group was significantly higher, and the activity of SOD in the lung tissue was significantly lower (all p<0.05). Compared with that in the control group, the content of LDH, TNF-α and MDA in the MH group was significantly higher, and the activity of SOD was significantly lower (all p<0.05). However, the differences in SOD activity, LDH activity between the PQ and MH groups were not statistically significant (all p > 0.05). There were significant differences in MDA and TNF-α content between the PQ group and MH group (all p<0.05). MH decreased the production of malondialdehyde and TNF-α to protect against the lung injury caused by PQ poisoning, but it had no significant effect on the activity of LDH and SOD. There were significant differences in metabolomics between the MH group and the PQ poisoning group, primarily in bile acid biosynthesis and metabolism of cholesterol, nicotinate, nicotinamide, alanine, aspartate, glutamate, glycine, threonine, serine, phenylalanine and histidine. Therefore, this study highlights that MH has non-invasive mechanisms and may be a promising tool to treat lung injury induced by PQ poisoning.
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