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      Home / AgTech & Research

      New research links diquat herbicide to gut damage and broader organ toxicity

      Editors avatar Editors
      June 11, 2025, 10:00 am
      June 11, 2025, 10:00 am
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      AgTech & Research
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      New research links diquat herbicide to gut damage and broader organ toxicity
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      Diquat, a herbicide banned in the European Union, the United Kingdom, and Switzerland, continues to be applied to crops across the United States despite mounting evidence of its health risks. A new scientific review has found that diquat not only harms the liver and kidneys, long recognized as vulnerable organs, but also severely damages the intestines, potentially triggering a chain reaction that affects other critical organs.

      Published in Frontiers in Pharmacology in May 2025, the review analyzed over 100 studies and concluded that the intestines are a primary target of diquat toxicity. The herbicide, commonly used on potatoes, rapeseed, sugarcane, and cotton, was found to compromise the gut barrier, kill beneficial bacteria, impair nutrient absorption, and trigger chronic inflammation.

      According to the researchers, these intestinal injuries may drive further harm through the so-called “gut-organ axis,” a biological network that connects the gut to other parts of the body. This suggests that diquat’s effects may extend far beyond the gastrointestinal tract, contributing to damage in the liver, kidneys, lungs, and possibly leading to multiple organ dysfunction syndrome (MODS).

      “Diquat primarily enters the body through the digestive tract, leading to poisoning,” the researchers wrote. “Its core toxic mechanism involves oxidative stress caused by reactive oxygen species, which directly damages the intestinal lining and exacerbates systemic inflammation.”

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      Widespread use despite regulatory bans

      Diquat, like its chemical counterpart paraquat, is a bipyridyl herbicide that kills plants by producing reactive oxygen species (ROS). While paraquat is banned in over 70 countries due to its toxicity and links to Parkinson’s disease, diquat remains registered with the U.S. Environmental Protection Agency for use as a non-selective contact herbicide.

      In contrast, the EU and several other jurisdictions have banned diquat over concerns about its environmental persistence and health effects. The substance can remain active for days in water and even longer in soil, where it binds to particles and may enter the food chain. Despite these concerns, diquat continues to be exported to countries like Brazil, where paraquat use was prohibited in 2020.

      Intestinal damage as a central concern

      The review emphasizes the intestine’s critical role in mediating diquat’s toxic effects. The herbicide was shown to:

      • Shorten intestinal villi and deepen crypts, impairing nutrient absorption
      • Damage tight junction proteins, weakening the gut’s barrier function
      • Promote the release of pro-inflammatory cytokines
      • Disrupt the balance of gut microbiota, reducing beneficial microbes like Lactobacillus

      The resulting imbalance affects the production of microbial metabolites essential for disease resistance and intestinal repair, making the gut more susceptible to further injury.

      Broader systemic impacts

      Beyond the gut, diquat’s toxic profile may affect multiple organs:

      • Kidneys: Induces acute injury through membrane damage and inflammatory signaling
      • Liver: Disrupts cellular energy metabolism, promotes inflammation and immune responses
      • Lungs: Produces oxidative molecules that can damage lung tissue
      • Other: May interfere with autophagy, a cellular process that removes damaged proteins

      These interactions could lead to systemic toxicity and complications such as MODS, although human data remains limited.

      Call for further study and risk mitigation

      The researchers stress the need for human epidemiological studies to verify the findings from animal models, which often do not capture the effects of long-term, low-level exposure. They also call for improved toxicity models and targeted detoxification strategies focusing on intestinal health.

      A better understanding of diquat’s toxicological mechanisms, the authors argue, is essential for managing poisoning cases, assessing related herbicides, and informing environmental recovery in contaminated areas.

      diquat
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