Herbicide injury caused from photosystem I (PS I) inhibitors including (bipyridilium herbicides) paraquat (Cyclone, Gramoxone) and diquat (Reglone, Reward). These are non-selective, contact-acting herbicides producing rapid necrosis of contacted plant tissues.
- Non-selective necrosis of plant foliage.
- Leaf water-soaking on all treated tissues within hours of treatment.
- Necrosis of contacted foliage within 4 to 6 hours.
- Spotting and necrotic lesions on fruit contacted by the spray droplets.
- High doses applied to the stem of plants can cause stem cankers even in woody plants.
Plant Entry and Symptom Expression
Foliar applied, nontranslocated contact herbicides causing rapid destruction of cell membranes. PS-I inhibitor herbicides do not have soil residual activity. Photosystem I inhibitor injury symptoms are visible on all treated tissues within hours of application and plant death within one to two days. Increased speed of PS I activity in bright sunlight, high humidity and/or moist soil. Amount of tissue necrosis on treated plants depends on the amount of spray contact – leaf spot when small amounts of drift occur; necrosis of leaves and green stems with sufficient spray coverage.
PS I inhibitor injury may be confused with symptoms from:
- Bentazon and bromoxynil (PS II rapid action) cell membrane destruction.
- PPO inhibitor herbicides (such as acifluorfen flumioxazin, and lactofen).
- Glufosinate (glutamine synthetase).
- High salt concentration resulting in desiccation.
- Drought related leaf necrosis.
- Excess concentration of crop oils, surfactants and other spray adjuvants.
- Gasoline, diesel fuel and other petroleum products may also display contact herbicide symptomology.
Herbicide Mode of Action Category
WSSA – 22
HRAC – D
Applied Weed Science: Including the Ecology and Management of Invasive Plants (3rd Edition), Merrill Ross & Carol Lembi, pages 165, 170-172.
Publication date: Sept. 10, 2015
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