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.
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.
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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