Herbicide injury caused from protoporphyrinogen oxidase (PPO, PPG or protox) inhibitors including acifluorfen, flumioxazin, oxyfluorfen, fomesafen, sulfentrazone, oxadiazon, and others.
- Interveinal chlorosis, bronzing, desiccation and then necrosis.
- Foliar necrosis – spots, margins or general necrosis depending on the amount of spray exposure.
- Petiole and tender stem necrosis.
- Fruit lesions and necrosis.
- Leaf mid-vein reddening followed by necrosis.
- Dark red leaf spots followed by necrotic leaf spots.
PPO inhibitors can be applied pre or postemergence leading to foliar absorption in seedlings and some upward translocation. Light is needed to activate assimilated PPO inhibitors causing rapid cell membrane destruction on young seedling leaves, petioles and stems shortly after emergence. Spray drift to foliage results in rapid necrosis of tender tissues. More mature leaves and stems may not express symptoms. Various PPO herbicides display like symptomologies but may differ due to application timing and differential sensitivity in crops and weeds.
PPO inhibitor injury may be confused with symptoms from:
- Cell membrane disruptors such as paraquat, diquat, herbicidal oils and fatty acids.
- Classical PS II, as-triazine such as metribuzin.
- Rapid action PS II, benzothiadiazole such as bentazon.
- Desiccation, salt injury, frost damage.
Applied Weed Science: Including the Ecology and Management of Invasive Plants (3rd Edition), Merrill Ross & Carol Lembi, pages 168, 178-179, 273-277
Publication date: Dec. 11, 2015
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