Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2009637 | Pesticide Biochemistry and Physiology | 2010 | 6 Pages |
Abstract
Using a unicellular cyanobacterium, Synechococcous elongatus PCC7942, we have shown that cytosolic acidification, O2â; H2O2 production and photosystem II-inactivation are the causes of cell death from bentazone/bromoxynil incubations. Butyric acid evoked solely pH lowering response and yet inhibited PS II activity indicating that herbicide-caused acidification is sufficient to kill the cyanobacterial cells, but other factors like excess H2O2 production due to an imbalance in the peroxide sequestration machinery might be contributory. While the activities of superoxide dismutase and pyrogallol peroxidase increased consequent to herbicide incubations and displayed oligomeric states with mobility shift, catalase and glutathione peroxidase though present remained insensitive.
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Authors
Palash Kumar Das, Suvendra Nath Bagchi,