Silicon tackles butachlor toxicity in rice seedlings by regulating anatomical characteristics, ascorbate-glutathione cycle, proline metabolism and levels of nutrients.

Reckless use of herbicides like butachlor (Buta) in the fields represents a serious threat to crop plants, and hence to their productivity. Silicon (Si) is well known for its implication in the alleviation of the effects of abiotic stresses; however, its role in mitigating Buta toxicity is not yet known. Therefore, this study was carried out to explore the role of Si (10 µM) in regulating Buta (4 µM) toxicity in rice seedlings. Buta reduced growth and photosynthesis, altered nitric oxide (NO) level and leaf and root anatomy, inhibited enzyme activities of the ascorbate-glutathione cycle (while transcripts of associated enzymes, increased except OsMDHAR), as well as its metabolites (ascorbate and glutathione) and uptake of nutrients (Mg, P, K, S, Ca, Fe, etc. except Na), while addition of Si reversed Buta-induced alterations. Buta stimulated the expression of Si channel and efflux transporter genes- Lsi1 and Lsi2 while the addition of Si further greatly induced their expression under Buta toxicity. Buta increased free proline accumulation by inducing the activity of Δ-pyrroline-5-carboxylate synthetase (P5CS) and decreasing proline dehydrogenase (PDH) activity, while Si reversed these effects caused by Buta. Our results suggest that Si-governed mitigation of Buta toxicity is linked with favorable modifications in energy flux parameters of photosynthesis and leaf and root anatomy, up-regulation of Si channel and transporter genes, ascorbate-glutathione cycle and nutrient uptake, and lowering in oxidative stress. We additionally demonstrate that NO might have a crucial role in these responses.