Abstract
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 Δ1-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.
Highlights
Reckless use of herbicides like butachlor (Buta) in the fields represents a serious threat to crop plants, and to their productivity
The results showed that Buta accelerated reactive oxygen species (ROS) accumulation which resulted in significant amount of lipid peroxidation (LPO) and membrane disruption (MD) in rice seedlings
Under Si+Buta combination, ROS accumulation, LPO and MD were noticeably decreased. These results indicate that Si addition regulates ROS accumulation, LPO and MD in rice seedlings under Buta toxicity; less oxidative stress, better growth, was noticed under Si+Buta combination, as compared to Buta treatment alone
Summary
Reckless use of herbicides like butachlor (Buta) in the fields represents a serious threat to crop plants, and to their productivity. Herbicides including Buta generally inhibit growth of weeds by affecting the biosynthesis of photosynthetic pigments[13,14] and either electron carriers or enzymes partaking in photosynthesis[15,16,17] Due to their negative interactions with metabolic processes, herbicides including Buta have been reported to cause oxidative stress by inducing the accumulation of reactive oxygen species (ROS) that enhanced lipid peroxidation, and disturbed the fluidity of membranes[2,18,19,20]. This study was aimed to explore the role of Si in regulating Buta toxicity in rice seedlings by evaluating growth, photosynthesis, leaf and root anatomical characteristics, oxidative stress, the ascorbate-glutathione cycle, proline metabolism and the regulation of nutrients. Our study has important physiological and ecotoxicological implications and paves the way to follow-up studies on the role of Si under herbicide toxicity in important crops
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