Selenium amelioration of arsenic toxicity in rice shows genotypic variation: A transcriptomic and biochemical analysis.

The toxic metalloid arsenic (As) is consumed mostly through contaminated rice. Therefore, reducing its accumulation and maintaining nutrient homeostasis in crop plants are imperative to ensure food safety. However, there is a dearth of information on the interrelationship between nutrient homeostasis and the regulatory mechanisms of arsenic-selenium (As-Se) interactive pathways responsible for stress tolerance. In the present study, experiments were conducted in hydroponically grown 12-day-old seedlings of rice (Oryza sativa L.) varieties (Pusa Basmati1 and IR64) treated with arsenite (AsIII) (150 μM), selenium (SeVI) (20 μM), and As + Se. It was observed that selenium supplementation ameliorated As toxicity by reducing its accumulation and retrieving As-induced nutrient deficiency. Significant decrease in As accumulation, H2 O2 content, and fluorescent intensity of nitric oxide (NO), reactive oxygen species (ROS), and superoxide radical (O2 .-) along with cell death with Se supplementation in both rice varieties demonstrated the protective role of Se as a probable ROS quencher. Addition of Se increased the enzyme activities of thiol metabolism and induced differential transcript accumulation patterns of sulfur-related genes. Nutrient level positively correlated with the differential expression pattern of NPK-related genes that play roles in metabolism and nutrient availability in both varieties. Though Pusa Basmati1 (PB1) showed higher tolerance to As, IR64 overcomes As toxicity more efficiently than PB1 in the presence of Se, which highlights that IR64 is a better performer in the presence of Se. Overall, this study provides novel insight into the role of Se in As-stressed rice genotypes through alteration of nutrient transporters and thiol-related genes.