Abstract

Cadmium (Cd) is one of the prominent environmental hazards, affecting plant productivity and posing human health risks worldwide. Although salicylic acid (SA) and nitric oxide (NO) are known to have stress mitigating roles, little was explored on how they work together against Cd-toxicity in rice. This study evaluated the individual and combined effects of SA and sodium nitroprusside (SNP), a precursor of NO, on Cd-stress tolerance in rice. Results revealed that Cd at toxic concentrations caused rice biomass reduction, which was linked to enhanced accumulation of Cd in roots and leaves, reduced photosynthetic pigment contents, and decreased leaf water status. Cd also potentiated its phytotoxicity by triggering reactive oxygen species (ROS) generation and depleting several non-enzymatic and enzymatic components in rice leaves. In contrast, SA and/or SNP supplementation with Cd resulted in growth recovery, as evidenced by greater biomass content, improved leaf water content, and protection of photosynthetic pigments. These signaling molecules were particularly effective in restricting Cd uptake and accumulation, with the highest effect being observed in “SA + SNP + Cd” plants. SA and/or SNP alleviated Cd-induced oxidative damage by reducing ROS accumulation and malondialdehyde production through the maintenance of ascorbate and glutathione levels, and redox status, as well as the better activities of antioxidant enzymes superoxide dismutase, catalase, glutathione S-transferase, and monodehydroascorbate reductase. Combined effects of SA and SNP were observed to be more prominent in Cd-stress mitigation than the individual effects of SA followed by that of SNP, suggesting that SA and NO in combination more efficiently boosted physiological and biochemical responses to alleviate Cd-toxicity than either SA or NO alone. This finding signifies a cooperative action of SA and NO in mitigating Cd-induced adverse effects in rice, and perhaps in other crop plants.

Highlights

  • Modern-environment and human health are continuously challenged by a plethora of pollutants, which are originated by both anthropogenic and geological activities [1]

  • In the current study, Cd-exposed rice plants exhibited significant losses of Chls and carotenoids together with disturbance in leaf water status (Table 1), which were reported in other plant species like mustard and maize [13,34,38]. These results indicated that accumulated levels of Cd in leaf tissues interfered with photosynthetic activity by reducing the supply of photosynthetic pigments and water, decreasing growth and biomass of Cd-stressed plants (Figure 1A,B; Table 1)

  • salicylic acid (SA) and/or sodium nitroprusside (SNP) was involved in uplifting the activities of superoxide dismutase (SOD) and CAT, which coordinately restricted elevation of O2− and H2O2 in the leaves of Cd-stressed rice plants. These results further indicated that the reduction of H2O2 in “SA + Cd,” “SNP + Cd,” and “SA + SNP + Cd” plants by the actions of SOD and CAT (Figure 3A,B) did not require a rise in the activities of ascorbate peroxidase (APX), dehydroascorbate reductase (DHAR), and glutathione reductase (GR) involved in the AsA-GSH cycle (Figure 3C,E,F)

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Summary

Introduction

Modern-environment and human health are continuously challenged by a plethora of pollutants, which are originated by both anthropogenic and geological activities [1] Among these pollutants, heavy metals have been evolved as one of the major contaminants, endangering the quality of lives of diverse habitants ranging from microbial communities to plants, animals, and humans [2,3]. Despite having cellular signaling roles at low concentrations, excessive ROS are highly reactive, and display differential degrees of toxicities to proteins, membrane lipids, and nucleic acids, leading to generation of oxidative stress [11]. One of the supports is to supply exogenous compounds, including signaling molecules like salicylic acid (SA) and nitric oxide (NO), which are known to modulate plant defense mechanisms in order to withstand deleterious effects of various abiotic stresses, including heavy metal toxicity [13,14]

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