Halogenated flame retardants in farmlands were observed to inhibit the growth of exposed crops. This study aimed to elucidate the mechanism of inhibition on rice by employing four representative polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs). The exposure to these contaminants at 200 nM led to a decrease of 0.63–0.95 fold in rice below-ground biomass and 0.49–0.66 fold in yield, and a corresponding 4%–10% increase in soluble sugars in leaves. PBDEs and PCBs were found to significantly disrupt the synthesis, decomposition, and transport of sugars in leaves, the three pivotal determinants of crop growth. Notably, these compounds promoted a 1.41- to 7.60-fold upregulation of the triose phosphate translocator, significantly enhancing soluble sugar synthesis. Conversely, a 0.45–0.97 fold downregulation was observed for sucrose transporters, thus impeding the leaf-to-shoot efflux of soluble sugars. Furthermore, PBDEs and PCBs were favorably bound to fructose-1,6-bisphosphate aldolase (FBA), inducing its substrate-specific dysfunction in fructose-1,6-diphosphate decomposition (3%–14%). Overall, PBDE and PCB exposure promoted a notable intracellular accumulation of soluble sugars in rice leaves, a typical symptom of plant diabetes, since the intensified synthesis of soluble sugars in leaves and the repressed decomposition and transportation of soluble sugars to other storage organs, thus impeding crop growth. This study provided an insightful understanding of the toxic effects and molecular mechanisms of halogenated flame retardants, highlighting their role in abnormal sugar accumulation and growth inhibition in crops and offering vital information for the risk assessment and administration of these compounds to guarantee the safety of agricultural products.
The co-occurrence of 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) and copper (Cu) in agricultural fields pose significant implications for crop growth and grain production. This study explored their individual and combined effects on rice crops and elucidated the underlying mechanisms combining in vivo , in vitro , and in silico investigations. Both BDE-47 and Cu inhibited shoot biomass, whereas root biomass exhibited distinct profiles: BDE-47 inhibited it, while Cu promoted it, at environmentally relevant exposure concentrations. This phenomenon was attributed to differences in sucrose transport between the source (shoot) and sink (root). Furthermore, metabolic, transcriptional, and translational analyses unveiled that this process was modulated by the NAC23-Tre6P-SnRK1a signaling pathway, with the dysfunction of fructose-1,6-diphosphate aldolase (FBA) and alterations in intracellular sucrose level serving as the crucial negative factors. Both contaminants bound to FBA, disrupting glucose signal transmission and upregulating SnRK1a expression. Additionally, BDE-47 suppressed sucrose levels, thereby reducing NAC23 activity and inhibiting sucrose transport. Conversely, Cu significantly elevated sucrose levels, mitigating the adverse effects of SnRK1a on NAC23 and enhancing sucrose transport. Interestingly, the coexistence of Cu with BDE-47 synergistically inhibited sucrose transport, further reducing root biomass and lowering the toxicity threshold of BDE-47 on rice crops. This study offered novel insights into the signaling regulatory mechanisms governing the differential impacts of BDE-47 and Cu on rice growth and yield production, facilitating more accurate assessments of their phytotoxicity and informing scientific regulatory frameworks for croplands.