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Unveiling the impacts of biodegradable microplastics on cadmium toxicity, translocation, transformation, and metabolome in lettuce
Summary
Researchers studied how biodegradable microplastics interact with cadmium contamination in lettuce and found that the combination worsened the toxic effects on plant growth compared to cadmium alone. The biodegradable plastics increased cadmium accumulation in the edible parts of the lettuce and altered how the metal was distributed within plant cells. The findings raise concerns about using biodegradable plastic mulch in soils already contaminated with heavy metals, as it may increase the amount of toxic metals that end up in food crops.
Biodegradable microplastics (BMPs) may impact the environmental fate and ecotoxicity of Cd, but the effect mechanism in soil-plant system remain poorly understood. This study investigated the impact of BMPs (poly(lactic acid) (PLA) and poly(butylene adipate terephthalate) (PBAT) microplastics) on the Cd toxicity, translocation, transformation, and metabolome in lettuce (Lactuca sativa L.) by pot experiments. The results show that co-exposure to BMPs and Cd synergistically inhibited the shoot growth. 0.2 % PLA MPs enhanced but 2.5 % PLA MPs inhibited the photosynthesis; however, the dose of PBAT MPs was negatively correlated with the content of chlorophyll a. Moreover, the presence of 2.5 % PBAT MPs increased the nitrate content of leaves by 9.5 % compared to single Cd exposure. The partial least squares path model (PLS-PM) indicates that BMPs exacerbated the inhibitory effects of Cd on lettuce growth. PLA MPs enhanced K, Ca, Cu, and Zn accumulation in root stele, whereas PBAT MPs promoted Fe and Mn enrichment in epidermis. Furthermore, co-exposure resulted in higher inorganic and water-soluble Cd proportions in shoots. PLA MPs elevated Cd contents in cell wall fractions of both roots and shoots, while PBAT MPs increased Cd contents in shoot cell walls and root cells and soluble Cd ratio in shoots. BMPs enhanced Cd toxicity and bioaccumulation by downregulating the expression of ABC transporters and phenylpropanoid biosynthesis pathways, and the relative abundance of related metabolites.
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