Mechanistic Insights into Cellular and Molecular Basis of Protein‐Nanoplastic Interactions

Abstract

Plastic waste is ubiquitously present across the world, and its nano/sub‐micron analogues (plastic nanoparticles, PNPs), raise severe environmental concerns affecting organisms’ health. Considering the direct and indirect toxic implications of PNPs, their biological impacts are actively being studied; lately, with special emphasis on cellular and molecular mechanistic intricacies. Combinatorial OMICS studies identified proteins as major regulators of PNP mediated cellular toxicity via activation of oxidative enzymes and generation of ROS. Alteration of protein function by PNPs results in DNA damage, organellar dysfunction, and autophagy, thus resulting in inflammation/cell death. The molecular mechanistic basis of these cellular toxic endeavors is fine‐tuned at the level of structural alterations in proteins of physiological relevance. Detailed biophysical studies on such protein‐PNP interactions evidenced prominent modifications in their structural architecture and conformational energy landscape. Another essential aspect of the protein‐PNP interactions includes bioenzymatic plastic degradation perspective, as the interactive units of plastics are essentially nano‐sized. Combining all these attributes of protein‐PNP interactions, the current review comprehensively documented the contemporary understanding of the concerned interactions in the light of cellular, molecular, kinetic/thermodynamic details. Additionally, the applicatory, economical facet of these interactions, PNP biogeochemical cycle and enzymatic advances pertaining to plastic degradation has also been discussed.

Comparative toxicity of polystyrene, polypropylene, and polyethylene nanoplastics on Artemia franciscana nauplii: a multidimensional assessment

“…For example, PS-NP and PP-NP are more hydrophobic and positively charged than PE-NP, which may influence their uptake, distribution, and accumulation in the cells. 64 Cdc48 , Clap , Had , and Cstb are associated with PS-NP and PP-NP, and these genes are involved in protein degradation or folding, which may be stimulated by PS-NP and PP-NP, but suppressed by PE-NP. Tcp1 , AP15 , and Ucp2 are linked to PE-NP, and these genes are related to mitochondrial function or oxidative stress, which may be enhanced by PE-NP, but lessened by PS-NP and PP-NP.…”