One of the challenges potentially limiting the continued widespread commercial development and application of engineered nanomaterials (ENMs) is the still perceived lack of knowledge on their potential toxic effects. Although evidence has been accumulating on the biological effects of ENMs at the level of cells, tissues, and organisms, wide differences in design make the results so far obtained not easily comparable. More importantly, risk assessment procedures are not sufficiently harmonized. Experimental data from assays involving fungi, plants, and animals have shown that mitochondria and chloroplasts are primary targets of metal-based ENMs. To provide a unifying picture of the molecular mechanisms of nanomaterial action, the aim of this perspective paper is to examine critically the current literature in this area: instances of mitochondrial and chloroplastic involvement in ENMs response are evaluated to describe the interplay between nuclear and organelle genomes observed in different organisms. This paper highlights critical parameters to consider when designing sustainable ENMs and suggests a standardized set of endpoints that can be sought when assessing the impact of ENMs exposure on environmental and human health.
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