Engineered Nanomaterial Activity at the Organelle Level: Impacts on the Chloroplasts and Mitochondria

Abstract

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 end points that can be sought when assessing the impact of ENMs exposure on environmental and human health.

Subtoxic dose of lithium cobalt oxide nanosheets impacts critical molecular pathways in trout gill epithelial cells

“…Engineered nanomaterials have been shown previously to disrupt the energy balance within cells, likely due to mitochondrial-related impacts. 51,52 Impacts to mitochondrial function may account for the upregulation of metabolism related pathways observed here. Furthermore, LCO NPs have been shown previously to adsorb phosphate in solution.…”

“…7 illustrates hypothesized connections and possible explanations for the observed regulated processes, which represent potential areas for future studies. The upregulation of metabolism related processes by both subtoxic and toxic NP doses suggests energy imbalance or depletion, possibly due to mitochondrial disfunction, 51,52 and cellular attempt to restore balance. We hypothesize this energy imbalance could result from NP-induced hypoxia, as suggested by the observed upregulation of pathways related to decreased oxygen levels and hypoxia by both the toxic and subtoxic doses at 24 and 48 hours.…”

Nano-ZnO-Induced Drought Tolerance Is Associated with Melatonin Synthesis and Metabolism in Maize

“…Positive effects on chloroplast and mitochondria have been reported for various metal oxide nanoparticles. For instance, nano-TiO 2 protects the chloroplast and mitochondria from environmental stress via increasing antioxidant enzyme activities and up-regulating At3g23990 [34,35]. Similarly, the single-walled carbon nanotubes increase the photosynthetic activity and the threshold of electron transport due to their protective effects on lipid membranes in chloroplast [36].…”

In Vivo-In Vitro Comparative Toxicology of Cadmium Sulphide Quantum Dots in the Model Organism Saccharomyces cerevisiae

“…From a physiological and molecular point of view, it has been demonstrated that ENMs increase the Reactive Oxygen Species (ROS) production within the cells. These excessive ROS interact negatively with all cell compartments, in particular affecting cell membranes and the energy production at the level of the mitochondria [43]. However, it remains unclear whether the generation of intracellular ROS could derive only from a direct interaction at the level of the mitochondria or if the ROS production at the level of the cytosol was also involved [43].…”

“…These excessive ROS interact negatively with all cell compartments, in particular affecting cell membranes and the energy production at the level of the mitochondria [43]. However, it remains unclear whether the generation of intracellular ROS could derive only from a direct interaction at the level of the mitochondria or if the ROS production at the level of the cytosol was also involved [43]. Measures of the cell redox state utilizing parameters related to the GSH oxidation state confirmed that in both tolerant and sensitive mutants, treated with CdS QDs, the oxidation level of glutathione was higher than in the not treated control (Figure 5, Tables S7 and S8).…”