Proteomic and lipidomic analysis of primary mouse hepatocytes exposed to metal and metal oxide nanoparticles

Abstract

20The global analysis of the cellular lipid and protein content upon exposure to metal and metal oxide 21 nanoparticles (NPs) can provide an overview of the possible impact of exposure. Proteomic analysis has 22 been applied to understand the nanoimpact however the relevance of the alteration on the lipidic profile 23 JOURNAL OF INTEGRATED OMICS A METHODOLOGICAL JOURNALHTTP://WWW.JIOMICS.COM Journal of Integrated Omicshas been underestimated. In our study, primary mouse hepatocytes were treated with ultra-small (US) 24

Energy Starvation in Daphnia magna from Exposure to a Lithium Cobalt Oxide Nanomaterial

“…This could be the result of the overlap of the redox potential of these metabolic processes with the ENM conduction band, of oxidative metal release, or of the combination of these or other redox processes. The conservation of these redox-dependent processes for energy metabolism across eukaryotes, , and the conservation of energy metabolism across species more broadly, in combination with the observation of changes in energy metabolism in response to metal oxide ENM exposure across metal types and biological systems, ,− ,, suggests that this may be a fruitful avenue of future nanotoxicity research, both from the standpoint of chemistry and biology.…”

“…These results accord with metabolic impacts seen from LCO and other metal oxides in the literature including changes in metabolic gene expression in C. riparius larvae and trout gill cells exposed to LCO, 30,48 changes in expression of oxidative phosphorylation genes in human lung cells following TiO 2 exposure, 18 reduced in NADH dehydrogenase activity and ATP production in mammalian cells exposed to a range of metal oxide ENMs, 8 and metabolic changes observed in components of the TCA cycle and ETC from exposure to numerous metal oxide ENMS in different biological systems. [14][15][16][17]19 Metal oxide ENMs have also been shown to impact the function of mitochondria in both yeast and plants, as well as the function of plant chloroplasts. 52 Thus, evidence both provided by this study as well as that available in the literature suggests that metabolic impacts of metal oxide ENMs may be a mechanism of nanotoxicity applicable across species and particle types.…”

“…In fact, numerous studies have demonstrated the metabolic impacts of metal oxide ENM exposures across cell and animal models. These include: a 5-fold increase in gluconeogenesis in rat liver cells exposed to ZnO ENM concentrations as low as 2.5 μg/cm 2 , an effect not accountable by ion dissolution alone; significant negative impacts on primary production and respiration in algae exposed to nano-TiO 2 at 0.3 mg/L over 20 d; a 4-fold decline in activity of tricarboxylic acid (TCA) cycle enzyme aconitase in 1 mg/L ZnO ENM-exposed white sucker liver; reduced expression of 11 TCA cycle genes in CuO ENM-exposed Pseudomonas aeruginosa bacteria at 10 mg/L; decreases in TCA cycle metabolites succinate, citrate, and α-ketoglutarate in kidney of ZnO-exposed rats at 100 mg/kg; declines in TCA cycle metabolites citrate, fumarate, and malate by 4, 3, and 5-fold, respectively, in Caenorhabditis elegans exposed to nano-TiO 2 at 7.7 mg/L; greater than 2-fold changes in expression of 115 electron transport chain (ETC) genes in human lung cells exposed to TiO 2 ENMs at 800 mg/L; greater than 2-fold increased expression of ETC proteins ATP-synthase and ETF-α in mouse liver cells exposed to TiO 2 ENMs at 1 mg/L and ETC protein cytochrome b-c1 from exposure to ZnO and CuO ENMs at 5 mg/mL; and 5-fold declines in NADH dehydrogenase activity and ATP production in mammalian cells exposed to Co 3 O 4 , Cr 2 O 3 , Ni 2 O 3 , CuO, Mn 2 O 3 , CoO, and ZnO ENMs at concentrations as low as 10 mg/L . In spite of this evidence, the broad implication of the impact of a range of metal oxide ENMs on as universally conserved processes as energy metabolism has not been recognized.…”