It’s official! Our provisionally-accepted manuscript, “Physiological hepatic response to zinc oxide nanoparticle exposure in the white sucker, Catostomus commersonii,” was revised and has now received final acceptance in the journal Comparative Biochemistry and Physiology – Part C: Toxicology and Pharmacology. We’re proud to say that the editors informed us of the good news a little over 21 hours after we resubmitted the manuscript.
Among the authors for this manuscript are Chris and both of his honours students, Neal Callaghan and Patrick Gormley. In addition, Tyson MacCormack and one of his alumni, current UPEI veterinary student Kathryn Butler are also authors. All research was carried out in the MacCormack Lab.
Updates will be made as soon as information is available with regards to publication status and DOI. In the meantime, we present an abstract for your convenience.
Physiological hepatic response to zinc oxide nanoparticle exposure in the white sucker, Catostomus commersonii
Christopher Anthony Dieni*, Neal Ingraham Callaghan, Patrick Thomas Gormley, Kathryn Marie Alison Butler, Tyson James MacCormack
* To whom correspondence should be addressed: Department of Chemistry and Biochemistry, Mount Allison University, Barclay Chemistry Building, 63C York Street, Sackville, New Brunswick, Canada, E4L 1G8. Email: email@example.com. Tel: 506-364-2588. Fax: 506-364-2455
Liver toxicity of commercially relevant zinc oxide nanoparticles (nZnO) was assessed in a benthic freshwater cypriniform, the white sucker (Catostomus commersonii). Exposure to nZnO caused several changes in levels of liver enzyme activity, antioxidants, and lipid peroxidation end products consistent with an oxidative stress response. Aconitase activity decreased by ~65% but tended to be restored to original levels upon supplementation with Fe2+, indicating oxidative inactivation of the 4Fe-4S cluster. Furthermore, glucose-6-phosphate dehydrogenase activity decreased by ~29%, and glutathione levels increased by ~56%. Taken together, these suggest that nZnO induces hepatic physiological stress. Each assay was then validated by using a single liver homogenate or plasma sample that was partitioned and treated with nZnO or Zn2+, the breakdown product of nZnO. It was found that Zn2+, but not nZnO, increased detected glutathione reductase activity by ~14% and decreased detected malondialdehyde by ~39%. This indicates that if appreciable nZnO dissolution occurs in liver samples during processing and assay, it may skew results, with implications not only for this study, but for a wide range of nanotoxicology studies focusing on nZnO. Finally, in vitro incubations of cell-free rat blood plasma with nZnO failed to generate any significant increase in malondialdehyde or protein carbonyl levels, or any significant decrease in ferric reducing ability of plasma. This suggests that at the level tested, any oxidative stress caused by nZnO is the result of a coordinated physiological response by the liver.
Assay validation, fish, liver response, nanotoxicity, oxidative stress, zinc oxide nanoparticles