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Reversible Inhibition of Iron Oxide Nanozyme by Guanidine Chloride.

ABSTRACT: Nanozymes have been widely applied in bio-assays in the field of biotechnology and biomedicines. However, the physicochemical basis of nanozyme catalytic activity remains elusive. To test whether nanozymes exhibit an inactivation effect similar to that of natural enzymes, we used guanidine chloride (GuHCl) to disturb the iron oxide nanozyme (IONzyme) and observed that GuHCl induced IONzyme aggregation and that the peroxidase-like activity of IONzyme significantly decreased in the presence of GuHCl. However, the aggregation appeared to be unrelated to the quick process of inactivation, as GuHCl acted as a reversible inhibitor of IONzyme instead of a solo denaturant. Inhibition kinetic analysis showed that GuHCl binds to IONzyme competitively with H₂O₂ but non-competitively with tetramethylbenzidine. In addition, electron spin resonance spectroscopy showed that increasing GuHCl level of GuHCl induced a correlated pattern of changes in the activity and the state of the unpaired electrons of the IONzymes. This result indicates that GuHCl probably directly interacts with the iron atoms of IONzyme and affects the electron density of iron, which may then induce IONzyme inactivation. These findings not only contribute to understanding the essence of nanozyme catalytic activity but also suggest a practically feasible method to regulate the catalytic activity of IONzyme.

SUBMITTER: Mo WC

PROVIDER: S-EPMC7301555 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Reversible Inhibition of Iron Oxide Nanozyme by Guanidine Chloride.

Mo Wei-Chuan WC Yu Jia J Gao Li-Zeng LZ Liu Ying Y Wei Yan Y He Rong-Qiao RQ

Frontiers in chemistry 20200611

Nanozymes have been widely applied in bio-assays in the field of biotechnology and biomedicines. However, the physicochemical basis of nanozyme catalytic activity remains elusive. To test whether nanozymes exhibit an inactivation effect similar to that of natural enzymes, we used guanidine chloride (GuHCl) to disturb the iron oxide nanozyme (IONzyme) and observed that GuHCl induced IONzyme aggregation and that the peroxidase-like activity of IONzyme significantly decreased in the presence of GuH ...[more]

PMID: 32596209

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Project description:Rational:Salmonella Enteritidis (S. Enteritidis) is a globally significant zoonotic foodborne pathogen which has led to large numbers of deaths in humans and caused economic losses in animal husbandry. S. Enteritidis invades host cells and survives within the cells, causing resistance to antibiotic treatment. Effective methods of elimination and eradication of intracellular S. Enteritidis are still very limited. Here we evaluated whether a new intracellular antibacterial strategy using iron oxide nanozymes (IONzymes) exerted highly antibacterial efficacy via its intrinsic peroxidase-like activity in vitro and in vivo.Methods: The antibacterial activities of IONzymes against planktonic S. Enteritidis, intracellular S. Enteritidis in Leghorn Male Hepatoma-derived cells (LMH), and liver from specific pathogen free (SPF) chicks were investigated by spread-plate colony count method and cell viability assay. Changes in levels of microtubule-associated protein light chain 3 (LC3), a widely used marker for autophagosomes, were analyzed by immunoblotting, immunofluorescence, and electron microscopy. Reactive oxygen species (ROS) production was also assessed in vitro. High-throughput RNA sequencing was used to investigate the effects of IONzymes on liver transcriptome of S. Enteritidis-infected chicks. Results: We demonstrated that IONzymes had high biocompatibility with cultured LMH cells and chickens, which significantly inhibited intracellular S. Enteritidis survival in vitro and in vivo. In addition, co-localization of IONzymes with S. Enteritidis were observed in autophagic vacuoles of LMH cells and liver of chickens infected by S. Enteritidis, indicating that IONzymes mediated antibacterial reaction of S. Enteritidis with autophagic pathway. We found ROS level was significantly increased in infected LMH cells treated with IONzymes, which might enhance the autophagic elimination of intracellular S. Enteritidis. Moreover, orally administered IONzymes decreased S. Enteritidis organ invasion of the liver and prevented pathological lesions in a chicken-infection model. Non-target transcriptomic profiling also discovered IONzymes could change hepatic oxidation-reduction and autophagy related gene expressions in the S. Enteritidis infected chickens. Conclusion: These data suggest that IONzymes can increase ROS levels to promote the antibacterial effects of acid autophagic vacuoles, and thus suppress the establishment and survival of invading intracellular S. Enteritidis. As a result, IONzymes may be a novel alternative to current antibiotics for the control of intractable S. Enteritidis infections.

Project description:BackgroundIron oxide nanoparticles (IONPs) have been extensively studied in different biomedical fields. Recently, the non-cytotoxic concentration of IONPs induced cell-specific response raised concern of their safety. Endothelial cell exposure was unavoidable in their applications, while whether IONPs affect the phenotype of vascular endothelial cells is largely unknown. In this work, the effect of IONPs on endothelial-to-mesenchymal transition (EndMT) was investigated in vitro and in vivo.ResultsThe incubation with γ-Fe2O3 nanoparticles modified with polyglucose sorbitol carboxymethyether (PSC-Fe2O3) at non-cytotoxic concentration induced morphological changes of human umbilical vein endothelial cells (HUVECs) from cobblestone-like to spindle mesenchymal-like morphology, while PSC-Fe2O3 mostly stay in the culture medium and intercellular space. At the same time, the endothelial marker CD31 and VE-cadherin was decreased along with the inhibitory of angiogenesis properties of HUVEC. Meanwhile, the mesenchymal marker α-smooth muscle actin (α-SMA) and fibroblast specific protein (FSP) was up regulated significantly, and the migration ability of the cells was enhanced. When ROS scavenger mannitol or AA was supplemented, the EndMT was rescued. Results from the in vivo study showed that, expression of CD31 was decreased and α-SMA increased in the liver, spleen and kidney of mice given PSC-Fe2O3, and the density of collagen fibers in the liver sinusoid of mice was increased. The supplementary mannitol or AA could reverse the degree of EndMT in the tissues. Mechanistic study in vitro indicated that the level of extracellular hydroxyl radicals (·OH) was up regulated significantly by PSC-Fe2O3, which induced the response of intracellular ROS and resulted in the EndMT effect on HUVECs.ConclusionThe PSC-Fe2O3 was capable of inducing EndMT in the endothelial cells at acutely non-cytotoxic dose due to its intrinsic peroxidase-like activity, though they were few taken up by endothelial cell. The EndMT effect on HUVEC can be rescued by ROS scavenger in vitro and in vivo.

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Reversible Inhibition of Iron Oxide Nanozyme by Guanidine Chloride.

Publications

Reversible Inhibition of Iron Oxide Nanozyme by Guanidine Chloride.

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