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The acidic transformed nano-VO₂ causes macrophage cell death by the induction of lysosomal membrane permeabilization and Ca²⁺ efflux.

ABSTRACT: Because of its outstanding thermochromic characteristics and metal-insulator transition (MIT) property, nano-vanadium dioxide (abbreviated as nano-VO₂ or nVO₂) has been applied widely in electrical/optical devices and design of intelligent window. However, the biological effect of nVO₂ is not well understood, especially when affected by environmental factors or living organisms. For VO₂ is an amphoteric oxide, we simulated pH's influence to nVO₂'s physicochemical properties by exposure nVO₂ in water of different pH values. We found that nVO₂ transformed to a new product after exposure in acidic water for two weeks, as revealed by physicochemical characterization such as SEM, TEM, XRD, and DLS. This transformation product formed in acidic water was referred as (acidic) transformed nVO₂). Both pristine/untransformed and transformed nVO₂ displayed no obvious toxicity to common epithelial cells; however, the acidic transformed nVO₂ rapidly induced macrophage cell death. Further investigation demonstrated that transformed nVO₂ caused macrophage apoptosis by the induction of Ca²⁺ efflux and the following mitochondrial membrane permeabilization (MMP) process. And a more detailed time course study indicated that transformed nVO₂ caused lysosomal membrane permeabilization (LMP) at the earlier stage, indicating LMP could be chosen as an earlier and sensitive end point for nanotoxicological study. We conclude that although nVO₂ displays no acute toxicity, its acidic transformation product induces macrophage apoptosis by the induction of LMP and Ca²⁺ efflux. This report suggests that the interplay with environmental factors or living organisms can results in physicochemical transformation of nanomaterials and the ensuing distinctive biological effects.

SUBMITTER: Xu S

PROVIDER: S-EPMC5598166 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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The acidic transformed nano-VO2 causes macrophage cell death by the induction of lysosomal membrane permeabilization and Ca2+ efflux.

Xu Shaohai S Xu Shengmin S Chen Shaopeng S Fan Huadong H Luo Xun X Sun Yuxiang Y Wang Jun J Yuan Hang H Xu An A Wu Lijun L

Toxicology reports 20150610

Because of its outstanding thermochromic characteristics and metal-insulator transition (MIT) property, nano-vanadium dioxide (abbreviated as nano-VO2 or nVO2) has been applied widely in electrical/optical devices and design of intelligent window. However, the biological effect of nVO2 is not well understood, especially when affected by environmental factors or living organisms. For VO2 is an amphoteric oxide, we simulated pH's influence to nVO2</ ...[more]

PMID: 28962423

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Project description:Mitochondrial Ca2+ handling is accomplished by balancing Ca2+ uptake, primarily via the Ru360-sensitive mitochondrial calcium uniporter (MCU), Ca2+ buffering in the matrix and Ca2+ efflux mainly via Ca2+ ion exchangers, such as the Na+/Ca2+ exchanger (NCLX) and the Ca2+/H+ exchanger (CHE). The mechanism of CHE in cardiac mitochondria is not well-understood and its contribution to matrix Ca2+ regulation is thought to be negligible, despite higher expression of the putative CHE protein, LETM1, compared to hepatic mitochondria. In this study, Ca2+ efflux via the CHE was investigated in isolated rat cardiac mitochondria and permeabilized H9c2 cells. Mitochondria were exposed to (a) increasing matrix Ca2+ load via repetitive application of a finite CaCl2 bolus to the external medium and (b) change in the pH gradient across the inner mitochondrial membrane (IMM). Ca2+ efflux at different matrix Ca2+ loads was revealed by inhibiting Ca2+ uptake or reuptake with Ru360 after increasing number of CaCl2 boluses. In Na+-free experimental buffer and with Ca2+ uptake inhibited, the rate of Ca2+ efflux and steady-state free matrix Ca2+ [mCa2+]ss increased as the number of administered CaCl2 boluses increased. ADP and cyclosporine A (CsA), which are known to increase Ca2+ buffering while maintaining a constant [mCa2+]ss, decreased the rate of Ca2+ efflux via the CHE, with a significantly greater decrease in the presence of ADP. ADP also increased Ca2+ buffering rate and decreased [mCa2+]ss. A change in the pH of the external medium to a more acidic value from 7.15 to 6.8∼6.9 caused a twofold increase in the Ca2+ efflux rate, while an alkaline change in pH from 7.15 to 7.4∼7.5 did not change the Ca2+ efflux rate. In addition, CHE activation was associated with membrane depolarization. Targeted transient knockdown of LETM1 in permeabilized H9c2 cells modulated Ca2+ efflux. The results indicate that Ca2+ efflux via the CHE in cardiac mitochondria is modulated by acidic buffer pH and by total matrix Ca2+. A mechanism is proposed whereby activation of CHE is sensitive to changes in both the matrix Ca2+ buffering system and the matrix free Ca2+ concentration.

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The acidic transformed nano-VO₂ causes macrophage cell death by the induction of lysosomal membrane permeabilization and Ca²⁺ efflux.

Publications

The acidic transformed nano-VO<sub>2</sub> causes macrophage cell death by the induction of lysosomal membrane permeabilization and Ca<sup>2+</sup> efflux.

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