Mitochondrial dysfunction induced by ultra-small silver nanoclusters with a distinct toxic mechanism

Dong, Ping; Li, Jia-Han; Xu, Shiping; Wu, Xiaojuan; Xiang, Xun; Yang, Qiqi; Jin, Jian-Cheng; Liu, Yi; Jiang, Feng-Lei

doi:10.1016/j.jhazmat.2016.01.017

Cited by 39 publications

(15 citation statements)

References 78 publications

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“…It is well known that prolonged inflammatory responses involving ROS generation, such as those experienced with chronic NP exposure, impairs mitochondrial function. ROS‐induced stress from TiO 2 , ZnO, Ag, SiO 2 , and cationic liposome NPs has been shown to damage the mitochondrial membrane via oxidation of membrane lipids, alteration of membrane potential, and change in permeability through both mitochondrial permeability transition pore (MPT)‐dependent and independent pathways . Increases in intracellular Ca 2+ levels as a result of ROS generation further contribute to mitochondrial damage by disrupting the normal rate and functioning of ATP synthesis .…”

Section: Np Exposure Leads To Release Of Endogenous Danger Signalsmentioning

confidence: 99%

“…When mitochondrial function is compromised, mtDNA is capable of translocating into the cytosol through MPT pores, as with Ag NP exposure, leaking through gaps in severely damaged membrane, as with cation‐NP exposure, or through Bax/Bak pore formation during apoptosis . Once in the cytosol, mtDNA acts as a DAMP, binding intracellular DNA recognition receptors and activating proinflammatory type 1 interferon responses, especially NLRs and TLR9.…”

Section: Np Exposure Leads To Release Of Endogenous Danger Signalsmentioning

confidence: 99%

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Nanoparticles and danger signals: Oral delivery vehicles as potential disruptors of intestinal barrier homeostasis

Vita

Royse

Pullen

2019

Journal of Leukocyte Biology

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Gut immune system homeostasis involves diverse structural interactions among resident microbiota, the protective mucus layer, and a variety of cells (intestinal epithelial, lymphoid, and myeloid). Due to the substantial surface area in direct contact with an "external" environment and the diversity of xenobiotic, abiotic, and self-interactions coordinating to maintain gut homeostasis, there is enhanced potential for the generation of endogenous danger signals when this balance is lost. Here, we focus on the potential generation and reception of damage in the gut resulting from exposure to nanoparticles (NPs), common food and drug additives. Specifically, we describe recent evidence in the literature showing that certain NPs are potential generators of damage-associated molecular patterns, as well as potential immune-stimulating molecular patterns themselves. K E Y W O R D SATP, DAMP, mtDNA, NAMP, Nanoparticles, NLRP3Over the past decade, the commercial use of NPs by the food and biomedical industries has seen immense growth. The small, nanoscale size of NPs confers unique physicochemical properties that allow them to be effective oral delivery mechanisms for pharmaceuticals, food flavors, nutrient additives, and more. The accepted size range of NPs is not straightforward, varying across different biomedical and engineering disciplines and government agencies. 10,11 Although certain sources indicate that a typical NP is 1-100 nm in three dimensions, other sources consider accepted dimensions (one or more) for NPs to include <200 nm, 12 <500 nm, 13 or as large as <1000 nm. 14,15 The ASTM International definition provides for either two or three dimensions at the nanoscale, 16 whereas the ISO definition indicates nanoscale in three dimensions. 17 In an officially issued

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Section: Np Exposure Leads To Release Of Endogenous Danger Signalsmentioning

confidence: 99%

Section: Np Exposure Leads To Release Of Endogenous Danger Signalsmentioning

confidence: 99%

Nanoparticles and danger signals: Oral delivery vehicles as potential disruptors of intestinal barrier homeostasis

Vita

Royse

Pullen

2019

Journal of Leukocyte Biology

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“…Mitochondrial permeabilization was tested by using an ultraviolet-visible spectrophotometer (UNICO, USA) to measure the absorbance at 540 nm for 8 min at 25°C. 31…”

Section: Mitochondrial Swellingmentioning

confidence: 99%

Mitochondrial toxicity of organic arsenicals: membrane permeability transition pore opening and respiratory dysfunction

Fan

Yuan

et al. 2018

Toxicol. Res.

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In order to clarify the mitochondrial toxicity mechanism of the organic arsenical (2-methoxy-4-(((4-(oxoarsanyl) phenyl) imino) methyl) phenol), research was carried out at the sub-cell level based on the previous finding that the compound can damage the mitochondria by triggering a burst of ROS. After investigating its influence on isolated mitochondria , it was demonstrated that a high dose of with short-term exposure can induce mitochondrial swelling, decrease the membrane potential, enhance the permeability of H and K, and induce membrane lipid peroxidation, indicating that it can result in an MPT process in a ROS-mediated and Ca-independent manner. Additionally, MPT was also aggravated as a result of impairment of the membrane integrity and membrane fluidity. In addition, short-term incubation between mitochondria and compound promoted the inhibition of respiratory chain complexes I, II, III and IV, as well as damage to the respiration process, which supported the previous finding about the burst of ROS. On the other hand, after long-term exposure by the organic arsenical, mitochondrial metabolic dysfunction was triggered, which was in accordance with perturbation of the respiratory chain complexes as well as the respiration process. This work systematically sheds light on the mitochondrial toxicity mechanism of the organic arsenical , including induction of the MPT process and inhibition of respiratory metabolism, which provides a potential target for organic arsenicals as anti-tumor drugs.

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“…The liver mitochondria were separated and purified through gradient centrifugation. 27,28 The protocols were performed at 0-4°C. The rat liver was quickly sheared and washed with solution A three times.…”

Section: Isolation Of Mitochondriamentioning

confidence: 99%

Mitochondrial toxicity induced by a thiourea gold(i) complex: mitochondrial permeability transition and respiratory deficit

Jin

et al. 2018

Toxicol. Res.

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Mitochondrial dysfunction induced by ultra-small silver nanoclusters with a distinct toxic mechanism

Cited by 39 publications

References 78 publications

Nanoparticles and danger signals: Oral delivery vehicles as potential disruptors of intestinal barrier homeostasis

Nanoparticles and danger signals: Oral delivery vehicles as potential disruptors of intestinal barrier homeostasis

Mitochondrial toxicity of organic arsenicals: membrane permeability transition pore opening and respiratory dysfunction

Mitochondrial toxicity induced by a thiourea gold(i) complex: mitochondrial permeability transition and respiratory deficit

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