Dysfunction of methionine sulfoxide reductases to repair damaged proteins by nickel nanoparticles

Feng, Po Hao; Huang, Ya; Chuang, Kai Jen; Chen, Kuan Yuan; Lee, Kang Yun; Ho, Shu-Chuan; Bien, Mauo Ying; You, Yang; Chuang, Hsiao Chi

doi:10.1016/j.cbi.2015.05.003

Cited by 13 publications

(6 citation statements)

References 37 publications

(43 reference statements)

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“…ROS are reactive molecular species with an unpaired electron in their outer orbit 29 , so they can easily extract a second electron from a neighboring molecule. Previous reports showed that BPDE is formed due to protein adduct caused by benzo[a]pyrene 30 and metals 31 . Our results showed that significant BPDE protein damage occurred by DEP exposure of A549 cells.…”

Section: Discussionmentioning

confidence: 99%

Protein oxidation and degradation caused by particulate matter

Lai

Lee

Bai

et al. 2016

Sci Rep

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Particulate matter (PM) modulates the expression of autophagy; however, the role of selective autophagy by PM remains unclear. The objective of this study was to determine the underlying mechanisms in protein oxidation and degradation caused by PM. Human epithelial A549 cells were exposed to diesel exhaust particles (DEPs), urban dust (UD), and carbon black (CB; control particles). Cell survival and proliferation were significantly reduced by DEPs and UD in A549 cells. First, benzo(a)pyrene diolepoxide (BPDE) protein adduct was caused by DEPs at 150 μg/ml. Methionine oxidation (MetO) of human albumin proteins was induced by DEPs, UD, and CB; however, the protein repair mechanism that converts MetO back to methionine by methionine sulfoxide reductases A (MSRA) and B3 (MSRB3) was activated by DEPs and inhibited by UD, suggesting that oxidized protein was accumulating in cells. As to the degradation of oxidized proteins, proteasome and autophagy activation was induced by CB with ubiquitin accumulation, whereas proteasome and autophagy activation was induced by DEPs without ubiquitin accumulation. The results suggest that CB-induced protein degradation may be via an ubiquitin-dependent autophagy pathway, whereas DEP-induced protein degradation may be via an ubiquitin-independent autophagy pathway. A distinct proteotoxic effect may depend on the physicochemistry of PM.

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Section: Discussionmentioning

confidence: 99%

Protein oxidation and degradation caused by particulate matter

Lai

Lee

Bai

et al. 2016

Sci Rep

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“…These include protein and lipid peroxidation, the formation of DNA-protein crosslinks and DNA breakage. Protein oxidation is considered to be one of the main causes of cell death, resulting in accumulation of aberrant proteins and the loss of their function [69]. As cells are part of a huge membrane system, lipid peroxidation also results in a loss of membrane permeability and integrity.…”

Section: Apoptosis Pathways Involved In Enp Cytotoxicitymentioning

confidence: 99%

Engineered nanoparticles induce cell apoptosis: potential for cancer therapy

Yang

2016

Oncotarget

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Engineered nanoparticles (ENPs) have been widely applied in industry, commodities, biology and medicine recently. The potential for many related threats to human health has been highlighted. ENPs with their sizes no larger than 100 nm are able to enter the human body and accumulate in organs such as brain, liver, lung, testes, etc, and cause toxic effects. Many references have studied ENP effects on the cells of different organs with related cell apoptosis noted. Understanding such pathways towards ENP induced apoptosis may aid in the design of effective cancer targeting ENP drugs. Such ENPs can either have a direct effect towards cancer cell apoptosis or can be used as drug delivery agents. Characteristics of ENPs, such as sizes, shape, forms, charges and surface modifications are all seen to play a role in determining their toxicity in target cells. Specific modifications of such characteristics can be applied to reduce ENP bioactivity and thus alleviate unwanted cytotoxicity, without affecting the intended function. This provides an opportunity to design ENPs with minimum toxicity to non-targeted cells.

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“…16 Exposure of A549 cells to Ni NPs also caused increased protein oxidation, such as methionine oxidation, and decreased oxidized protein repair and degradation, as evidenced by downregulation of methionine repairing enzymes, such as methionine sulfoxide reductase A (MSRA) and methionine sulfoxide reductase B3 (MSRB3), and autophagy marker LC3. 17 Increased protein expression of antioxidant response-associated protein HO-1, but not Nrf2, was found in A549 cells exposed to Ni NPs. 18 However, others found no significant increase in ROS in BEAS-2B 24 or A549 cells 19 after Ni NP exposure.…”

Section: Cytotoxic Effects Of Ni Nps On Human Lung Cells In Vitromentioning

confidence: 92%