Oxidative stress by inorganic nanoparticles

Tee, Jie Kai; Ong, Choon Nam; Bay, Boon Huat; Ho, Han Kiat; Leong, David Tai

doi:10.1002/wnan.1374

Cited by 103 publications

(68 citation statements)

References 178 publications

(320 reference statements)

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“…Besides cytotoxicity, previous study also found that silica coating significantly reduce DNA damage induced by ZnO nanorods [51]. Comparison between ZnO NPs and SiO 2 NPs also found that ZnO NPs are more toxic [52, 53, 54, 55]. …”

Section: Resultsmentioning

confidence: 98%

Reducing ZnO nanoparticles toxicity through silica coating

Chia

Leong

2016

Heliyon

Self Cite

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ZnO NPs have good antimicrobial activity that can be utilized as agents to prevent harmful microorganism growth in food. However, the use of ZnO NPs as food additive is limited by the perceived high toxicity of ZnO NPs in many earlier toxicity studies. In this study, surface modification by silica coating was used to reduce the toxicity of ZnO NPs by significantly reducing the dissolution of the core ZnO NPs. To more accurately recapitulate the scenario of ingested ZnO NPs, we tested our as synthesized ZnO NPs in ingestion fluids (synthetic saliva and synthetic gastric juice) to determine the possible forms of ZnO NPs in digestive system before exposing the products to colorectal cell lines. The results showed that silica coating is highly effective in reducing toxicity of ZnO NPs through prevention of the dissociation of ZnO NPs to zinc ions in both neutral and acidic condition. The silica coating however did not alter the desired antimicrobial activity of ZnO NPs to E. coli and S. aureus. Thus, silica coating offered a potential solution to improve the biocompatibility of ZnO NPs for applications such as antimicrobial agent in foods or food related products like food packaging. Nevertheless, caution remains that high concentration of silica coated ZnO NPs can still induce undesirable cytotoxicity to mammalian gut cells. This study indicated that upstream safer-by-design philosophy in nanotechnology can be very helpful in a product development.

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Section: Resultsmentioning

confidence: 98%

Reducing ZnO nanoparticles toxicity through silica coating

Chia

Leong

2016

Heliyon

Self Cite

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“…The protein function is specific to one conformation and an alteration can cause important cell injuries [114]. Both AgNPs and Ag + ions have been shown to interact with proteins, thereby leading to altered conformation, deactivation and even degradation [112,[115][116][117]. When AgNPs bind to proteins, they form corona structures and can express genes involved in DNA damage [112].…”

Section: Discussionmentioning

confidence: 99%

Genotoxicity of Silver Nanoparticles

et al. 2020

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Silver nanoparticles (AgNPs) are widely used in diverse sectors such as medicine, food, cosmetics, household items, textiles and electronics. Given the extent of human exposure to AgNPs, information about the toxicological effects of such products is required to ensure their safety. For this reason, we performed a bibliographic review of the genotoxicity studies carried out with AgNPs over the last six years. A total of 43 articles that used well-established standard assays (i.e., in vitro mouse lymphoma assays, in vitro micronucleus tests, in vitro comet assays, in vivo micronucleus tests, in vivo chromosome aberration tests and in vivo comet assays), were selected. The results showed that AgNPs produce genotoxic effects at all DNA damage levels evaluated, in both in vitro and in vivo assays. However, a higher proportion of positive results was obtained in the in vitro studies. Some authors observed that coating and size had an effect on both in vitro and in vivo results. None of the studies included a complete battery of assays, as recommended by ICH and EFSA guidelines, and few of the authors followed OECD guidelines when performing assays. A complete genotoxicological characterization of AgNPs is required for decision-making.

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“…More importantly, the higher level of TUNEL staining in the ZnO NP-treated group implied that keratinocyte apoptosis was increased and that the histological foundation for epidermal renewal capacity was impaired. Oxidative stress is generally thought to play a pivotal role in the mechanism by which nanomaterials damage cells [31]. The higher level of 8-OHdG staining in the ZnO NP-treated group revealed that ZnO NPs promoted DNA damage related to oxidative stress in pathological keratinocytes.…”

Section: Discussionmentioning

confidence: 87%

“…GSH prevents proteins from being damaged by ROS by oxidizing their own thiol groups [32]. The MDA level indicates the extent of lipid peroxidation [31]. The disturbance of GSH antioxidant system and the increased MDA level in the ZnO NP-treated group revealed the potential mechanism by which ZnO NPs promote in ammation and keratinocyte apoptosis in pathological skin.…”

Section: Discussionmentioning

confidence: 99%

ZnO NPs delay the recovery of psoriasis-like skin lesions through promoting inflammation and keratinocyte apoptosis via nuclear translocation of phosphorylated NF-κB p65 and cysteine deficiency

Lai

Wang

Zhu

et al. 2020

Preprint

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Background This study aimed to confirm the safety and risk of applying zinc oxide nanoparticles (ZnO NPs) to pathological skin, such as psoriasis-like skin. The majority of previous studies confirmed the safety of applying ZnO NPs to normal skin. However, we know very little about the risks of using sunscreen, cosmetics and topical drugs containing ZnO NPs for individuals with skin diseases. In addition, some studies claimed that ZnO NPs can penetrate normal or pathological skin, and ZnO NPs have frequently been reported to have proinflammatory and lethal effects in vitro. Therefore, it is necessary to evaluate the safety of applying ZnO NPs to pathological skin. Results ZnO NPs passed through gaps between keratinocytes and entered stratum basale of epidermis and dermis in imiquimod (IMQ)-induced psoriasis-like skin lesions. Application of a ZnO NP-containing suspension for 3 connective days delayed the healing of the epidermal barrier; increased the expression levels of inflammatory cytokines; promoted keratinocyte apoptosis and disturbed redox homeostasis. In vitro, ZnO NPs promoted TNF-α, IL-1β and IL-6 secretion and apoptosis of recombinant-human-TNF-α-stimulated HaCaT cells. NF-κB, ERK, p38 and JNK inhibitors blocked ZnO NP-induced inflammation. JSH-23, an inhibitor of the nuclear translocation of p-NF-κB p65, and NAC, an acetylated precursor of L-cysteine, not only inhibited the ZnO NP-induced inflammation but also inhibited apoptosis and cysteine deficiency. Neither erastin nor RSL3 induced p-NF-κB p65 nuclear translocation, but they did reduce cysteine biosynthesis. Additionally, ferropstatin-1, an inhibitor of lipid peroxidation, partially rescued ZnO NP-induced decreases in cell viability and cysteine content. Conclusions ZnO NPs delay the recovery of psoriasis-like skin lesions through promoting inflammation and keratinocyte apoptosis via the nuclear translocation of phosphorylated NF-κB p65 and cysteine deficiency. This work reminds the public that ZnO NPs are not safe for pathological skin, especially in inflammatory skin diseases such as psoriasis, and has revealed a partial mechanism by which ZnO NPs delay the recovery of pathological skin, promoting the appropriate use of ZnO NPs.

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Oxidative stress by inorganic nanoparticles

Cited by 103 publications

References 178 publications

Reducing ZnO nanoparticles toxicity through silica coating

Reducing ZnO nanoparticles toxicity through silica coating

Genotoxicity of Silver Nanoparticles

ZnO NPs delay the recovery of psoriasis-like skin lesions through promoting inflammation and keratinocyte apoptosis via nuclear translocation of phosphorylated NF-κB p65 and cysteine deficiency

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