The Essential Toxin: Impact of Zinc on Human Health

Plum, Laura M.; Rink, Lothar; Haase, Hajo

doi:10.3390/ijerph7041342

Cited by 1,248 publications

(748 citation statements)

References 164 publications

(174 reference statements)

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“…There are several conflicting results showing how zinc can be anti-or pro-apoptotic depending on the zinc concentration used. Moreover, it has been observed that both zinc deficiency and supplementation induced apoptosis in the same cellular model [48].…”

Section: A Nf-κb and Other Signalling Pathwaymentioning

confidence: 97%

Zinc in Infection and Inflammation

Gammoh¹,

Rink²

2017

Preprint

Self Cite

187

139

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Abstract:Micronutrient homeostasis is a key factor in maintaining a healthy immune system. Zinc is an essential micronutrient that is involved in the regulation of the innate and adaptive immune responses. The main cause of zinc deficiency is malnutrition. Zinc deficiency leads to cell-mediated immune dysfunctions among other manifestations. Consequently, such dysfunctions lead to a worse outcome in the response towards bacterial infection and sepsis. For instance, zinc is an essential component of the pathogen-eliminating signal transduction pathways leading to neutrophil extracellular traps formation, as well as inducing cell-mediated immunity over humoral immunity by regulating specific factors or differentiation. Additionally, zinc deficiency plays a role in inflammation, mainly elevating inflammatory response as well as damage to host tissue. Zinc is involved in the modulation of the proinflammatory response by targeting Nuclear Factor Kappa B, a transcription factor that is the master regulator of proinflammatory responses. It is also involved in controlling oxidative stress and regulating inflammatory cytokines. Zinc plays an intricate function during an immune response and its homeostasis is critical for sustaining proper immune function. This review will summarize the latest findings concerning the role of this micronutrient during the course of infections and inflammatory response and how the immune system modulates zinc depending on different stimuli.

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Section: A Nf-κb and Other Signalling Pathwaymentioning

confidence: 97%

Zinc in Infection and Inflammation

Gammoh¹,

Rink²

2017

Preprint

Self Cite

187

139

View full text Add to dashboard Cite

show abstract

“…50 The intracellular dissolution hypothesis could explain the decreased mitochondrial activity observed in ZnO-treated cells. Zinc ions have been shown to be proapoptotic under certain circumstances 51 and the solubilized ZnO released from the endosomes could be causing toxicity by inhibiting energy metabolism. [51][52][53] However, as Figure 10 shows, none of the three particles had any influence on the rate of proliferation of the cells.…”

Section: Zinc Oxidementioning

confidence: 99%

Minimal Intestinal Epithelial Cell Toxicity in Response to Short- and Long-Term Food-Relevant Inorganic Nanoparticle Exposure

McCracken

Zane

Knight

et al. 2013

Chem. Res. Toxicol.

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Toxicity of commercial nanoparticles of titania, silica, and zinc oxides is being investigated in this in vitro study. Particles of these compositions are found in many food items, and thus this study is directed toward particle behavior in simulated digestion media and their interaction with intestinal epithelial cell line C2BBe1, a clone of Caco-2 cells, originally isolated from a human colon cancer. Even though the primary particle size of all three particles was below 50 nm, the particles appeared as aggregates in culture media with a negatively charged surface. In the presence of pepsin (pH 2), the charge on the titania became positive, and silica was almost neutral and aggregated extensively, whereas ZnO dissolved. For silica and titania, treatment with simulated intestinal digestive solution led to a strongly negatively charged surface and particle sizes approaching values similar to those in media. On the basis of infrared spectroscopy, we concluded that the surface of silica and titania was covered with bile salts/proteins after this treatment. Transmission electron microscopy indicated that the C2BBe1 cells internalized all three particles. Toxicity assays included investigation of necrosis, apoptosis, membrane damage, and mitochondrial activity. Titania and SiO2 particles suspended in media at loading levels of 10 μg/cm2 exhibited no toxicity. With ZnO at the same loading level, mild toxicity was observed based only on the LDH assay and decrease of mitochondrial activity and not necrosis or apoptosis. Titania particles exposed to the simulated digestion media exhibited mild toxicity based on decrease of mitochondrial activity, likely due to transport of toxic bile salts via adsorption on the particle surface.

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“…The inability to tightly control zinc transport rapidly leads to cellular dysfunction and death (46). For example, zinc exposure ubiquitinates and degrades the yeast zinc uptake transporter ZRT1 (23).…”

Section: Discussionmentioning

confidence: 99%