THE EFFECT OF ZINC ON ANAPHYLAXIS <i>in vivo</i> IN THE GUINEA‐PIG

Cho, C.H.; Dai, Soter; Ogle, C. W.

doi:10.1111/j.1476-5381.1977.tb07542.x

Cited by 12 publications

(4 citation statements)

References 8 publications

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“…In a murine model of ovalbumin-induced lung allergic hypersensitivity, zinc deprivation enhanced airway inflammation and epithelial damage (16). Similarly, brief exposure to aerosolized zinc sulfate protected guinea pigs against allergic bronchoconstriction and prevented most pulmonary complications associated with this model (5). In our investigation, we observed that zinc deprivation led to a substantial increase in lung epithelial susceptibility to extrinsic apoptosis and contributed to a loss of barrier function.…”

Section: Discussionmentioning

confidence: 82%

Zinc modulates airway epithelium susceptibility to death receptor-mediated apoptosis

Bao

Knoell

2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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The accelerated loss of lung epithelium through activation of extrinsic apoptosis is believed to play a causative role in lung pathogenesis. Previous investigations have shown that zinc is required to sustain lung epithelial cell viability under stress conditions and that depletion of intracellular zinc predisposes cells to apoptosis. In this investigation, we determined whether intracellular zinc deficiency enhanced the susceptibility of primary, differentiated cultures of human lung epithelium to death receptor-mediated apoptosis, leading to barrier dysfunction. Cultures obtained from multiple donors were exposed to stimuli that provoke death receptor-mediated apoptosis and depleted of intracellular zinc with a zinc-specific chelating agent. Transepithelial resistance, paracellular transport, caspase-8 and caspase-3 activity, and apoptosis were measured. Activation of extrinsic apoptosis or zinc chelation alone resulted in a nominal increase in caspase function and apoptosis without major evidence of barrier disruption. Activation of extrinsic apoptosis in addition to zinc depletion resulted in an abrupt decrease in transepithelial resistance, a substantial increase in apoptosis, and an increased paracellular leak. Cultures were rescued by supplementation with zinc sulfate. Further analysis revealed that exogenous zinc facilitates cell survival through activation of the phosphatidylinositol 3-kinase/Akt signaling pathway. We conclude that intracellular zinc is a vital factor in lung epithelium that protects cells from death receptor-mediated apoptosis and barrier dysfunction.

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Section: Discussionmentioning

confidence: 82%

Zinc modulates airway epithelium susceptibility to death receptor-mediated apoptosis

Bao

Knoell

2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Effects on histamine release may explain the protection by Zn sulphate aerosols against OVA-induced bronchoconstriction in guinea pigs [205] as well as inhibition by Zn gluconate of IgEdependent contraction of guinea pig trachea [206]. Zn also blocks eosinophil cationic protein release from eosinophils [207].…”

Section: Functional Consequencesmentioning

confidence: 97%

“…Issues that will need to be considered are Zn dosages, type of Zn compound, route of administration and concurrent therapy. While Zn has been administered into the nasal cavity by electrolysis to treat hay fever in humans [215] and by nebulization to prevent allergen-induced bronchoconstriction in sensitized guinea pigs [205], the most practical, natural and safest route is orally. In addition, Richter and colleagues [188] have demonstrated that addition of Zn to the drinking water was effective in decreasing airway eosinophilia in mice.…”

Section: Zinc Supplementationmentioning

confidence: 99%

Zinc and its Specific Transporters as Potential Targets in Airway Disease

Murgia

Lang

Truong-Tran

et al. 2006

CDT

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The dietary group IIb metal zinc (Zn) plays essential housekeeping roles in cellular metabolism and gene expression. It regulates a number of cellular processes including mitosis, apoptosis, secretion and signal transduction as well as critical events in physiological processes as diverse as insulin release, T cell cytokine production, wound healing, vision and neurotransmission. Critical to these processes are the mechanisms that regulate Zn homeostasis in cells and tissues. The proteins that control Zn uptake and compartmentalization are rapidly being identified and characterized. Recently, the first images of sub-cellular pools of Zn in airway epithelium have been obtained. This review discusses what we currently know about Zn in the airways, both in the normal and inflamed states, and then considers how we might target Zn metabolism by developing strategies to monitor and manipulate airway Zn levels in airway disease.

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“…In contrast brief exposures to zinc sulphate aerosols have been shown to protect against allergic bronchoconstriction in guinea pigs, possibly by blocking histamine release from mast cells 51 . Zinc has also been shown to directly decrease the incidence of respiratory infections in young children from developing countries.…”

Section: Is Zinc Beneficial or Detrimental For Respiratory Diseases?mentioning

confidence: 99%

New insights into the role of zinc in the respiratory epithelium

et al. 2001

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Summary Over the past 30 years, many researchers have demonstrated the critical role of zinc (Zn), a group IIb metal, in diverse physiological processes, such as growth and development, maintenance and priming of the immune system, and tissue repair. This review will discuss aspects of Zn physiology and its possible beneficial role in the respiratory epithelium. Here we have detailed the mechanisms by which Zn diversely acts as: (i) an antioxidant; (ii) an organelle stabilizer; (iii) an anti-apopototic agent; (iv) an important cofactor for DNA synthesis; (v) a vital component for wound healing; and (vi) an anti-inflammatory agent. This paper will also review studies from the authors' laboratory concerning the first attempts to map Zn in the respiratory epithelium and to elucidate its role in regulating caspase-3 activated apoptosis. We propose that Zn, being a major dietary anti-oxidant has a protective role for the airway epithelium against oxyradicals and other noxious agents. Zn may therefore have important implications for asthma and other inflammatory diseases where the physical barrier is vulnerable and compromised.

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THE EFFECT OF ZINC ON ANAPHYLAXIS in vivo IN THE GUINEA‐PIG

Cited by 12 publications

References 8 publications

Zinc modulates airway epithelium susceptibility to death receptor-mediated apoptosis

Zinc modulates airway epithelium susceptibility to death receptor-mediated apoptosis

Zinc and its Specific Transporters as Potential Targets in Airway Disease

New insights into the role of zinc in the respiratory epithelium

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