Pathophysiology of Zinc

Chvapil, Miloš; Elias, Sharon; Ryan, Janet N.; Zukoski, Charles F.

doi:10.1016/b978-0-12-366851-6.50010-7

Cited by 24 publications

(10 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…C h v a pil et at. reported a stabilization of lysosomal membrane by Zn^+ [1], an inhibition of endogenous and CCU-stimulated peroxidation of membrane lipid by Zn++ in vitro [2], and reduced ability of collagen to aggregate platelets in the presence of Zn++ [3], In either case, stabilizing effect of Zn^+ follows the uptake of Zn++ onto the membrane. Furthermore, bivalent metal ions are shown to contract or expand the phospholipid monolayer.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of the Terminal Stage of Complement-Mediated Lysis (Reactive Lysis) by Zinc and Copper Ions

Yamamoto

Takahashi

1975

Int Arch Allergy Immunol

View full text Add to dashboard Cite

The effect of various metal ions, Fe⁺⁺, Fe⁺⁺⁺, Cu⁺⁺, Zn⁺⁺, Co⁺⁺, on the terminal stage of reactive lysis (a form of complement-mediated hemolysis in which only late-acting components of complement are required) was studied. Only Cu⁺⁺ and Zn⁺⁺ exhibited an inhibitory effect on the lysis of EC5678 (sheep erythrocytes reacted with C56, C7 and C8) induced by C9. The mode of action of these metal ions was further explored. Both Cu⁺⁺ and Zn⁺⁺ inhibited the formation of hemolytically active EC56789 from EC5678 and C9. Their effect appeared to be primarily due to the inhibition of C9 binding to EC5678 through their reversible interaction with C9. Furthermore, Cu⁺⁺ is shown to inactivate irreversibly the hemolytic activity of EC5678. EC5678 pretreated with Cu⁺⁺ was capable of binding C9, but the resulting EC56789 was hemolytically inactive. Besides their effect on complement, both metal ions were shown to affect directly the erythrocyte membrane, since the mechanical lysis of hemolytic intermediate cells (E, EC567, EC5678) was suppressed by Cu⁺⁺ and Zn⁺⁺. The lysis of EC56789, a process of internal activation, was also inhibited by both Cu⁺⁺ and Zn⁺⁺.

show abstract

Section: Discussionmentioning

confidence: 99%

Inhibition of the Terminal Stage of Complement-Mediated Lysis (Reactive Lysis) by Zinc and Copper Ions

Yamamoto

Takahashi

1975

Int Arch Allergy Immunol

View full text Add to dashboard Cite

show abstract

“…Other evidence indicating the interference of zinc with lipid peroxidation in vivo was presented by Radomski and Wood (53) and Chvapil et al (46). They showed that lung edema induced by exposing mice to hyperbaric oxygen or N02 can be prevented by adequate treatment of animals with zinc or manganese.…”

Section: Effect Of Zincmentioning

confidence: 89%

“…This refers to the direct interaction of the metal with membrane constituents, and with enzymes affecting membrane components and the process leading to the induction of lipid peroxidation, etc. Some of these aspects have been reviewed (46)(47)(48). The lysosomal theory of tissue injury proved to be of paramount importance in understanding the dynamics of events after the effect of physical, chemical, or biological noxious agents.…”

Section: Effect Of Zincmentioning

confidence: 99%

Pharmacology of fibrosis and tissue injury

Chvapil¹

1974

Environ Health Perspect

Self Cite

View full text Add to dashboard Cite

Methods controlling tissue fibrosis are classified into those specifically inhibiting various metabolic aspects of collagen selectively in the injured tissue (ascorbic acid deficiency, effect of agent chelating Fe 2+ , proline analogs, lathyrogens). The most promising method seems to be the blocking of crosslinks formation among collagen molecules by β-aminopropionitrile, a competitive inhibitor of a crosslinking enzyme, lysyl oxidase. The second group of methods is called nonspecific, as they affect any stage of inflammatory process preceding the activation of fibroblasts. The importance of activated macrophages in the stimulation of fibroblast is discussed. Finally, a new concept is proposed, indicating the function of zinc ions in the control of the integrity of biomembrances, tissue reactivity to noxious agents. It is suggested that zinc may control NADPH dependent lipid peroxidation at the membrane level by inhibiting NADPH oxidase activity. The implication of these ideas to lung fibrosis induced by silica or asbestos is discussed.

show abstract

“…Zinc inhibits certain activities of mast cells [20-221, neutrophils [23], macrophages [24,25], spermatozoa, and platelets [24,261, and it antagonizes the action of calcium in the erythrocyte [27-291. However, the molecular mechanism of zinc inhibition of cells, and the molecular mechanism of zinc antagonism of calcium effects, are unknown.…”

Section: Introductionmentioning

confidence: 99%

Zinc inhibition of calmodulin: A proposed molecular mechanism of zinc action on cellular functions

et al. 1979

View full text Add to dashboard Cite

Calcium stimulates, and zinc inhibits, a wide variety of cell types. In the erythrocyte, we have found calcium and zinc to have antagonist actions in a variety of systems. An important mechanism for calcium effects on cells is activation of calmodulin. Calmodulin is a small ubiquitous protein which, when activated by calcium, has a large array of cellular regulatory functions. We now report that calmodulin function is inhibited by low concentrations of zinc. Zinc inhibition of calmodulin provides a rational molecular mechanism for the diverse cellular inhibitory effects of zinc, as well as for zinc's antagonism of calcium effects.

show abstract

Pathophysiology of Zinc

Cited by 24 publications

References 72 publications

Inhibition of the Terminal Stage of Complement-Mediated Lysis (Reactive Lysis) by Zinc and Copper Ions

Inhibition of the Terminal Stage of Complement-Mediated Lysis (Reactive Lysis) by Zinc and Copper Ions

Pharmacology of fibrosis and tissue injury

Zinc inhibition of calmodulin: A proposed molecular mechanism of zinc action on cellular functions

Contact Info

Product

Resources

About