Antiradical and chelating effects in flavonoid protection against silica-induced cell injury

Our plain-English summary of Antiradical and chelating effects in flavonoid protection against silica-induced cell injury, by V.A. Kostyuk, A.I. Potapovich (Archives of Biochemistry and Biophysics, 1998).

The study

• Authors: V.A. Kostyuk, A.I. Potapovich
• Journal: Archives of Biochemistry and Biophysics
• Published: 1998;355(1):43-8
• Cited by: 43 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Quercetin, dihydroquercetin, and rutin are capable of scavenging superoxide anion (rate constants of the reaction with superoxide at pH 10 were 1.7 x 10(5), 1.5 x 10(5), and 0.5 x 10(5) M-1 s-1, respectively). At the same time rutin and quercetin but not dihydroquercetin are iron ion chelators. These substances were used to elucidate the role of radical scavenging and iron chelating in flavonoid protection against asbestos-induced oxidative cellular injury. Exposure of rat peritoneal macrophages to chrysotile asbestos fibers resulted in "frustrated" phagocytosis, cell injury, and a LDH release. Quercetin, dihydroquercetin, and rutin were effective in protecting the phagocytic cells against injury caused by asbestos. Moreover, these flavonoids exhibited cellular protection in the same order of effectiveness as that observed for the quenching of superoxide: quercetin > dihydroquercetin > rutin. Exposure of human red blood cells to asbestos fibers also caused progressive cell injury and lysis. Quercetin and rutin protected the red cells (quercetin > rutin), whereas dihydroquercetin was ineffective in preventing asbestos-induced hemolysis. The protective ability of quercetin and rutin may be related to their iron-chelating activity. Due to this these flavonoids can be located on asbestos surface in sites of initiation of free radical reactions and their antiradical moieties can scavenge reactive oxygen species immediately after the appearance. Thus, both antiradical and chelating effects appear to be involved in the flavonoid protection against silica-induced cell injury.

Copyright 1998 Academic Press.

In plain English

This was a laboratory study on isolated cells. The authors tested whether three plant compounds called flavonoids (quercetin, dihydroquercetin and rutin) protected cells from damage caused by natural chrysotile asbestos fibers. They used macrophages (immune cells) taken from the abdominal cavity of Wistar rats and red blood cells from healthy human blood donors. In chemical tests, all three compounds neutralized superoxide, a reactive form of oxygen. Quercetin and rutin bound iron, but dihydroquercetin did not. All three compounds reduced asbestos damage to the rat macrophages. Quercetin was most effective, then dihydroquercetin, then rutin. The iron-binding chemicals EDTA and deferoxamine did not protect them. In red blood cells, quercetin and rutin protected against asbestos-caused bursting, but dihydroquercetin did not. Adding EDTA to the fibers first reduced or removed that protection. The authors concluded that both radical-neutralizing and iron-binding effects appear to be involved. Their title calls this "silica-induced" injury, although the fiber tested was chrysotile asbestos. They said part of their explanation rested on indirect evidence.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Laboratory (in vitro) experiments on isolated rat macrophages and human red blood cells, plus chemical tests of the compounds
• Who was studied: Peritoneal (abdominal cavity) macrophages from Wistar rats, and red blood cells from healthy human donor blood obtained from a hospital blood bank. Results were reported as means of 4 to 6 measurements per condition. Place and dates of the experiments were not stated.
• Exposure: Natural chrysotile asbestos fibers from Tuva, Russia, added to the cell suspensions at a final concentration of 2 mg/ml. They were tested with and without the flavonoids quercetin, dihydroquercetin and rutin, and with comparison chemicals: the antioxidants BHT and alpha-tocopherol, and the iron binders EDTA and deferoxamine.
• Main results:
  • In chemical tests, quercetin, dihydroquercetin and rutin all reacted with superoxide, with rate constants at pH 10 of 1.7, 1.5 and 0.5 times 10 to the 5th power per molar per second, respectively.
  • Quercetin and rutin formed complexes with iron. Dihydroquercetin did not, or did so very poorly.
  • In rat macrophages exposed to chrysotile, all three flavonoids reduced a marker of fat oxidation (TBARS) and protected the cells from injury (measured as release of the enzyme LDH). By LDH release, the order of effectiveness was quercetin, then dihydroquercetin, then rutin.
  • In the macrophages, BHT and alpha-tocopherol fully blocked TBARS formation but did not reduce LDH release.
  • In the macrophages, the iron binders EDTA and deferoxamine had no effect on asbestos cell damage.
  • In human red blood cells exposed to chrysotile, quercetin and rutin protected against bursting (hemolysis). Dihydroquercetin, alpha-tocopherol, EDTA and deferoxamine did not.
  • In some experiments, fibers were treated with the compounds and then separated and moved into fresh solution before the red cells were added. Quercetin and rutin still prevented hemolysis.
  • 1 mg of chrysotile took up approximately 20 nmol of quercetin, 12 nmol of dihydroquercetin and 9 nmol of rutin.
  • EDTA was added to the fibers before the flavonoids, at an equal concentration. This reduced the red-cell protection by roughly 60% for quercetin and 70% for rutin.
  • At four times the flavonoid concentration, EDTA added first left quercetin and rutin completely ineffective.
• The authors' conclusion: The authors concluded that both radical-scavenging and iron-binding effects appear to be involved in flavonoid protection against what they call silica-induced cell injury. The experiments used chrysotile asbestos.
• Limitations the authors state:
  • The authors described their comparison of the compounds' iron-binding properties as only indirect evidence for their explanation. That explanation is that the compounds differ in where they attach to the asbestos fibers.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Chrysotile.

Medical terms in this study, explained in our Lexicon: Superoxide, Macrophage, Chrysotile, Phagocytosis, LDH Release, Reactive Oxygen Species (ROS).

Related studies

• Influence of metal ions on flavonoid protection against asbestos-induced cell injury — V.A. Kostyuk, A.I. Potapovich, et al. (2001)
• Protective effect of natural flavonoids on rat peritoneal macrophages injury caused by asbestos fibers — V.A. Kostyuk, A.I. Potapovich, et al. (1996)
• Comparative study of antioxidant properties and cytoprotective activity of flavonoids — A.I. Potapovich, V.A. Kostyuk (2003)
• N-acetyl L-cysteine attenuates oxidant-mediated toxicity induced by chrysotile fibers — F. Afaq, P. Abidi, et al. (2000)
• Chrysotile inhibits glutathione-dependent protection against the onset of lipid peroxidation in rat lung microsomes — J.M. Arif, I. Ahmad, et al. (1996)
• Inhibitory effects of anti-oxidants on apoptosis of a human polyclonal T-cell line, MT-2, induced by an asbestos, chrysotile-A — F. Hyodoh, A. Takata-Tomokuni, et al. (2005)

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