Tobacco-borne siderophoric activity

Our plain-English summary of Tobacco-borne siderophoric activity, by M.W. Qian, J.W. Eaton (Archives of Biochemistry and Biophysics, 1989).

The study

• Authors: M.W. Qian, J.W. Eaton
• Journal: Archives of Biochemistry and Biophysics
• Published: 1989;275(1):280-8
• Cited by: 31 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The proinflammatory and carcinogenic effects of cigarette smoking are well known. Recent evidence indicts iron as a powerful promoter of inflammatory processes and, perhaps not coincidentally, the lungs and alveolar macrophages of smokers contain abnormally large amounts of iron. Furthermore, ferruginous compounds such as asbestos exert a powerful synergy with smoking in the causation of pulmonary neoplasia. Indeed, elements in tobacco smoke and asbestos synergistically damage DNA through reactions mediated by the (probably iron-dependent) formation of hydroxyl radical. These considerations prompted the hypothesis that tobacco smoke might contain substances capable of "delocalizing' iron. We find that one or more substances in organic extracts of smoke and unburned tobacco will transfer iron from an aqueous to an immiscible organic phase. This organic solvation requires the prior reduction of iron which can be effected by elements in smoke extracts. The translation of iron into organic phase is dependent on time and on the concentration of iron within the aqueous phase. Organic condensates of smoke will leach iron from rich forms of asbestos (amosite and crocidolite). Perhaps most importantly, exposure of intact human cells (erythrocytes) to dried residues of such condensates causes the accumulation of iron. This iron is evidently intracellular because it is inaccessible to powerful extracellular iron chelator such as deferoxamine. This tobacco-borne siderophoric activity may help explain some of the pathologic consequences of tobacco use as pulmonary inflammation and neoplasia.

In plain English

This was a laboratory study at the University of Minnesota Medical School. It tested whether substances in tobacco smoke can bind iron and move it; it did not study people or measure disease. The authors collected cigarette smoke (mainly Camel nonfilter) in chloroform and also soaked unburned tobacco in chloroform. When these extracts were shaken with iron dissolved in water, iron moved into the chloroform. Pure chloroform moved no detectable iron. The authors estimated the smoke extract could transfer up to 1.0 mM iron. Transfer was greatest between pH 6 and 7 and depended on a water-soluble substance that converted iron to its reduced (ferrous) form. When 2 mg of amosite or crocidolite asbestos was shaken with smoke condensate, iron was slowly leached from both. Human red blood cells exposed to dried smoke condensate took up iron that washing with the iron-binding drug deferoxamine did not remove. The authors concluded this activity may help explain some effects of tobacco use, such as pulmonary inflammation and neoplasia. They noted that the strength of the iron binding could not be measured accurately.

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) biochemistry experiments using tobacco smoke extracts, asbestos fibers and human red blood cells
• Who was studied: No human or animal subjects. The materials were chloroform condensates of cigarette smoke (mainly Camel nonfilter, with results confirmed for other brands), chloroform extracts of unburned Camel tobacco, amosite and crocidolite asbestos, and red blood cells from fresh human blood. The work was done at the University of Minnesota Medical School, Minneapolis.
• Exposure: Chloroform condensates of cigarette smoke combined with iron solutions, with 2 mg of amosite (asbestiform grunerite) or crocidolite (asbestiform riebeckite), each roughly 15% iron by weight, and with human red blood cells
• Main results:
  • Smoke extract moved iron from water into chloroform. The authors estimated up to 1.0 mM iron could be transferred. Extracts of unburned tobacco had similar capacity.
  • Pure chloroform, the control, moved no detectable iron.
  • At the lowest iron concentration in the water (0.1 mM), almost 80% of the iron moved into the organic phase.
  • Iron transfer depended strongly on pH and was greatest between pH 6 and 7.
  • Reduced (ferrous) iron was moved up to 10 times as efficiently as ferric iron. A water-soluble reducing substance in the smoke extract was needed for the effect.
  • Under optimal conditions the extract could bind over 50 nmol of iron per mg of extracted tar, almost 0.1 mg of iron per cigarette.
  • Smoke condensate leached iron from amosite and crocidolite in relatively large amounts, more slowly than it moved free iron. Controls with pure chloroform showed no organic-soluble iron.
  • Human red blood cells incubated with dried smoke condensate took up iron from the surrounding liquid. Uptake rose with the amount of condensate. Cells incubated without added iron showed no iron accumulation.
  • In experiments with radioactive iron, at 120 minutes the red cell samples given the highest dose of dried smoke residue had taken in approximately 30% of the added isotope.
  • Washing the red cells with deferoxamine, an iron-binding drug, did not remove the iron they had taken up. The authors took this to mean the iron was inside the cell or at least within the cell membrane.
• The authors' conclusion: The authors concluded that this iron-binding ('siderophoric') activity of tobacco may help explain some pathologic consequences of tobacco use, such as pulmonary inflammation and neoplasia.
• Limitations the authors state:
  • The strength (affinity) of iron binding by smoke substances could not be measured accurately, because standard methods do not apply to the two-layer system used.
  • The nature of the competition with water-soluble iron binders (EDTA, citrate) was uncertain.
  • The reducing substance in smoke was not identified.

Topics

Medical terms in this study, explained in our Lexicon: Carcinogenic, Alveolar Macrophage, Causation, Hydroxyl Radical, Amosite, Crocidolite, Inflammation.

Related studies

• Retinoid signaling and activator protein-1 expression in ferrets given beta-carotene supplements and exposed to tobacco smoke — X.D. Wang, C. Liu, et al. (1999)
• Cigarette smoke, asbestos, and small irregular opacities — W. Weiss (1984)
• Cigarette smoke increases the penetration of asbestos fibers into airway walls — D. McFadden, J. Wright, et al. (1986)
• Effects of cigarette smoke and asbestos on airway, vascular and mesothelial cell proliferation — H. Sekhon, J. Wright, et al. (1995)
• Cigarette smoke makes airway and early parenchymal asbestos-induced lung disease worse in the guinea pig — V. Tron, J.L. Wright, et al. (1987)
• Synergistic effects of mineral fibres and cigarette smoke on the production of tumour necrosis factor by alveolar macrophages of rats — Y. Morimoto, M. Kido, et al. (1993)

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