Microsomal lipid peroxidation and oxy-radicals formation are induced by insoluble iron-containing minerals

Our plain-English summary of Microsomal lipid peroxidation and oxy-radicals formation are induced by insoluble iron-containing minerals, by M. Fontecave, M. Jaouen, D. Mansuy, et al (Biochemical and Biophysical Research Communications, 1990).

The study

• Authors: M. Fontecave, M. Jaouen, D. Mansuy, D. Costa, R. Zalma, H. Pezerat
• Journal: Biochemical and Biophysical Research Communications
• Published: 1990;173(3):912-8
• Cited by: 13 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Lipid peroxidation, measured by malondialdehyde formation is induced in rat liver microsomes by insoluble iron-containing minerals (pyrite, magnetite, nemalite and an iron ore, minette de Lorraine) which are generally found either in iron mines or as contaminants of asbestos fibers. In spin-trapping studies using DMPO as a spin trap those minerals are also found to catalyze the oxidation of formate to carboxylate radicals by oxygen, via the formation of hydroxyl radicals. The two processes are mainly due to the presence of redox active iron at the surface of the solid particles and thus are greatly inhibited by desferrioxamine, a strong iron chelator. However, these reactions are not correlated.

In plain English

In this laboratory study, the authors tested 9 insoluble iron-containing minerals on liver microsomes (cell fractions) from rats. One of them was nemalite, a fibrous brucite they described as a known contaminant of some chrysotile fibers. They measured lipid peroxidation, a form of oxidative damage to fats, and used spin trapping to detect reactive oxygen radicals. Magnetite, air-aged pyrite, nemalite and an iron ore called minette de Lorraine produced high lipid peroxidation. The other minerals, and freshly ground pyrite, did not significantly increase it. In the radical tests, all minerals except haematite, goethite and freshly ground pyrite gave a signal. With pyrite and nemalite, catalase cut that signal by 80%, and desferrioxamine, an iron-binding compound, stopped it completely. The two effects did not match: chlorite and biotite strongly promoted radical formation but caused no lipid peroxidation, which the authors said was not clear. The authors concluded that the results give a molecular basis for the possible role of some iron compounds in lung cancers among iron miners. No asbestos fibers were tested in this study.

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) experiment: lipid peroxidation assays in rat liver microsomes and spin-trapping (EPR) tests for oxy-radicals
• Who was studied: Liver microsomes from male Sprague-Dawley rats pretreated with sodium phenobarbital, exposed to 9 insoluble iron-containing mineral samples
• Exposure: The minerals were haematite, goethite, magnetite, siderite, pyrite (freshly ground and air-aged), nemalite (fibrous brucite in which about 8% of magnesium is replaced by ferrous iron), chlorite, biotite and the iron ore minette de Lorraine. Microsome incubations used 2 or 5 mg of mineral; spin-trapping tests used 45 mg. Nemalite was chosen as a contaminant of some chrysotile fibers.
• Main results:
  • In rat liver microsomes, magnetite, air-aged pyrite, nemalite and minette de Lorraine induced high production of malondialdehyde (MDA), a marker of lipid peroxidation.
  • The other minerals did not significantly raise lipid peroxidation above the basal rate.
  • Pyrite was active only after being left in air; freshly ground pyrite was completely inactive.
  • Desferrioxamine strongly inhibited lipid peroxidation caused by nemalite and pyrite, but had no effect on lipid peroxidation caused by magnetite.
  • Pyrite (air-aged) and nemalite had iron readily accessible to the chelator bipyridyl. Magnetite, chlorite, biotite and freshly ground pyrite had no bipyridyl-chelatable iron.
  • In spin-trapping tests, most minerals caused oxidation of formate to carboxylate radicals; only haematite, goethite and freshly ground pyrite were totally inactive.
  • In tests with pyrite and nemalite, catalase inhibited carboxylate radical formation by 80%, and desferrioxamine inhibited it completely.
  • The reaction took place at the surface of the mineral particles, not in the surrounding solution.
  • Lipid peroxidation and radical formation were not correlated: chlorite and biotite strongly promoted formate oxidation but did not cause lipid peroxidation.
• The authors' conclusion: The authors concluded that the ability of some iron-containing compounds to increase microsomal lipid peroxidation and oxy-radical generation gives a molecular basis for their possible activity as inducers or promoters of lung cancers among iron miners.
• Limitations the authors state:
  • The authors could not explain why chlorite and biotite, which had no bipyridyl-accessible iron, were such strong catalysts of formate oxidation.

Topics

Medical terms in this study, explained in our Lexicon: Hydroxyl Radical.

Related studies

• Fibre-induced lipid peroxidation leads to DNA adduct formation in Salmonella typhimurium TA104 and rat lung fibroblasts — P.J. Howden, S.P. Faux (1996)
• The stimulatory effects of asbestos on NADPH-dependent lipid peroxidation in rat liver microsomes — M. Fontecave, D. Mansuy, et al. (1987)
• The ability of mineral dusts and fibres to initiate lipid peroxidation. Part I: parameters which determine this ability — M. Gulumian (1999)
• Chrysotile inhibits glutathione-dependent protection against the onset of lipid peroxidation in rat lung microsomes — J.M. Arif, I. Ahmad, et al. (1996)
• Iron enhances uptake of mineral particles and increases lipid peroxidation in tracheal epithelial cells — B. Keeling, K.Y. Li, et al. (1994)
• Effect of mineral particles containing iron on primary cultures of rabbit tracheal epithelial cells: possible implication of oxidative stress — C. Guilianelli, A. Baeza-Squiban, et al. (1993)

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