Our plain-English summary of Biological autoxidation. II. Cholesterol esters as inert barrier antioxidants. Self-assembly of porous membrane sacs. An hypothesis, by S.H. Kon (Medical Hypotheses, 1978).
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The study
- Author: S.H. Kon
- Journal: Medical Hypotheses
- Published: 1978;4(6):559-80
- Cited by: 1 article, as counted by NIH iCite
- Read it: PubMed · Publisher
Abstract
The antioxidation defenses recognized thus far appear too weak. Needed are inert barriers to encapsulate foci of activated oxygen (FAOs) and contain their spreading. These capsules must: 1. self-assemble nonenzymatically and spontaneously in face of adversity; 2. resist oxidation and dissolution in water; and 3. be moderately fluid and elastic enough to withstand flexing by tissues. Evidence shows activated oxygen: a. is produced by common cholesterolester (CE)-raising agents; b. boosts accumulation of CEs; and c. splits low-density lipoproteins (LDL), thus releasing CE-rich coalescence-prone lipid micelles. I am proposing that CEs, combined with polar lipids, are uniquely suited to form inert-lipid antioxidation barriers (ILABs). Porous ILAB capsules self-assemble from lipid micelles released by oxidatively degraded LDL. The capsules are thermodynamically unstable but elastic, durable and capable of self-repair through oxidation of ambient LDL. All capsules tend to contract into spheres. Enclosed needle-like "foreign bodies", such as asbestos, puncture the contracting capsules. Hence the odd bulbous architecture of asbestos bodies. ILABs protect from--and their failure initiates and promotes--carcinogenesis and atherosclerosis. ILABs may be mediators of membrane biogenesis. The loss of arterial flexibility in atherosclerosis protects ILAB capsules from breakage.
In plain English
This article was a hypothesis paper. The author did not report new experiments, measurements or studies of people. Drawing on previously published laboratory and animal work, the author proposed that cholesterol esters, combined with polar lipids, form inert, elastic capsules (called "labosomes") that seal off spots in tissue where activated oxygen is produced. Under this proposal, the capsules assemble on their own from fatty particles released when low-density lipoproteins are broken down by activated oxygen. For asbestos, the author proposed that a capsule forming around a needle-shaped fiber would be sausage-shaped, would tend to round off, and would be punctured by the fiber. The author suggested that repeated rupture of such capsules, with the gaps filling with an iron-protein coagulum produced by the fiber, may account for the bulbous shape of asbestos bodies. The author also cited earlier work reporting that the carcinogenicity of foreign bodies, including asbestos, increases as their degree of dispersion decreases. The article did not name a specific asbestos fiber type. The author concluded that these ideas required further exploration, including their possible involvement in carcinogenesis and atherosclerosis.
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: hypothesis paper (theoretical proposal based on previously published literature; no new data)
- Who was studied: No people or animals were studied by the author; the paper discusses previously published laboratory, animal and human findings
- Exposure: Asbestos fibers, discussed generally as needle-shaped rigid foreign bodies (no fiber type named); the wider paper concerns activated oxygen and cholesterol esters
- Main results:
- Proposed (not measured): a capsule formed around an asbestos fiber tends to round off and is punctured by the fiber
- Proposed: voids in and between the resulting odd shapes fill with an iron-protein coagulum produced by the asbestos fiber
- Proposed: repeated disruption of these capsules may account for the bulbous structure of asbestos bodies
- Cited from other work (reference 70), not this paper's finding: carcinogenicity of foreign bodies, including asbestos, increases as their degree of dispersion decreases
- Proposed: hardening of arteries may be the body's defense against breakage of these capsules
- The authors' conclusion: The author concluded that the proposed concepts require further exploration, including their involvement in autoxidation diseases, possibly including carcinogenesis and atherosclerosis
Topics
Medical terms in this study, explained in our Lexicon: Asbestos Bodies, Carcinogenesis, Flexibility.
Related studies
- Biological autoxidation. I. Decontrolled iron: an ultimate carcinogen and toxicant: an hypothesis — S.H. Kon (1978)
- Changes in cholesterol and triglyceride concentrations in the Vanguard population of the Carotene and Retinol Efficacy Trial (CARET) — B. Cartmel, J. Dziura, et al. (2005)
- HPLC-FLD determination of NBD-cholesterol, its ester and other metabolites in cellular lipid extracts — X.Z. Cao, T.Y. Mi, et al. (2013)
- Beta-carotene and other carotenoids as antioxidants — S.A. Paiva, R.M. Russell (1999)
- The protective role of antioxidants in the defence against ROS/RNS-mediated environmental pollution — B. Poljšak, R. Fink (2014)
- The potential role of antioxidant vitamins in preventing cardiovascular diseases and cancers — S. Hercberg, P. Galan, et al. (1998)
Browse more research in Medical Hypotheses, or return to medical research.
Cited on this site
How to cite it
Cite the study
S.H. Kon. Biological autoxidation. II. Cholesterol esters as inert barrier antioxidants. Self-assembly of porous membrane sacs. An hypothesis. Medical Hypotheses 1978;4(6):559-80. doi:10.1016/0306-9877(78)90047-6. PMID: 748727.
Cite our summary
“Biological autoxidation. II. Cholesterol esters as inert barrier antioxidants. Self-assembly of porous membrane sacs. An hypothesis.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/biological-autoxidation-ii-cholesterol-esters-as-inert-barrier.
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