Chemico-biological Interactions

Our medical research library holds 8 studies published in Chemico-biological Interactions (1980–2024). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 8 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it.

About the journal

• Publisher: Elsevier
• Published: 1969 to the present, Ireland
• Language: English
• ISSN: 0009-2797 (print), 1872-7786 (electronic)
• Its record in the NLM Catalog

2020s

• Mechanisms of action of mineral fibres in a placental syncytiotrophoblast model: An in vitro toxicology study. S. Fantone, G. Tossetta, L. Cianfruglia, et al. 2024;390:110895. PubMed · Publisher

  Abstract

  Asbestos has been widely used due to its unique characteristics. It is known that exposure to asbestos causes serious damage to health but one species, chrysolite, is still used because it is considered less toxic and not biopersistent in some countries. The aim of our study was to investigate if cellular process underlying the proliferation, differentiation and cell death of placental tissues could be modify in presence of asbestos fibres (50 μg/ml final concentration), long chrysolite fibres (CHR-L) and short chrysolite fibres (CHR-S), using BeWo cell line, an in vitro model that mimics the syncytiotrophoblast (STB), the outer layer of placental villi. Our data demonstrated that none of the fibres analysed alter syncytiotrophoblast formation but all of them induce ROS formation and reduced cell proliferation. Moreover, we showed that only CHR-L fibre induced was able to induce irreversible DNA alterations that carried cells to apoptosis. In fact, BeWo cells exposed to CHR-L fibre showed a significant increase in cleaved CASP3 protein, a marker of apoptosis. These data suggest that CHR-L may induce death of the placental villi leading to impaired placental development. The impairment of placental development is the basis of many gestational pathologies such as preeclampsia and intrauterine growth retardation. Since these pathologies are very dangerous for foetal and maternal life, we suggest to the gynaecologists to carefully evaluate the area of maternal residence, the working environment, the food used, and the materials used daily to avoid contact with these fibres as much as possible.

  Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.

2010s

• Molecular mechanisms of asbestos-induced lung epithelial cell apoptosis. G. Liu, R. Beri, A. Mueller, et al. 2010;188(2):309-18. Review PubMed · Publisher

  Abstract

  Asbestos causes pulmonary fibrosis (asbestosis) and malignancies (bronchogenic lung cancer and mesothelioma) by mechanisms that are not fully elucidated. Accumulating evidence show that alveolar epithelial cell (AEC) apoptosis is a crucial initiating and perpetuating event in the development of pulmonary fibrosis following exposure to a wide variety of noxious stimuli, including asbestos. We review the important molecular mechanisms underlying asbestos-induced AEC apoptosis. Specifically, we focus on the role of asbestos in augmenting AEC apoptosis by the mitochondria- and p53-regulated death pathways that result from the production of iron-derived reactive oxygen species (ROS) and DNA damage. We summarize emerging evidence implicating the endoplasmic reticulum (ER) stress response in AEC apoptosis in patients with idiopathic pulmonary fibrosis (IPF), a disease with similarities to asbestosis. Finally, we discuss a recent finding that a mitochondrial oxidative DNA repair enzyme (8-oxoguanine DNA glycosylase; Ogg1) acts as a mitochondrial aconitase chaperone protein to prevent oxidant (asbestos and H(2)O(2))-induced AEC mitochondrial dysfunction and intrinsic apoptosis. The coupling of mitochondrial Ogg1 to mitochondrial aconitase is a novel mechanism linking metabolism to mitochondrial DNA that may be important in the pathophysiologic events resulting in oxidant-induced toxicity as seen in tumors, aging, and respiratory disorders (e.g. asbestosis, IPF). Collectively, these studies are illuminating the molecular basis of AEC apoptosis following asbestos exposure that may prove useful for developing novel therapeutic strategies. Importantly, the asbestos paradigm is elucidating pathophysiologic insights into other more common pulmonary diseases, such as IPF and lung cancer, for which better therapy is required.

  Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.

1990s

• Effect of chrysotile asbestos on cytochrome P-450-dependent monooxygenase and glutathione-S-transferase activities in rat lung. Q. Rahman, S.G. Khan, S. Ali. 1990;75(3):305-13. PubMed · Publisher

  Abstract

  The in vitro and in vivo effect of a carcinogenic variety of asbestos, chrysotile, both on xenobiotic metabolizing enzymes such as benzo[a]pyrene hydroxylase, epoxide hydrolase as well as glutathione-S-transferase activities and microsomal lipid peroxidation in rat lung were examined. The in vitro incubation of chrysotile with microsomes significantly adsorbed heme proteins, cytochrome P-450 and P-448 with the concomitant decrease in the dependent monooxygenase activities. The prolonged incubation of this mineral fibre with microsomes also resulted in the release of heme. It also led to the depletion in the activities of epoxide hydrolase and glutathione-S-transferase. However, it induced lipid peroxidation. When these in vitro effects were validated in vivo, the exposure to early stages produced similar alterations as observed in in vitro studies. However, reverse pattern in the alterations was observed after 90 days of exposure except in the case of lipid peroxidation which remained induced.

1980s

• The involvement of ionic interactions during asbestos-induced enzyme release from polymorphonuclear leukocytes. J.G. Elferink, M. Deierkauf, J.A. Kramps, et al. 1989;72(1-2):215-27. PubMed · Publisher

  Abstract

  Chrysotile asbestos permeabilizes the plasma membrane of rabbit polymorphonuclear leukocytes (PMNs) which is evident from the release of the cytoplasmic enzyme lactate dehydrogenase (LDH) from the cell. When Ca2+ is present in the medium exocytosis is observed, evident from the release of the granule associated enzyme lysozyme which is not liberated in the absence of Ca2+. Asbestos-induced enzyme release is inhibited by polyanions or by removal of positive charges on asbestos, and resembles enzyme release induced by synthetic polycations. Pretreatment of PMNs with neuraminidase does not affect the ability of asbestos to induce enzyme release from these cells. Asbestos induces release of glucose from glucose-loaded liposomes, and this effect can be inhibited by the polyanion poly-D-glutamic acid. The results are compatible with the view that positive charges play a decisive role in the interaction between PMNs and asbestos, and that the primary target of asbestos could be the lipid bilayer of the membrane. The interaction results in a permeabilized plasma membrane. When Ca2+ is present in the medium it moves into the cell and causes exocytosis of the granule enzyme lysozyme. Inhibition of cytotoxicity by polyanion may cause a diminished Ca2+-influx and hence inhibition of lysozyme release.

• Hydroxyl radical production in the presence of fibres by a Fenton-type reaction. M. Gulumian, J.A. van Wyk. 1987;62(1):89-97. PubMed · Publisher

  Abstract

  Glass fibres are considered to be inert and therefore thought to present no real hazard to the health of people who inhale them. Results in the present study however indicate that these fibres are able to produce hydroxyl radicals in the presence of hydrogen peroxide by a Fenton-type reaction. Since hydroxyl radical is implicated in lipid peroxidation, single-strand DNA breaks and carcinogenesis, care should be exercised when dealing with glass fibres.

• Effect of particulates on metabolism and mutagenicity of benzo[a]pyrene. D.R. Bevan, W.E. Manger. 1985;56(1):13-28. PubMed · Publisher

  Abstract

  Mechanisms of co-carcinogenicity of particulates, such as iron oxide and asbestos, and benzo[a]pyrene (B[a]P) are not completely understood. Particulates dramatically alter rates of uptake of B[a]P into membranes, a factor which could account for co-carcinogenicity. However, B[a]P must be activated to reactive forms to be carcinogenic and mutagenic so alterations in metabolism of B[a]P by particulates also could result in co-carcinogenesis. To elucidate mechanisms of particulate-B[a]P co-carcinogenesis, we have correlated rates of uptake of B[a]P into microsomes with metabolism of B[a]P and with mutagenicity of B[a]P in the Ames test. In general, aryl hydrocarbon hydroxylase (AHH) activity paralleled rates of uptake of B[a]P, though some inhibition of AHH activity by particulates which was not attributable to availability of B[a]P was evident. This inhibition was studied further by assaying separately mixed function oxidase and epoxide hydrase activities in the presence of particulates. Both chrysotile and iron oxide inhibited O-deethylation of 7-ethoxyresorufin and hydration of B[a]P-4,5-oxide. To determine effects of this inhibition on activation of B[a]P to reactive forms, we studied profiles of metabolites of B[a]P and mutagenicity of B[a]P. The only alteration in profiles of B[a]P metabolites produced by particulates was that due to effects on rates of uptake. Similarly, mutagenicity of B[a]P was positively correlated with rates of uptake into microsomes. We conclude that the predominant effects of chrysotile and iron oxide are in altering rates of uptake of particle-adsorbed B[a]P. Changes in uptake rates then result in alterations of B[a]P metabolism and mutagenicity.

• Lipid peroxidation in microsomes induced by crocidolite fibres. M. Gulumian, F. Sardianos, T. Kilroe-Smith, et al. 1983;44(1-2):111-8. PubMed · Publisher

  Abstract

  When rat liver and lung microsomes were incubated with crocidolite fibres, a substantial increase in lipid peroxidation was observed. Increasing concentrations of this fibre in the incubation mixture, produced a concomitant induction in microsomal lipid peroxidation. This increase was very rapid as the reaction was almost complete within 10 min. The ability of these fibres to induce this process after a short period of incubation seems to be due to their binding to the microsomes. The iron present in the structure of crocidolite is thought to be responsible for catalysing the peroxidation. The formation of free radicals by asbestos and possible pathological sequelae are discussed.

• Benzo[a]pyrene uptake into rat liver microsomes: effects of adsorption of benzo[a]pyrene to asbestos and non-fibrous mineral particulates. J.R. Lakowicz, D.R. Bevan. 1980;29(2):129-38. PubMed · Publisher

  Abstract

  The fluorescence yield of benzo[a]pyrene (BP) increases dramatically upon its transfer from the surface of particulates to rat liver microsomes. Adsorption of BP to Canadian chrysotile, anthophyllite, hematite and silica results in greatly enhanced uptake rates into microsomes when compared to uptake from a microcrystalline dispersion of BP. The fibrous minerals chrysotile and anthophyllite were more effective than silica and hematite in enhancing BP uptake. Simple mixtures of BP microcrystals and particles did not display enhanced transport, indicating that adsorption of BP to the particulate surface is necessary for enhanced microsomal uptake. BP was not released into microsomes from carbon black. We suggest that particulate-enhanced availability of BP may be of significance in the co-carcinogenesis between particulates and polynuclear aromatic hydrocarbons. However, other mechanisms are also possible, and are not excluded by our experiments. The fluorescence methodology, described in this paper provides a novel and convenient means to quantify microsomal uptake of BP and thereby investigate further the mechanisms of cocarcinogenesis.

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