Drug and Chemical Toxicology

Our medical research library holds 8 studies published in Drug and Chemical Toxicology (1987–1994). 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. 6 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it. For 1 study PubMed has no abstract for, we give the abstract printed in the article or, where there is none, a summary we wrote from it, each labeled as such.

About the journal

• Publisher: Taylor & Francis Group
• Published: 1977 to the present, United States
• Language: English
• ISSN: 0148-0545 (print), 1525-6014 (electronic)
• Its record in the NLM Catalog

1990s

• Effects of Aramid, a high strength synthetic fiber, on respiratory cells in vitro. J.P. Marsh, B.T. Mossman, K.E. Driscoll, et al. 1994;17(2):75-92. PubMed · Publisher

  Abstract

  Industry continues to develop synthetic fibers for new technologies and as replacements for asbestos, a toxic and carcinogenic fiber. To determine whether the in vitro effects of the aromatic polyamide fiber, Aramid (Kevlar, Twaron), resembled those induced by asbestos, fibers were surveyed for (1) cytotoxicity as measured by total cell protein, and (2) proliferative capacity as measured by [3H]thymidine incorporation, colony forming efficiency (CFE), and ornithine decarboxylase (ODC) activity in two target cells of mineral dust-induced lung damage, hamster tracheal epithelial (HTE) cells and rat lung (RL90) fibroblasts. Results of cytotoxicity tests indicated that Aramid was as toxic to HTE and RL90 cells as were crocidolite and chrysotile asbestos when expressed on both an equal mass and equal fiber number basis. In HTE cells, Aramid caused a statistically significant increase in [3H]thymidine incorporation and CFE and produced a dose-dependent induction of ODC enzyme activity. Proliferative effects by asbestos or Aramid were not observed in RL90 fibroblasts. Thus, when tested over a respirable size range, Aramid exhibited many of the same effects on epithelial cells in vitro as did asbestos, including increased radiolabeled nucleotide incorporation into DNA and induction of ODC enzyme activity.

• Protective role of ascorbic acid against asbestos induced toxicity in rat lung: in vitro study. S.G. Khan, S. Ali, Q. Rahman. 1990;13(2-3):249-56. PubMed · Publisher

  Abstract

  Asbestos fibers adsorb cytochrome P-450 and P-448 proteins from rat lung micosomal fractions and liberate heme from cytochrome P-448 on prolonged incubation in vitro. further, fibers, decrease the activities of benzo(a)pyrene hydroxylase and glutathione-S-transferase in microsomal and cytosolic fractions respectively. Mineral fibers also stimulate both the enzymatic (NADPH-induced) and non-enzymatic (Fe2(+)-induced) lipid peroxidation in microsomal fractions. Preincubation of microsomal and cytosolic fractions with a physiological concentration of ascorbic acid ameliorates, to a large extent, the changes induced by asbestos fibers.

1980s

• A possible mechanism of chrysotile asbestos toxicity. G.L. Fisher, B.T. Mossman, A.R. McFarland, et al. 1987;10(1-2):109-31. PubMed · Publisher

  Abstract

  In vitro evaluations of heat treated and/or irradiated chrysotile asbestos indicate the importance of electron transfer in determining the biological outcome of asbestos exposure. Regardless of the assay system used, all show the same trends. Namely, heat treatment reduces cytotoxicity while heat treatment in combination with irradiation increases activity over heat treatment alone. Furthermore, studies of BSA and DNA binding consistently indicate a lower molecular adsorption for heated asbestos. BSA and DNA adsorption are similar for untreated, irradiated and heated or irradiated samples. Physical and chemical analyses indicate that the size and elemental composition are unaffected by the treatment processes. X-ray diffraction indicates no change in the crystal structure of chrysotile asbestos. IR spectroscopy suggests that heat treatment affects the external hydroxyl group population while heat treatment and irradiation may repopulate this functional group. A proposed mechanism consistent with the biological and physical characterization is based upon electron transfer from the chrysotile asbestos matrix to biological receptors.

• Asbestos exposure dose-bronchoalveolar milieu response in asbestos workers and the sheep model: evidences of a threshold for chrysotile-induced fibrosis. R. Bégin, S. Massé, M. Rola-Pleszczynski, et al. 1987;10(1-2):87-107. PubMed · Publisher

  Abstract

  Epidemiological studies of asbestos workers have proposed a linear dose-response relationship between asbestos cumulative exposure indices and the incidence of asbestos-related lung diseases. However, for chrysotile, several studies have not observed such a linear relationship in low exposure workers. To further study the relationship of chrysotile exposure dose - lung tissue response, we designed in the sheep model one experiment of one exposure at variable intensity and one experiment with variable rates of individual exposures. In the first study, 6 groups of 6 sheep were exposed to either 0, 1, 10, 25, 50 or 100 mg chrysotile in 100 ml saline and lung lavage analyses carried out at day 0, 12, 24, 40 and 60 after. Histopathology was done at day 60. In the second experiment, 4 groups of 12 sheep were exposed to 100 ml saline every week or every two weeks, 100 mg chrysotile in 100 ml saline every week or every two weeks. In the second experiment, lung damage was assessed by changes in vital capacity (VC), lung compliance (Cst) and profusion of chest radiographic opacities (PO). On BAL in the control sheep, there were small and transient early increases in total cells/ml, macrophages/ml, neutrophils/ml, lactate dehydrogenase (LDH)/ml, alkaline phosphatase (AK)/ml, beta-glucuronidase (beta G)/ml and procollagen lll/ml. In the 1, 10, 25, and 50 mg asbestos sheep groups, there were no significant differences. However, in the 100 mg asbestos sheep, there were significant sustained increases in total cells/ml (3-6 times controls), macrophages/ml (2-6 times controls), neutrophils/ml (60-600 times controls), LDH/ml (5-10 times controls), AK/ml (1.5-2 times controls), beta G/ml (3-5 times controls), procollagen lll/ml (2 times controls) and IgG (1.5-3 times controls). These data were correlated with histopathological findings. In the sheep exposed weekly to chrysotile, significant changes in VC, Cst and PO occurred at mean cumulative exposure dose of 1.2 g whereas in the sheep exposed every 2 weeks, similar changes in VC, Cst and PO occurred at the cumulative exposure dose of 3.6 g (P less than 0.05). In conclusion, our data suggest that there is a threshold for chrysotile-induced fibrosis. This level cannot be considered adequately in term of cumulative exposure dose but must take into account intensity and rate of individual exposures.

• Asbestos in peripheral lung culture a species comparison of pulmonary tissue response. M.E. Placke, G.L. Fisher. 1987;10(1-2):133-56. PubMed · Publisher

  Abstract

  We have recently developed culture techniques to allow the long-term maintenance of adult peripheral lung tissue in vitro from a variety of mammalian species including hamster, rat, bovine, and human. The technique involves perfusion of the major airways with agarose gel and culture media followed by thin sectioning and culture on porous surgical foam. Cross sections of lung lobes 1-2 mm thick have been cultured for periods beyond four weeks with maintenance of structural and biochemical integrity of the lung. In vitro exposure of lung explants to crocidolite asbestos through the airways produced fibrotic and hyperplastic lesions similar to those reported after in vivo exposure. The incidence and severity of interstitial fibrous was concentration-dependent, including the human specimens, and the morphologic appearance of the lesions was similar in explants derived from each species. The lung explant model is well suited for further mechanistic evaluations of asbestos-induced lung lesions. It is notable that the pulmonary lesions were produced without the possibility for recruitment of hematogenous inflammatory cell populations.

• Cytotoxicity of respirable dusts from industrial minerals: comparison of two naturally occurring and two man-made silicates. D. Nadeau, L. Fouquette-Couture, D. Paradis, et al. 1987;10(1-2):49-86. PubMed · Publisher

  Abstract

  The membranolytic and cytotoxic properties of two naturally occurring (chrysotile asbestos; attapulgite clay) and two man-made (Fiberfrax, an aluminium-silicate, and xonotlite, a calcium silicate) industrial minerals were compared. "Short" fiber fractions of chrysotile and Fiberfrax were obtained by sedimentation in demineralized water, while the attapulgite and xonotlite samples were used as obtained. The aluminium silicate fibers were found to be non- hemolytic, while for the other three silicates, chrysotile had the strongest hemolysis potential, followed very closely by xonotlite; attapulgite was less hemolytic than the former two silicates, but was nevertheless highly hemolytic to the rat erythrocytes. Using rat pulmonary alveolar macrophages, the in vitro cytotoxicity assays showed that with fresh cell monolayers, all four silicates were equivalent in causing cell damages at a dose of 250 micrograms; at a lower dose (50 micrograms), the intensity of the cytotoxic effect was in the decreasing order: Fiberfrax greater than attapulgite greater than chrysotile greater than xonotlite. With one day-old cultured cell monolayers, a dose of 250 micrograms of the silicates fibers was less cytotoxic, with the exception of the attapulgite fibers which remained essentially as cytotoxic as with the fresh cell monolayers. The reduced cytotoxic response was especially noticeable with the chrysotile fibers. At 50 micrograms, the cytotoxicity scale of the mineral dusts with one day-old cell monolayers was essentially the same as the one obtained with the fresh cell monolayers, that is: Fiberfrax approximately equal to attapulgite greater than chrysotile greater than or equal to xonotlite. Overall, these in vitro tests imply: 1) that all four industrial silicates tested can be considered to be "biologically active"; 2) that on the basis of their different reactivities with the two types of cell culture conditions used, their biological reactivity in vivo might be quite distinct. This might be especially true for at least the chrysotile, attapulgite and xonotlite short fibers, considering that these three types of silicate dusts have very similar dimensions. Moreover, for the chrysotile and attapulgite samples, fiber numbers is probably not an important factor, since the density of the two silicates is roughly the same. The unaltered cytotoxic responses of the American attapulgite fibers in the two macrophage assays correlate well with the fact that short attapulgite fibers seems to have a stronger in vivo reactivity than short chrysotile fibers. In fact, it might be the strongest of the four industrial silicates tested.(ABSTRACT TRUNCATED AT 400 WORDS)

• Implication of active oxygen species as second messengers of asbestos toxicity. B.T. Mossman, J.P. Marsh, M.A. Shatos, et al. 1987;10(1-2):157-80. PubMed · Publisher

  Summary

  This chapter tested the hypothesis that cell damage by crocidolite and chrysotile asbestos involves the generation of active oxygen species. It summarized the authors' earlier work and reported new in vitro experiments with RL-82 rat lung fibroblasts. Earlier work had shown that superoxide dismutase and hydroxyl radical scavengers (mannitol, DMTU, sodium benzoate) inhibited crocidolite- and long chrysotile-associated 75Selenium release from hamster tracheal epithelial cells, while DABCO, a singlet oxygen scavenger, did not. In the first new experiment, UICC crocidolite was pretreated with 1, 5 and 10 mM of the iron chelators deferoxamine or Tiron, washed, and added to fibroblasts at 10 and 15 µg/cm2. Viability was assessed by trypan blue exclusion after 24 hours (N = 3 per group). Untreated crocidolite at these doses gave a decreased viability index of approximately 65% and 50%, respectively, compared with controls. Chelation significantly inhibited asbestos-associated cell death (p<.001) at all chelator concentrations. In the second experiment, a xanthine-xanthine oxidase superoxide-generating system was added at nontoxic concentrations. Xanthine alone had no effect, but xanthine plus xanthine oxidase (0.5 and 1.0 U/ml) increased both collagen and noncollagen protein synthesis at 48 and 72 hours. The authors concluded that asbestos damages cells primarily via reactive oxygen intermediates and that iron on the crocidolite fiber is a major factor in producing the hydroxyl radical.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

  In plain English

  This 1987 laboratory chapter summarized the authors' earlier work and reported new cell-culture experiments testing whether active oxygen species (oxygen free radicals) are involved in cell damage caused by asbestos. No people were studied; the work used rodent respiratory tract cells. In the new experiments, UICC crocidolite asbestos was first soaked in one of two iron-binding chemicals, deferoxamine or Tiron, and then added to rat lung fibroblast cells (RL-82). Untreated crocidolite at 10 and 15 ug/cm2 reduced the cells' viability. Fibers pretreated with either chemical caused significantly less cell death (p less than 0.001) at all chemical concentrations used. In a second experiment, a xanthine plus xanthine oxidase system that generates superoxide raised collagen and noncollagen protein production in the fibroblasts at 48 and 72 hours. Xanthine alone did not. The authors concluded that their studies suggest asbestos damages cells mainly by generating reactive oxygen intermediates, and that iron on crocidolite fibers is a major factor. They noted that the link to actual disease still had to be shown.

  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.

• Surface physico-chemical studies of chrysotile asbestos and related minerals. C. Jolicoeur, D. Poisson. 1987;10(1-2):1-47. Review PubMed · Publisher

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