Enhanced lipid peroxidation in lung lavage of rats after inhalation of asbestos

Petruska, Janet; Leslie, Kevin O.; Mossman, Brooke T.

doi:10.1016/0891-5849(91)90160-5

Cited by 42 publications

(13 citation statements)

References 44 publications

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“…Numerous in vitro studies have identified increased reactive oxygen species (ROS) generation as an initiating factor in cancer. The generation of ROS and the resulting oxidative stress may cause a breakdown of membrane lipids, an imbalance of intracellular calcium homeostasis and DNA breakage (Petruska et al, 1991;Clutton, 1997;Shukla et al, 2011). Here we report increased oxidative stress in Sh-SEA-treated cells.…”

Section: Discussionmentioning

confidence: 50%

Tumour-like phenotypes in urothelial cells after exposure to antigens from eggs of Schistosoma haematobium: An oestrogen–DNA adducts mediated pathway?

Botelho

Vale

Gouveia

et al. 2013

International Journal for Parasitology

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a b s t r a c tChronic infection with the blood fluke, Schistosoma haematobium, is associated with squamous cell carcinoma of the bladder. Previously, it has been shown that soluble extracts of mixed sex adult S. haematobium worms (SWAP) are tumourigenic, both in vitro and in vivo. In addition, oestrogen-related molecules in SWAP of S. haematobium down-regulate oestrogen receptors (ERs) alpha and beta in oestrogen responsive cells. Moreover, schistosome oestrogens occur in sera of persons with schistosomiasis haematobia and repress transcription of ERs in urothelial cells. Given that eggs of S. haematobium are the developmental stage directly responsible for urogenital disease during schistosomiasis haematobia, we suspected that soluble antigens from S. haematobium eggs exhibit similar or more potent tumorigenic capacity. Here we investigated the tumorigenic potential of soluble egg antigens (Sh-SEA) of S. haematobium and the endocrine system in favouring parasitism by schistosomes. The findings confirmed that 6.25 lg/ml of Sh-SEA was enough to stimulate cell proliferation, reduce apoptosis and increase oxidative stress of Sh-SEA-exposed urothelial cells. In addition, genotoxic effects of Sh-SEA on these cells were determined by using alkaline single-cell gel electrophoresis (Comet). Furthermore, Liquid Chromatography Diode Array Detection Electron Spray Ionisation Mass Spectrometry indicated the presence of catechol-oestrogens in S. haematobium SEA. A prospective oestrogen-DNA adduct mediated pathway in S. haematobium egg induced bladder cancer is also discussed. Ó

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Section: Discussionmentioning

confidence: 50%

Tumour-like phenotypes in urothelial cells after exposure to antigens from eggs of Schistosoma haematobium: An oestrogen–DNA adducts mediated pathway?

Botelho

Vale

Gouveia

et al. 2013

International Journal for Parasitology

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“…Markers of cellular permeability and damage were also augmented at most of the time points both in the amosite and in the high-dose LA groups. Increased protein in BAL fluid, likely due to increased epithelial permeability, was reported previously in rats exposed to amphibole asbestos by inhalation (Petruska et al 1991) and IT instillation (Ishihara et al 1999;Adamis et al 2001). LDH was elevated in both FIGURE 9.…”

Section: Discussionmentioning

confidence: 55%

Pulmonary Inflammatory and Fibrotic Responses in Fischer 344 Rats After Intratracheal Instillation Exposure to Libby Amphibole

Padilla-Carlin

Schladweiler

Shannahan

et al. 2011

Journal of Toxicology and Environmental Health, Part A

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Increased incidences of asbestosis have been reported in workers from Libby, MT, associated with exposures to amphibole-contaminated vermiculite. In this study pulmonary and histopathological changes were investigated following Libby amphibole (LA) exposure in a rat model. Rat respirable fractions of LA and amosite (aerodynamic diameter <2.5 μm) were prepared by water elutriation. Male F344 rats were exposed to single doses of either saline (SAL), amosite (0.65 mg/rat), or LA (0.65 or 6.5 mg/rat) by intratracheal instillation. At times from 1 d to 3 mo after exposure, bronchoalveolar lavage (BAL) was performed and right and left lungs were removed for reverse-transcription polymerase chain reaction (RT-PCR) and histopathological analysis, respectively. Data indicated that 0.65 mg amosite resulted in a higher degree of pulmonary injury, inflammation, and fibrotic events than LA at the same mass dose. Exposure to either amosite or high dose LA resulted in higher levels of cellular permeability and injury, inflammatory enzymes, and iron binding proteins in both BAL fluid and lung tissue at most time points when compared to SAL controls. However, mRNA expression for some growth factors (e.g., platelet-derived growth factor [PDGF]-A and transforming growth factor [TGF]-1β), which contribute to fibrosis, were downregulated at several time points. Furthermore, histopathological examination showed notable thickening of interstitial areas surrounding the alveolar ducts and terminal bronchioles. On a mass dose basis, amosite produced a greater acute and persistent lung injury for at least 3 mo after exposure. However, further testing and analysis of LA are needed with regard to the dose metric to fully evaluate its potential fibrogenicity and carcinogenicity.

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“…This evidence is supported by the results of the TEM analyses. The reaction of particles with cell membranes results in the generation of ROS, and the generated oxidative stress may cause a breakdown of membrane lipids, imbalance of intracellular calcium homeostasis, and alterations in metabolic pathways (32)(33)(34). The imbalance of calcium homeostasis finally results in calcium-dependent endonuclease activation, which is believed to initiate chromatin fragmentation, another key feature of apoptotic cells (35,36).…”

Section: Discussionmentioning

confidence: 99%

Evidence that ultrafine titanium dioxide induces micronuclei and apoptosis in Syrian hamster embryo fibroblasts.

Rahman

Lohani

Dopp

et al. 2002

Environ Health Perspect

355

218

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Inhaled ultrafine titanium dioxide (UF-TiO2) particles cause pronounced pulmonary inflammation, in contrast to fine TiO2. Previous studies provide evidence for the production of reactive oxygen species by alveolar macrophages, after overloading with UF-TiO2 particles and cytotoxicity of UF-TiO2 in rat lung alveolar macrophages. UF-TiO2 also causes pulmonary fibrosis and lung tumors in rats. UF-TiO2 particles are photogenotoxic, but in general, information on the genotoxicity of UF-TiO2 is still limited. We studied the potential of UF-TiO2 (particle size less than or equal to 20 nm) and fine TiO2 (particle size > 200 nm) to induce chromosomal changes, which can be monitored by the formation of micronuclei (MN) in Syrian hamster embryo (SHE) cells. We also analyzed UF-TiO2-treated cells for apoptosis induction. The MN assay revealed a significant increase in MN induction (p less than or equal to 0.05) in SHE cells after treatment with UF-TiO2 (1.0 micro g/cm2) for 12 hr (mean, 24.5 MN/1,000 cells), 24 hr (mean, 31.13 MN/1,000 cells), 48 hr (mean, 30.8 MN/1,000 cells), 66 hr (mean, 31.2 MN/1,000 cells), and 72 hr (mean, 31.3 MN/1,000 cells). Bisbenzimide staining of the fixed cells revealed typical apoptotic structures (apoptotic bodies), and the apoptosis-specific "DNA ladder pattern" resulting from internucleosomal cleavage was identified by gel electrophoresis. Furthermore, transmission electron microscopy of the exposed cells revealed the typical chromatin compaction of apoptosis.

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Enhanced lipid peroxidation in lung lavage of rats after inhalation of asbestos

Cited by 42 publications

References 44 publications

Tumour-like phenotypes in urothelial cells after exposure to antigens from eggs of Schistosoma haematobium: An oestrogen–DNA adducts mediated pathway?

Tumour-like phenotypes in urothelial cells after exposure to antigens from eggs of Schistosoma haematobium: An oestrogen–DNA adducts mediated pathway?

Pulmonary Inflammatory and Fibrotic Responses in Fischer 344 Rats After Intratracheal Instillation Exposure to Libby Amphibole

Evidence that ultrafine titanium dioxide induces micronuclei and apoptosis in Syrian hamster embryo fibroblasts.

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