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2 edition of role of oxidant damage in asbestos genotoxicity. found in the catalog.

role of oxidant damage in asbestos genotoxicity.

Christopher James Turver

role of oxidant damage in asbestos genotoxicity.

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Published by Brunel University in Uxbridge .
Written in English


Edition Notes

ContributionsBrunel University. Department of Biochemistry.
The Physical Object
Pagination273p. :
Number of Pages273
ID Numbers
Open LibraryOL20755383M

  Jaurand MC, Mechanisms of fiber-induced genotoxicity, Environ Health Perspect. ;(Suppl 5) Upadhyay D, Kamp DW. Asbestos-induced pulmonary toxicity: role of DNA damage and apoptosis, Exp Biol Med (Maywood). ; Cited by: The significant roles of oxidant enzymes in ROS scavenging also have been suggested by studies with transgenic plants. Wang et al. () demonstrated that overexpression of pea (Pisum sativum) MnSOD in rice showed reduced electrolyte leakage compared to WT leaf slices after polyethylene glycol treatment, which could induce drought Cited by: The direct evidence of the role of oxidative DNA damage and its repair is proven by hereditary syndromes (MUTYH-associated polyposis, NTHL1-associated tumor syndrome), where germline mutations cause loss-of-function in glycosylases of base excision repair, thus enabling the accumulation of oxidative DNA damage and leading to the adenoma. Most interestingly, the genomic damage caused by moderate micronutrient deficiency is of the same order of magnitude as the levels of damage caused by exposure to high doses of environmental toxins (Kym, ; Dangour et al., ; Wald et al., ). Folates and other B-complex vitamins perform key functions in biological processes pivotal to Cited by: 3.

  Occupational exposures to hazardous chemicals in paints cause serious health hazards in painters. The present study was designed to evaluate the possibility of hematotoxic and genotoxic effects of paint chemicals among painters in Assiut Governorate, Egypt. In addition the role of oxidative stress and apoptosis in mechanism of such toxic effects were studied. A case control study was performed Author: Nahed Abdel Maksoud, Khaled Abdel Aal, Nagwa Ghandour, Mona El-Baz, Eman Shaltout.


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role of oxidant damage in asbestos genotoxicity. by Christopher James Turver Download PDF EPUB FB2

The role of oxidant damage in asbestos genotoxicity Author: Turver, C. ISNI: Awarding Body: University of Brunel Current Institution: Brunel University Date of Award: Availability of Full Text: Access from EThOS. There are some evidences about the role of asbestos-induced oxidative stress and symptoms in individuals who chronically are exposed to asbestos.

For example, high levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in workers' blood samples is one of the markers of DNA damage in workers who were exposed to by: 4. The spectrum of mutations induced in the omentum of lacI-transgenic rats treated with crocidolite was compatible with 8-oxoGua playing an important role in mutation induction, thus supporting the potential significance of this lesion for the biological effects of asbestos.

In view of the probable role of oxidative DNA and chromosome damage in asbestos carcinogenicity, it is possible that such types of damage Cited by: Exposure to asbestos causes cellular damage, leading to asbestosis, bronchogenic carcinoma, and mesothelioma in humans.

The pathogenesis of asbestos-related diseases is complicated and still poorly understood. Studies on animal models and cell cultures have indicated that asbestos fibers generate reactive oxygen and nitrogen species (ROS/RNS) and cause oxidation and/or nitrosylation of.

Multiple roles of oxidants in the pathogenesis of asbestos-induced diseases Article Literature Review in Free Radical Biology and Medicine 34(9) June with Reads. (15) In addition to eliciting this inflammatory response, asbestos can generate reactive oxygen and nitrogen species, which lead to DNA structure damage and induce genotoxicity, thus favoring the.

The genotoxicity of asbestos fibers is generally mediated by reactive oxygen species (ROS) and by insufficient antioxidant protection. To further elucidate which radicals are involved in asbestos-mediated genotoxicity and to which extent, we have carried out experiments with the metal chelators deferoxamine (DEF) and phytic acid (PA), and with the radical scavengers superoxide dismutase Cited by:   Persistent asbestos fibers cause the generation of reactive oxygen species (ROS) and oxidative tissue damage that are implicated in the pathogenesis of asbestos-induced cancers [4,5].

Inhaled asbestos fibers permeate into the lung, and ultimately to the pleural surface, where they are taken up by tissue phagocytes, primarily macrophages [ 7, 8 ].Cited by:   If generation of ROS is one of the major pathways for arsenic-mediated genotoxicity, then it should be expected to induce specific DNA lesions consistent with oxidative damage.

One of the most common oxidative DNA lesions is 8-hydroxy-2′-deoxyguanosine (8-OHdG).Cited by:   The in vitro and in vivo data addressing the causal role of ROS and RNS in asbestos-induced DNA/chromosomal damage and mutagenesis in target cells/tissues was previously summarized.

The interrelations between ROS and RNS and other asbestos-induced biological activities (i.e., apoptosis, P53 expression and inflammation) are analyzed below, if.

Overproduction of reactive oxygen and nitrogen species can result from exposure to environmental pollutants, such as ionising and nonionising radiation, ultraviolet radiation, elevated concentrations of ozone, nitrogen oxides, sulphur dioxide, cigarette smoke, asbestos, particulate matter, pesticides, dioxins and furans, polycyclic aromatic hydrocarbons, and many other compounds present in the Cited by: Mitochondria-Derived Reactive Intermediate Species Mediate Asbestos-Induced Genotoxicity and Oxidative Stress–Responsive Signaling Pathways causing generation of oxidants, chromosomal damage.

Dong H, Buard A, Renier A, Lévy F, Saint-Etienne L, Jaurand MC. Role of oxygen derivatives in the cytotoxicity and DNA damage produced by asbestos on rat pleural mesothelial cells in vitro. Carcinogenesis. Jun; 15 (6)– Dong HY, Buard A, Cited by: Asbestos causes oxidant production that becomes localized in mitochondria.

To determine whether oxidants are produced and localized to mitochondria after exposure of RPM cells to asbestos or H 2 O 2 ( μM for 30 min), we used CSLM to illustrate colocalization of the oxidant probe Red CC-1 with MitoTracker Green, a mitochondrial-selective dye (). Cited by:   Their role in the initiation and progression of cellular and mitochondrial DNA damage (cDNA and mtDNA), membrane lipid peroxidation, and oxidative damage to proteins and enzymes is crucial.

Also, airborne particulate matter (PM 10 and PM 2. 5) are microparticles or nanoparticles which can penetrate the respiratory system, entering deep into Author: Athanasios Valavanidis. Oxidative Stress. Oxidative stress is defined as an imbalance between oxidant production and antioxidant capacity, and has been implicated in the vascular damage associated with cardiovascular pathologies, such as atherosclerosis, diabetes, and hypertension.4,5.

With regard to genotoxicity testing and cancer risk assessment, particles and fibers form a rather specific group among all toxicants. First, the physicochemical behavior of fibrous and nonfibrous Author: Roel Schins. In vitro genotoxicity of asbestos substitutes induced by coupled stimulation of dissolved high-valence ions and oxide radicals.

Environmental Science and Pollution Research25 (23), DOI: /s Several studies have also shown that p dependent transcription has an important role in asbestos-induced DNA damage and apoptosis [].

Finally, asbestos-induced PARP activation in lung epithelial cells and mesothelial cells leads to apoptosis [, ]. This chapter reviews the effects of vitamin C on metal-induced genotoxicity. By focusing on cutting-edge studies, including our own results in experiments with vanadium(V) and chromium(VI), the suggestion that vitamin C can be used effectively to protect against or reduce the genotoxic effects induced by metal exposure by suppressing oxidative stress is particularly by: 3.

To test the hypothesis that asbestos-mediated cell injury is mediated through an oxidant-dependent mitochondrial pathway, isolated mesothelial cells were examined for mitochondrial DNA damage as de Cited by: Asbestos Mechanisms of Toxicity Workshop Asbestos – a group of highly fibrous silicate minerals that readily separate into long, thin, strong fibers that have sufficient flexibility to be woven are heat resistant and chemically inert, are electrical insulators and therefore are suitable.

(Gary et al., ) Serpentine. Lung represents an important target tissue when investigating the genotoxic effects of oxidant-producing compounds such as cigarette smoke, pollutants, and asbestos fibers.

In particular, the bronchial epithelium acts as a physicochemical barrier and plays a crucial role in initiating and augmenting defense mechanisms and is responsible for Cited by:   APA style: Mechanisms of the genotoxicity of crocidolite asbestos in mammalian cells: implication from mutation patterns induced by reactive oxygen species.

(Articles). It is well known that species derived from oxygen are cytotoxic and are involved in the etiology of cancer.

Several carcinogens during metabolism exert their effect by producing reactive oxygen species (ROS). One of the consequences of oxidative damage to cellular DNA is mutated.

It plays a vital role in the process of carcinogenesis (especially in the initiation and progression).Cited by: 3. Asbestos fibers induced nuclear DNA oxidative damage. Initially, we examined the role of mitochondria in asbestos-induced oxidative damage of the nuclear genome.

To do this, both parental and ρ 0 SAE cells were subjected to various doses of chrysotile and crocidolite exposure for 48 hr. The formation of 8-OHdG, a DNA lesion known to form upon oxidative damage, was measured Cited by: An early study showed that asbestos-induced oxidative DNA damage (8-hydroxydeoxyguanosine formation) was augmented by BSO and ameliorated by NAC, indicating that GSH modulates the genotoxic effects of asbestos.

In the present study, silica-induced DNA strand breaks were evaluated with a comet assay, and the inhibitory effect of NAC and the Cited by:   Asbestos fibers induced nuclear DNA oxidative damage.

Initially, we examined the role of mitochondria in asbestos-induced oxidative damage of the nuclear genome. To do this, both parental and ρ 0 SAE cells were subjected to various doses of chrysotile and crocidolite exposure for 48 hr. The formation of 8-OHdG, a DNA lesion known to form upon Cited by:   Human exposure to (certain forms of) crystalline silica (CS) potentially results in adverse effects on human health.

Since IARC has classified CS as a Group 1 carcinogen [1], which was confirmed in a later review in [2]. The genotoxic potential and mode of genotoxic action of CS was not conclusive in either of the IARC reviews, although a proposal for mode of actions was made in an Cited by: 9.

Environmental and occupational exposure to benzene from fuels is a major cause for concern for national and international authorities, as benzene is a known carcinogen in humans and there is no safe limit for exposure to carcinogens.

The objective of this study was to evaluate the genotoxic effects of chronic occupational exposure to benzene among two groups of workers: filling station workers Author: Isabele C.

Costa-Amaral, Leandro V. Carvalho, Marcus Vinicius C. Santos, Daniel Valente, Angélica. The book comprises 13 chapters covering ecotoxicology, cytotoxicity, nanotoxicity and genotoxicity mechanisms causing by the role and interactions of nanoparticles and free radicals with (RONS) and (ER) stress.

Endoplasmic Reticulum (ER) Stress as a mechanism for. The role of genotoxicity in asbestos-induced mesothelioma: an explanation for the differences in carcinogenic potential among fiber types. Inhal. Toxicol. 25, –67 ().Cited by: 1. Scientific Committee on Toxicity, Ecotoxicity and the Environment Brussels, C2/GF/csteeop/Asbestos /D In vivo genotoxicity of fibres, including chrysotile, can arise via a) direct mechanisms (primary genotoxicity), involving the generation of fibre components of Oberdörster () also discussed the role of dose, dimensions and File Size: KB.

The amphibole hypothesis. The structural properties of asbestos fibres have been the focal point of theories of the pathogenesis of asbestos induced diseases Amphibole fibres may be regarded as more toxic than chrysotile but this is an area of considerable disagreement.1 4 7 9 Compared with chrysotile, amphibole fibres accumulate more readily in the distal lung parenchyma, Cited by:   Asbestos fibers induced nuclear DNA oxidative damage.

Initially, we examined the role of mitochondria in asbestos-induced oxidative damage of the nuclear genome. To do this, both parental and [0] SAE cells were subjected to various doses of chrysotile and crocidolite exposure for 48 hr.

The rapidly emerging field of nanotechnology has offered innovative discoveries in the medical, industrial, and consumer sectors. The unique physicochemical and electrical properties of engineered nanoparticles (NP) make them highly desirable in a variety of applications.

However, these novel properties of NP are fraught with concerns for environmental and occupational by:   To date, no genetic model has been developed to address the role of oxidative damage in asbestos-induced genotoxicity or the role of XRCC1 in protecting human cells from asbestos-induced damage.

It is plausible that XRCC1 is involved in repair of asbestos-induced DNA damage because asbestos induces multiple DNA lesions that are repaired by XRCC1 -dependent.

Furthermore, we determined the role of mitochondrial DNA (mtDNA) alterations in promoting mitochondrial dysfunction and mitochondria respiration chain-derived oxidants in response to asbestos exposure. Additionally, this thesis investigated whether mitochondria-derived oxidants regulate redox-responsive signaling in asbestos-exposed SAE cells.

Nanoparticle toxicology Scientific state-of-the-art Ken Donaldson, University of Edinburgh Edinburgh, Scotland like asbestos Brain N a n o p a r t i c l e s Skin gut atheromatous plaques Lung Nose endothelium liver DNA damage-Genotoxicity Free inFile Size: 7MB.

Shukla A, Gulumian M et al (a) Multiple roles of oxidants in the pathogenesis of asbestos-induced diseases. Free Radic Biol Med 34(9)– PubMed Google Scholar Shukla A, Jung M et al (b) Asbestos induces mitochondrial DNA damage and dysfunction linked to the development of apoptosis.

Relevant books & reviews Hardy J.A. and Aust A.E. Iron in asbestos chemistry and carcinogenicity. Chem. Rev.Kamp D.W. and Weitzman S.A. The molecular basis of asbestos induced lung injury. Thorax,Kinnula t and antioxidant mechanisms of lung diseases caused by asbestos fibers.

Eur. Respir.The causal association between asbestos exposure and nonmalignant and malignant diseases of the lungs and mesothelial linings is well established and supported by epidemiologic, animal, and mechanistic toxicologic studies (IARC ). The biologic mechanisms responsible for asbestos .asbestos-induced DNA damage is prevented by iron chelators and antioxidants in cultured cells (Upadhyay and Kamp ).

Although the DNA repair pathways acti-vated by asbestos are largely unknown, the spectrum of DNA damage induced by asbestos suggests a role for single-strand breaks (SSBs) in asbestos-induced genotoxicity.

XRCC1.