7,12-Dimethylbenz[a]anthracene Induces Apoptosis in Murine Pre-B Cells through a Caspase-8–Dependent Pathway

Page, Todd J.; O'Brien, Scott; Jefcoate, Colin R.; Czuprynski, Charles J.

doi:10.1124/mol.62.2.313

Cited by 37 publications

(23 citation statements)

References 41 publications

(38 reference statements)

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“…These results may be contrasted with those obtained with a transformed, stromal cell-independent pre-B cell line, 70Z3 (Page et al, 2002). In studies with these transformed pre-B cells, DMBA induced a minimal and transient level of caspase-8 activity that preceded the relatively late (approximately 15-20 h) induction of caspase-3 activity.…”

Section: Discussioncontrasting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

“…Indeed, in vivo studies with DMBA suggest a role for TNFRs in the elimination of at least some hematopoietic cell types in the bone marrow (Page et al, 2002). In the absence of specific analysis of the fate of bone marrow B cells in particular (Page et al, 2002), it is difficult to tell whether TNFRs were in fact involved in DMBA-induced B cell death in vivo. However, several approaches described herein failed to implicate TNFR family members in early B cell apoptosis: 1) TNF-␣, TNF-␤, and LT-␤ mRNA were not detected by RT-PCR after DMBA treatment; 2) TNF-␣, as assessed by ELISA or surface expression, was not induced in DMBA-treated primary bone marrow stromal cells or in BMS2 cells; 3) inhibitory TNF-Ig and Fas-Ig failed to block apoptosis (data not shown); 4) bone marrow stromal cells from TNF-␣ Ϫ/Ϫ mice were as effective at inducing apoptosis as cells from wild-type mice; and 5) pro-B cells from TNFR1 Ϫ/Ϫ /TNFR2 Ϫ/Ϫ double knockout mice, Fas-defective BALB/c-lpr mice, or DR6 Ϫ/Ϫ mice were as susceptible to DMBA-induced apoptosis as wild-type cells.…”

Section: Discussionmentioning

confidence: 99%

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Environmental Chemical-Induced Bone Marrow B Cell Apoptosis: Death Receptor-Independent Activation of a Caspase-3 to Caspase-8 Pathway

Ryu¹,

Emberley²,

Schlezinger³

et al. 2005

Molecular Pharmacology

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Programmed cell death is a critical process in B lymphocyte development. Premature apoptosis in developing B cells could affect the repertoire and number of mature B cells produced. Of particular concern is the ability of environmentally ubiquitous polycyclic aromatic hydrocarbons (PAH) to induce B cell apoptosis within the bone marrow microenvironment in a clonally nonspecific way. Here, models of bone marrow B cell development were used to assess the role of the "extrinsic" apoptosis pathway in PAH-induced apoptosis and to compare PAH-induced apoptosis with that induced during clonal deletion. As

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Section: Discussioncontrasting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Environmental Chemical-Induced Bone Marrow B Cell Apoptosis: Death Receptor-Independent Activation of a Caspase-3 to Caspase-8 Pathway

Ryu¹,

Emberley²,

Schlezinger³

et al. 2005

Molecular Pharmacology

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“…DMBA has been found to produce immunotoxicity in bone marrow through the induction of apoptosis (Page et al, 2002), and recent studies showed that p53 knockout mice are resistant to the suppressive effects of DMBA on bone marrow (Heidel et al, 2000;Page et al, 2003). Many genotoxic chemicals that induce p53 are also immunosuppressive.…”

Section: (E) Potential Mechanisms Of Immunosuppression By Pahsmentioning

confidence: 99%

Integrating Field Analyses with Laboratory Exposures to Assess Ecosystems Health

Hellou¹,

Beach²,

Leonard³

et al. 2012

Polycyclic Aromatic Compounds

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initiated a programme on the evaluation of the carcinogenic risk of chemicals to humans involving the production of critically evaluated monographs on individual chemicals. The programme was subsequently expanded to include evaluations of carcinogenic risks associated with exposures to complex mixtures, life-style factors and biological and physical agents, as well as those in specific occupations. The objective of the programme is to elaborate and publish in the form of monographs critical reviews of data on carcinogenicity for agents to which humans are known to be exposed and on specific exposure situations; to evaluate these data in terms of human risk with the help of international working groups of experts in chemical carcinogenesis Publications of the World Health Organization enjoy copyright protection in accordance with the provisions of Protocol 2 of the Universal Copyright Convention. All rights reserved.The International Agency for Research on Cancer welcomes requests for permission to reproduce or translate its publications, in part or in full. Requests for permission to reproduce or translate IARC publications -whether for sale or for noncommercial distribution -should be addressed to WHO Press, at the above address (fax: +41 22 791 4806; email: permissions@who.int).The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the Secretariat of the World Health Organization concerning the legal status of any country, territory, city, or area or of its authorities, or concerning the delimitation of its frontiers or boundaries.The mention of specific companies or of certain manufacturers' products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.The IARC Monographs Working Group alone is responsible for the views expressed in this publication. IARC Library Cataloguing in Publication Data NOTE TO THE READERThe term 'carcinogenic risk' in the IARC Monographs series is taken to mean that an agent is capable of causing cancer under some circumstances. The Monographs evaluate cancer hazards, despite the historical presence of the word 'risks' in the title.Inclusion of an agent in the Monographs does not imply that it is a carcinogen, only that the published data have been examined. Equally, the fact that an agent has not yet been evaluated in a Monograph does not mean that it is not carcinogenic.The evaluations of carcinogenic risk are made by international working groups of independent scientists and are qualitative in nature. No recommendation is given for regulation or legislation.Anyone who is aware of published data that may alter the evaluation of the carcinogenic risk of an agent to humans is encouraged to make this information available to the Section of IARC Monographs, International Agency for...

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“…Many studies have suggested that PAHs are environmental immunosuppressive contaminants. PAHs, especially benzo(a)pyrene, not only harm the respiratory and immune system but also cause cell mutation and cancer, including lung and skin cancer (Hecht, 1999;Knize et al, 1999;Laupeze et al, 2002;Page et al, 2002;Yousef et al, 2002;van Grevenynghe et al, 2003). Unfortunately, the reduction of PAHs and PM from burning incense has received little attention.…”

Section: Introductionmentioning

confidence: 99%

Reducing Air Pollution Emissions from Burning Incense with the Addition of Calcium Carbonate

Yang

Lin

Peng

et al. 2012

Aerosol Air Qual. Res.

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A laboratory-scale study was performed to quantify the pollutant reduction effects from burning incense with the addition of CaCO 3 . Many studies have investigated the effects of burning incense on the quality of surrounding air, focusing primarily on particulate matter (PM) and polycyclic aromatic hydrocarbons (PAHs). However, the reduction of PM and PAHs from burning incense has received little attention. In our past study, we investigated nine types of commercially available incense and found that incense with a higher CaCO 3 content had lower PM and PAH emissions factors. Five to thirty percent of CaCO 3 was added to Liao and Chen incense powder, which are popular incense materials. The experimental results indicate that the reductions in the emissions of PM and PAHs from burning incense increased with along with amount of CaCO 3 additive. Mean PM reductions for 5.0%, 10.0%, 20.0%, and 30.0% CaCO 3 were 11 ± 2%, 15 ± 3%, 27 ± 1%, and 41 ± 3%, respectively. Mean particle-phase PAHs (P-PAHs) reductions were 9 ± 9%, 15 ± 5%, 22 ± 1%, and 28 ± 1%, respectively, and 5 ± 6%, 21 ± 1%, 21 ± 3%, and 30 ± 2% for total benzo[a]pyrene equivalent concentration (total BaP eq ), respectively. This study was performed to quantify the reduction of PM and PAH emissions from burning incense with increasing amounts of CaCO 3 . The findings of this study may serve as a guide to producing safer and less-polluting incense.

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7,12-Dimethylbenz[a]anthracene Induces Apoptosis in Murine Pre-B Cells through a Caspase-8–Dependent Pathway

Cited by 37 publications

References 41 publications

Environmental Chemical-Induced Bone Marrow B Cell Apoptosis: Death Receptor-Independent Activation of a Caspase-3 to Caspase-8 Pathway

Environmental Chemical-Induced Bone Marrow B Cell Apoptosis: Death Receptor-Independent Activation of a Caspase-3 to Caspase-8 Pathway

Integrating Field Analyses with Laboratory Exposures to Assess Ecosystems Health

Reducing Air Pollution Emissions from Burning Incense with the Addition of Calcium Carbonate

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