Metabolism of benzo[a]pyrene and 7,12-dimethylbenz[a]anthracene in cultured human fetal aortic smooth muscle cells

Bond, James A.; Kocan, Richard M.; Benditt, Earl P.; Juchau, Mont R.

doi:10.1016/0024-3205(79)90574-5

Cited by 47 publications

(6 citation statements)

References 5 publications

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“…Benzo[a]pyrene (B[a]P), 1 a polycyclic aromatic hydrocarbon present in tobacco smoke, is metabolized in tissue to mutagenic derivatives which form DNA adducts within target cells (4 -6). Considerable experimental evidence suggests that B[a]P accelerates smooth muscle proliferation and promotes atherosclerosis in animals ranging from chickens to rats (7)(8)(9)(10)13). In addition, we and others have detected B[a]P-related DNA adducts in atherosclerotic arteries (11)(12)(13).…”

mentioning

confidence: 99%

Benzo[a]pyrene Induces the Transcription of Cyclooxygenase-2 in Vascular Smooth Muscle Cells

Yan¹,

Subbaramaiah²,

Camilli³

et al. 2000

Journal of Biological Chemistry

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mentioning

confidence: 99%

Benzo[a]pyrene Induces the Transcription of Cyclooxygenase-2 in Vascular Smooth Muscle Cells

Yan¹,

Subbaramaiah²,

Camilli³

et al. 2000

Journal of Biological Chemistry

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“…Both dimethylbenz [a]anthracene and benzo [a]pyrene have been used extensively to initiate carcinogenesis in experimental animals (4,5). The enzymes that metabolize these carcinogens are present in the artery wall (6,7).…”

mentioning

confidence: 99%

Transforming gene in human atherosclerotic plaque DNA.

Penn¹,

Garte²,

Warren³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

114

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The monoclonal hypothesis equates atherosclerotic plaques with benign smooth muscle cell tumors and proposes that plaques can arise via mutational or viral events. Here, we provide direct evidence that molecular events, heretofore associated only with tumor cells, are common to plaque cells as well. Three distinct groups of human coronary artery plaque (hCAP) DNA samples transfected into NIH 3T3 cells gave rise to transformed foci. DNA samples from a panel of normal noncancerous human tissues, including coronary artery, were negative in the assay. Southern-blotted focus DNA yielded positive signals when hybridized to the 32P-labeled nick-translated repetitive human "Alu" DNA sequence. The DNA from cloned foci was used successfully in a second round of transfection. Focus DNA hybridized to nick-translated v-Ki-ras, v-Ha-ras, or N-ras probes failed to detect human fragments of these genes. Primary focus cells from each of five clones elicited tumors after injection into nude mice (6/42).Several distinct high molecular weight (>6.6 kilobases) bands were detected after BamHI-digested tumor DNA was hybridized to Alu. Preliminary characterization of these hCAP DNA-associated tumors indicates that they are similar to the fibrosarcomas that arise after injection of ras-transformed cells into nude mice. We propose that transforming genes in plaque cells behave in a manner analogous to the way in which oncogenes behave in cancer cells.

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“…Plaques increased in size in a dose-dependent fashion (4), and even a single injection at 5 weeks of age was sufficient to cause a marked increase in thymidine-labeling index of plaque SMC (5) within 1 week. Enzymes of the cytochrome P-450 system have been identified in both the adult artery wall (6,7) and in fetal aortic SMC (8). The analogy between plaques and benign tumors was strengthened by a recent demonstration that DMBA and methoxamine, administered in an initiation-promotion protocol, resulted in the appearance of microscopic, focal thoracic aorta plaques in cockerels (9).…”

Section: Viruses and Mutagens In Plaque Developmentmentioning

confidence: 99%

“…Finally, the tumors that arise in mice following injection of plaque DNA-transformed cells develop much more slowly than do most tumors arising following injection of cells containing activated oncogenes (7)(8)(9)(10)(11)(12)(13)(14)(15)(16) weeks for plaque DNA associated tumors versus < 2 weeks for activated ms-associated tumors). As yet, no reasonable explanation has been presented for why in plaque-associated tumors there is such a long latent period, as well as an extended period of development once the tumors become visible These questions are especially interesting because there are no other clear-cut differences between plaqueassociated tumors and ras-associated tumors.…”

Section: Prognosismentioning

confidence: 99%

Molecular Alterations Critical to the Development of Arteriosclerotic Plaques: A Role for Environmental Agents

Penn¹

1989

Environmental Health Perspectives

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Cardiovascular disease (CVD) is the single greatest cause of death in the United States and in Western Europe. There is strong epidemiologic evidence for an interaction of environmental and genetic factors in the development of clinically significant episodes of CVD. However, the specific contributions of each of these components to the onset and development of CVD remain unclear. According to the monoclonal hypothesis, arteriosclerotic plaques, the principal lesions associated with CVD, are monoclonal in origin and can be considered benign smooth muscle cells tumors of the artery wall. It follows that somatic cell alterations, possibly brought about by chemical mutagens or viruses, may play critical roles in plaque formation. During the past decade, evidence has been presented from a number of laboratories, including ours, that in animal model systems, both viruses and chemical carcinogens can play a key role in the appearance and development of arteriosclerotic plaques. We have recently provided evidence consistefit with the view that somatic cell alterations are critical to plaque development in man: DNA from human arteriosclerotic plaques transforms cells in vitro and injection of these transformed cells into nude mice results in tumor formation. Thus, plaque DNA behaves similarly to tumor DNA under defined assay conditions.

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Metabolism of benzo[a]pyrene and 7,12-dimethylbenz[a]anthracene in cultured human fetal aortic smooth muscle cells

Cited by 47 publications

References 5 publications

Benzo[a]pyrene Induces the Transcription of Cyclooxygenase-2 in Vascular Smooth Muscle Cells

Benzo[a]pyrene Induces the Transcription of Cyclooxygenase-2 in Vascular Smooth Muscle Cells

Transforming gene in human atherosclerotic plaque DNA.

Molecular Alterations Critical to the Development of Arteriosclerotic Plaques: A Role for Environmental Agents

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