An Overview of the Problem of Benzene Toxicity and Some Recent Data on the Relationship of Benzene Metabolism to Benzene Toxicity

Snyder, Robert; Sammett, David; Witmer, Charlotte; Kocsis, James J.

doi:10.1007/978-1-4613-3455-2_18

Cited by 4 publications

(1 citation statement)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The prolonged observation of MN cells may therefore be due to the continued induction of damage in newly formed cells. The evidence supporting this speculation was presented by Irons et al [198l] who observed radiolabeled benzene, hydroquinone, and catechol in the bone marrow of treated mice even at 7 days after exposure and Snyder et al [1982] who reported that benzene can be stored in the fat tissue of animals for a considerable period of time. Our study provides data to indicate that the effects from benzene exposure on chromosome damage and erythropoiesis perturbation persists in vivo for a long time after the cessation of exposure to benzene.…”

Section: Discussionmentioning

confidence: 92%

Persistence of micronuclei in peripheral blood normochromatic erythrocytes of subchronically benzene‐treated male mice

Rithidech¹,

Au²,

Ramanujam³

et al. 1988

Environ. mutagen

View full text Add to dashboard Cite

The kinetics of micronucleus (MN) induction and decline in blood normochromatic erythrocytes (NCE) of mice subchronically exposed to benzene was investigated during and after exposure. Swiss (ICR) male mice (lO/group) were given 0.0,36.6,73.2, and 146.4 mglkg body weight benzene by gavage daily for 14 days, except for days 5 and 10. The frequency of MN increased significantly (P < .001) during benzene treatment as a function of both concentration and time. Eleven days after exposure the levels of MN were higher than those observed at the end of exposure. After an initial rapid decline in the frequency of MN from 11 to 18 days postexposure, the decline became linear with time through 60 days postexposure. Using linear regression analysis, the MN level in each treatment group was predicted to reach control levels by approximately 85 days post-treatment. Dose-dependent suppression and recovery of erythropoiesis, estimated by polychromatic erythrocyte frequency, were observed in the 1st and 2nd weeks of exposure, respectively. Red blood cell (RBC) production was markedly increased in the first 3 weeks after benzene treatment. At later times the rate of production of the RBC returned to normal and may account for the linear decline observed in MN frequency. This research indicates that the frequency of MN is dose and duration dependent, while the decline in MN frequency after the end of benzene exposure can be related to changes in the kinetics of erythropoiesis.

show abstract

Section: Discussionmentioning

confidence: 92%

Persistence of micronuclei in peripheral blood normochromatic erythrocytes of subchronically benzene‐treated male mice

Rithidech¹,

Au²,

Ramanujam³

et al. 1988

Environ. mutagen

View full text Add to dashboard Cite

show abstract

Cytogenetic assays in genotoxic studies: Somatic cell effects of benzene and germinal cell effects of dibromochloropropane

Forti

Hrelia

et al. 1990

Teratog Carcinog Mutagen

View full text Add to dashboard Cite

We have reviewed the results of our cytogenetic studies to evaluate the usefulness of these assays in genotoxic studies. In one study, we observed unusual dose-response in lymphocyte chromosome aberration frequencies after exposure of mice to low doses of a chemical mixture (benzene, chloroprene, epichlorohydrin, and xylene). The frequency in the high dose group is lower than those of the medium and low dose groups. This reduction of genotoxicity is correlated with a significant induction of a detoxifying enzyme, glutathione-S-transferase. The data also suggest that extrapolation of effects from high to low doses for risk assessment may be erroneous. Using benzene as a model clastogen, we found that the clastogenic effect persists for a long time after termination of exposure in mice. This phenomenon is probably due to a gradual release of benzene from absorption of the chemical in body fat. In an inhalation study, we observed that chromosome aberrations are induced in mice after exposure to benzene at below the occupational exposure limit of 1 ppm. Since benzene is a ubiquitous environmental contaminant, it may interact with other environmental agents to modify its genotoxic effects. We found that a nongenotoxic drug, praziquantel, and a free radical scavenger, DMSO, can enhance or reduce respectively the clastogenic activities of benzene in mice. Both modifying agents acted by altering the metabolic pathways of benzene. In a study with rats, we showed that carcinogenic doses of benzene can induce chromosome aberrations in lymphocytes of rats long before the expression of cancer. With dibromochloropropane, we observed that this chemical can induce dominant lethality in rats.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

Influence of strain differences in mice on the metabolism and toxicity of benzene1, 2

Longacre

Kocsis

Snyder

1981

Toxicology and Applied Pharmacology

View full text Add to dashboard Cite

An Overview of the Problem of Benzene Toxicity and Some Recent Data on the Relationship of Benzene Metabolism to Benzene Toxicity

Cited by 4 publications

References 18 publications

Persistence of micronuclei in peripheral blood normochromatic erythrocytes of subchronically benzene‐treated male mice

Persistence of micronuclei in peripheral blood normochromatic erythrocytes of subchronically benzene‐treated male mice

Cytogenetic assays in genotoxic studies: Somatic cell effects of benzene and germinal cell effects of dibromochloropropane

Influence of strain differences in mice on the metabolism and toxicity of benzene1, 2

Contact Info

Product

Resources

About

An Overview of the Problem of Benzene Toxicity and Some Recent Data on the Relationship of Benzene Metabolism to Benzene Toxicity

Cited by 4 publications

References 18 publications

Persistence of micronuclei in peripheral blood normochromatic erythrocytes of subchronically benzene‐treated male mice

Persistence of micronuclei in peripheral blood normochromatic erythrocytes of subchronically benzene‐treated male mice

Cytogenetic assays in genotoxic studies: Somatic cell effects of benzene and germinal cell effects of dibromochloropropane

Influence of strain differences in mice on the metabolism and toxicity of benzene*1, *2

Contact Info

Product

Resources

About

Influence of strain differences in mice on the metabolism and toxicity of benzene1, 2