Studies on benzene mutagenesis. I. The micronucleus test

Díaz, M.M.; Reiser, Ana; Braier, L; Díez, Juan J.

doi:10.1007/bf01952286

Cited by 21 publications

(8 citation statements)

References 15 publications

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“…It may be postulated that the rise in the number of dividing cells may be due to recruitment of new cells into division and to annul the effect of cell death caused by benzene toxicity. Benzene-induced cell cycle delay in S phase was also observed in studies conducted on benzene mutagenesis by Diaz et al [16]. DAMC provides protection to the cells against benzene toxicity.…”

Section: Discussionsupporting

confidence: 52%

Chemoprevention of benzene-induced bone marrow and pulmonary genotoxicity

Raj

Malik

Parmar

et al. 2001

Teratog. Carcinog. Mutagen.

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Our earlier studies documented the ability of 7,8-diacetoxy-4-methylcoumarin (DAMC) to cause irreversible inhibition of cytochrome P-450 linked mixed function oxidases (MFO) mediated by membrane bound DAMC: protein transacetylase. Since P-450 catalyzed oxidation of benzene is crucial to its toxic effects, the action of DAMC and related analogues were considered promising in preventing the genotoxicity due to benzene. For this purpose rats were pretreated with various acetoxy-4-methylcoumarins (test compounds), which was followed by the administration of benzene either intratracheally (IT) or intraperitoneally (IP), and sacrificed 26 h after the injection of benzene. The incidence of micronuclei (MN) in bone marrow (BM) and lung (LG) were assessed by light and fluorescent microscopy, respectively. A dose-dependent induction of MN in BM and LG cells was observed in rats administered with benzene. A significant reduction in benzene-induced MN in BM and LG was observed as a result of DAMC administration to rats; a higher dose of DAMC resulted in greater inhibition of clastogenic action of benzene as revealed by MN incidence. 7,8-dihydroxy-4-methylcoumarin (DHMC), the deacetylated product of DAMC, demonstrated relatively lesser potency to inhibit the clastogenic action of benzene. This observation is consistent with the ability of DAMC to inhibit the formation of benzene oxide as well as to scavenge the oxygen radicals formed during the course of benzene metabolism. The fact that DHMC can only scavenge the oxygen radicals and is ineffective in inhibiting benzene oxidation in vivo explains the reduced capability of dihydroxy coumarin to prevent MN due to benzene. 7-Acetoxy-4-methylcoumarin (MAC) inhibits the MN due to benzene being roughly 50% of that produced by DAMC. DAMC is also effective in normalizing the cell cycle alterations produced by benzene in BM and LG. These observations further substantiate our hypothesis that the biological effects of acetoxy coumarins are mediated by the action of membrane bound transacetylase that catalyzes the acetylation of concerned proteins. Teratogenesis Carcinog. Mutagen. 21:181-187, 2001.

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Section: Discussionsupporting

confidence: 52%

Chemoprevention of benzene-induced bone marrow and pulmonary genotoxicity

Raj

Malik

Parmar

et al. 2001

Teratog. Carcinog. Mutagen.

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“…The MNT which was positive with benzene in mice [Diaz et al, 1980;Hite et al, 1980;Meyne and Legator, 1980;Siou et al, 19811 has offered a unique endpoint for the study of benzene [Gad-El-Karim et al, 19841, since it is performed on cells aValues significantly higher than untreated controls (p < 0.01). bValues significantly higher than benzene treatment alone (p < 0.01).…”

Section: Discussion the Micronucleus Testmentioning

confidence: 99%

Benzene myeloclastogenicity: A function of its metabolism

Gad-El-Karim

Ramanujam²,

Ahmed

et al. 1985

American J Industrial Med

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Using the micronucleus test we have found no significant difference between germ-free and conventional (non-germ-free) male CD-1 mice gavaged twice with 440 or 880 mg benzene/kg. Hence, the higher myeloclastogenicity observed previously with the p.o. (4-6 times) than with the i.p. route of benzene administration was ruled out as being due to the involvement of gut flora in benzene biotransformation. Pretreatment of males with 3-methylcholanthrene or beta-naphthoflavone, inducers of P-448 monooxygenase, but not phenobarbital, an inducer of P-450, significantly enhanced the myeloclastogenic effect of a single oral dose of benzene (440 mg/kg). Single oral doses of phenol, catechol, or hydroquinone (250, 150, and 200 mg/kg, respectively) failed to reproduce the potent myeloclastogenic effect of benzene. In fact, only hydroquinone was mildly clastogenic. The relation between benzene's myeloclastogenicity and metabolism is discussed.

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“…Together with toluene, ethylbenzene plus the ortho-, metaand para-xylene, benzene forms what is known as "BTEX compounds", BTEX constitutes the petroleum fraction with the highest water solubility, therefore, after oil spills, these compounds are the most likely to reach water reservoirs and cause various types of damage to the organisms present in the aquatic habitats. Several studies using single-cell gel assay have shown that BZN can effectively induce micronuclei and other types of DNA damage, in fish and other vertebrate cells (Diaz et al, 1980;Misra et al, 1987;Harper et al, 1989;Andreoli et al, 1997;Whysner et al, 2004;Maffei et al, 2005;Wetmore et al, 2008). Benzene can also induce structural and numerical chromosome aberrations, sister chromatid exchanges and micronuclei by various routes of exposure (WHO, 1993).…”

Section: Introductionmentioning

confidence: 99%

Micronucleus Test and Comet Assay in Erythrocytes of the Amazonian Electric Fish Apteronotus bonapartii Exposed to Benzene

Bücker

Carvalho²,

Conceição³

et al. 2024

Ecotoxicol. Environ. Contam.

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In this study we address the genotoxicity and putative mutagenic effects of benzene (BZN) in the erythrocytes of the electric fish Apteronotus bonapartii (Gymnotiformes, Apteronotidae) using the micronucleus test (MN) and comet assay, under controlled laboratory conditions. Electric fish were collected in the Solimões River, Manaus-AM, Brazil, and the specimens were exposed to 10 and 25 ppm concentrations of BZN, in 150L tanks. Blood samples were collected at 0 (T 0), 24, 48, 72 and 96 hours of exposure. For the concentration of 10 ppm BZN, the number of comets was significantly higher than T 0 levels after exposure of 48 hours, whereas the nuclear abnormalities (including MN) did not show any increase in relation to the controls (T 0) up to 96 hours. For the 25 ppm BZN, MN rates presented a significant increase after 72 hours, whereas other types of nuclear abnormalities increased in frequency after various exposure times, ranging from 24 to 72 hours. The number of comets increased significantly from 24 hours onwards for 25 ppm BZN. Both assays also showed a gradual increase in the number of damaged cells after longer exposure periods, indicating a time-dependent effect, especially at the highest BZN concentrations tested. This investigation reinforces the potential use of the endemic South American electric fish as a suitable genotoxicity biological model for biomonitoring purposes in the Amazon.

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Studies on benzene mutagenesis. I. The micronucleus test

Cited by 21 publications

References 15 publications

Chemoprevention of benzene-induced bone marrow and pulmonary genotoxicity

Chemoprevention of benzene-induced bone marrow and pulmonary genotoxicity

Benzene myeloclastogenicity: A function of its metabolism

Micronucleus Test and Comet Assay in Erythrocytes of the Amazonian Electric Fish Apteronotus bonapartii Exposed to Benzene

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