A review of the genotoxicity of ethylbenzene.

Ethylbenzene is an important industrial chemical that has recently been classified as a possible human carcinogen (IARC class 2B). It induces tumours in rats and mice, but neither the relevance of these tumours to humans nor their mechanism of induction is clear. Considering the carcinogenic potential of ethylbenzene, it is of interest to determine whether there is sufficient data to characterize its mode of action as either genotoxic or non-genotoxic.

Perspectives on the genotoxic risk of styrene.

Styrene is a highly reactive monomer widely used in the plastics industry. The potential for styrene to produce genotoxic effects has been studied extensively in experimental systems. Styrene can induce sister chromatid exchanges (SCE) and chromosome aberrations (CA) in vitro under test conditions that enhance metabolism of styrene to styrene 7,8-oxide (SO)or reduce detoxification of 50 by epoxide hydrolase.

Studies on the genotoxicity of beryllium sulphate in vitro and in vivo.

There is limited evidence that beryllium is a lung carcinogen to man, and several compounds of beryllium are carcinogenic to the lungs of the rat, rabbit and monkey. One such compound is beryllium sulphate (BeSO4.4H2O).

Assay-specific genotoxicity of N-nitrosodibenzylamine to the rat liver in vivo.

N-Nitrosodibenzylamine (NDBzA) is mutagenic to Salmonella typhimurium and induces DNA strand breaks in isolated rat hepatocytes, yet it is reported to be non-carcinogenic to the rat. Here we report that it is inactive in both the rat and mouse bone marrow micronucleus assays and in a rat liver autoradiographic assay for unscheduled DNA synthesis. It is, however, clearly active as a micronucleus-inducing agent and mitogen in the rat liver and is capable of inducing single-strand breaks in the DNA of rat liver.

Clastogenicity of tritiated thymidine to the mouse bone marrow.

Tritiated thymidine (3HTdR; 120 microCi/mouse) increases the incidence of micronucleated polychromatic erythrocytes (MPE) in bone marrow PE of both B6CF1 and CBA male mice. This effect observed in vivo reflects, the clastogenicity reported by other investigators for 3HTdR in vitro. Thymidine itself was concluded to be inactive in the assay at a dose-level 100 times greater than that required to show activity for 3HTdR.