Au W W, Morris D L, Legator M S
Department of Preventive Medicine and Community Health, University of Texas Medical Branch, Galveston 77555-1010.
Mutat Res. 1993 Aug;300(3-4):273-9. doi: 10.1016/0165-1218(93)90061-h.
2-Methoxyethanol (ethylene glycol monomethyl ether; EGME) is present in many industrial and consumer products, therefore, many individuals in the population are exposed to EGME. Although the toxicity of this compound is well documented its genotoxicity has not been adequately investigated using updated cytogenetic procedures. We have conducted studies to determine the clastogenic effects of EGME and its metabolite, methoxyacetaldehyde (MALD), in bone-marrow cells of B6C3F1 mice after their acute and subchronic exposure to the chemicals by the oral route. In addition, the effects after acute intravenous treatment with EGME were investigated. Mice treated with cyclophosphamide (CP) under similar experimental conditions were used as positive controls. Mice treated acutely with EGME or MALD were also implanted with bromodeoxyuridine tablets to label cells so that only cells at their first post-treatment mitoses were selected for chromosome analyses. Our data show that none of the concentrations of EGME (35-2500 mg/kg body weight) nor MALD (20-1000 mg/kg) caused any induction of chromosome aberrations even though cytotoxic doses were used. On the other hand, CP caused significant increases in chromosome damage. The data suggest that EGME and MALD are either non-clastogenic in vivo or that our mice are able to detoxify the two chemicals. In order to clarify these possibilities, pharmacokinetic and metabolic studies need to be conducted.
