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PubMed1975

Biochemical toxicology of unsaturated halogenated monomers.

Previous inhalation toxicity studies from our laboratory have shown that 1,1-dichloroethylene (1,1-DCE), 1,1-dibromoethylene (1,1-DBE), and 2-chloro-1,3,-butadiene (2-CBD) are more toxic to fasted rats than to fed rats. Vinyl chloride monomer (VCM) and 1,1-difluoroethylene (1,1-DFE) were not acutely hepatotoxic at 46,500 and 82,000 ppm, respectively, in normal male rats, whether fed or fasted. On a molar basis, 1,1-DBE and 1,1-DCE have similar toxicities while 2-CBD is less toxic. All three compounds produce similar elevation of serum transaminase and bloody ascites, although at differing times following differing exposure concentrations. 1,1-DCE produces massive midzonal hepatic necrosis with hepatic thrombosis and chromatolysis within 2 hr after a 4 hr exposure of fasted rats to 200 ppm. Subsequent to formation of this midzonal lesion, the central portion of the lobule collapses, accompanied by congestion, ascites, and in increased hematocrit in the rat. Serum transaminase and sorbital dehydrogenase are greatly elevated at 6 hr. This effect in fasted rats is associated with glutathione (GSH) depletion. Diethyl maleate (DEM) which depletes GSH in fed rats potentiates the injury associated with 1,1-DCE exposure as well as that produced by 2-CBD. Rats fed ad libitum and exposed to 1,1-DCE or 2-CBD at night, a time of low hepatic GSH concentration, exhibit enhancement of hepatotoxic response when compared to animals exposed during the day when GSH is high.

Alanine Transaminase↗
PubMed1977

Mutagenicity of halogenated alkanes and their derivatives.

The ability of a series of haloalkanes, haloethanols and haloacetaldehydes to induce mutations in Salmonella typhrimurium and preferentially to inhibit the growth of DNA polymerase-deficient E. coli (pol A(+)/pol A(-)) was investigated. For the haloalkanes investigated, the order of reactivities towards the E. coli pol A(+)/pol A(-), was: 1,1,2,2-tetrabromoethane > 1,1-dibromoethane > 1,1,2,2-tetrachlorethane > 1,2-dibromoethane = 1,5 dibromopentane > 1,2-dibromo-2-methylpropane > 1-bromo-2-chloroethane > 1,2-dichloroethane. In the standard Salmonella mutagenicity assay the order of these substances was 1,2-dibromoethane = 1,5-dibromopentane > 1,2-dibromo-2-methylpropane >/= 1-bromo-2-chloroethane > 1,1,2,2-tetrachloroethane = 1,1-dibromoethane > 1,2-dichloroethane. 1,1,2,2-Tetrabromoethane was negative in the standard assay but strongly mutagenic when tested in suspension. It would appear that the discrepancy between the two procedures is due to the fact that bactericidal mutagens cannot be scored reliably in the standard Salmonella assay. The order of reactivity of 2-haloethanols in E. coli pol. A(+)/pol A(-), was 2-iodo > 2-bromo-> 2-chloroethanol. In the Salmonella assay the order was 2-bromo-> 2 iodo- >2-chloro-ethanol. 2-Fluoroethanol and ethanol were devoid of activity in both assays. For the 2-haloacetaldehydes the reactivities in the E. coli system were 2-bromoethylacetate > 2-bromoacetaldehyde = acetaldehyde > 2-chloroacetaldehyde while in the Salmonella system the order was 2-bromoethylacetate > 2-chloroacetaldehyde. Acetaldehyde had minimal activity, while 2-bromoacetaldehyde was without activity but strongly bactericidal.

Acetaldehyde↗