Harvard University, Boston, Massachusetts, 1980 May; :1-5
Responses to toxic stress are reviewed. The following are examined: characterization of induced liver alkaline-phosphatase and other enzymes altered by toxic chemicals; the role of adrenal hormones and drugs on the toxicity and metabolism of halogenated hydrocarbons; the relationship of anticholinesterase action of organophosphates and increased adrenocortical activity; and the role of drugs, the environment and nutritional stress on neurological deficits produced by acrylamide (79061). Emphasis is placed on investigations of biochemical aspects of toxic stress induced by exposure to haloolefins, acrylamide, and metals. Toxic actions of 1,1- dichloroethylene (75354) (1,1-DCE), 2-chlorobutadiene (126998), 1,1- dibromoethylene (593920), vinyl-chloride-monomer (75014), acrylamide, copper (7440508), and mercury (7439976) are presented. The toxicity of 1,1-DCE is produced by hepatotoxic action in the absence of lipid peroxidation; a role for glutathione in the modulation of hepatotoxicity of 1,1-DCE is implicated. Inhalation tests in rats are cited for vinyl-chloride-monomer, in which hepatotoxicity does not occur; simultaneous inhalation of vinyl- chloride-monomer and 1,1-DCE at a ratio of 5:1 prevents the acute hepatotoxic effects of 1,1-DCE. A quantifiable method for measuring the functional neuromuscular deficit produced in rats by acrylamide is described. The method uses the rotorod principle and can assay the onset and duration of functional neuropathy in relation to sciatic nerve beta-glucuronidase.