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Toxicants, genetic control

Hill RN, Clemens TL, Liu DK, et al. 1975. Genetic control of chloroform toxicity in mice. Science 190 159-161. [Pg.271]

Mefabo//sm - The half-life of INH is widely variable and dependent on acetylator status. Isoniazid is primarily acetylated by the liver this process is genetically controlled. Fast acetylators metabolize the drug about 5 to 6 times faster than slow acetylators. Several minor metabolites have been identified, one or more of which may be reactive (monoacetylhydrazine is suspected), and responsible for liver damage. The rate of acetylation does not significantly alter the effectiveness of INH. However, slow acetylation may lead to higher blood levels of the drug, and thus to an increase in toxic reactions. [Pg.1713]

Immunological-mediated toxic-induced renal diseases are multifactorial Genetic control of metal-induced autoimmunity and nephropathy... [Pg.131]

See also Clean Air Act (CAA), (US) Clean Water Act (CWA) (US) Environmental Protection Agency (US) Food and Drug Administration (US) Genetically Engineered Foods Lead Mercury Occupational Safety and Health Act, US Organisation for Economic Cooperation and Development Polychlorinated Biphenyls (PCBs) Risk Assessment, Ecological Risk Assessment, Human Health Toxic Substances Control Act. [Pg.1012]

Genetic control of susceptibility to toxicants operates through a variety of mechanisms. One of these is metabolic. In animals, the murine Ah complex represents a "cluster" of genes exercising temporal control on tissue-specific regulatory genes... [Pg.9]

When the concentration of an inorganic ion is above the level where the body cannot return it to homeostasis through genetically controlled regulatory pathways, the ion is toxic. Therapy must be provided to a patient to decrease the toxicity of and ultimately remove the inorganic ion from the body. The most widely used method to remove ions from the body is chelation therapy. [Pg.50]


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