RANDOLPH J . MCMURTRY

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A recent clinical advance has been the discovery that many drug-induced hepatic diseases result from the metabolic activation of chemically stable drugs to potent alkylating agents by the liver. In addition to the liver, however, the kidney also contains active enzyme systems capable of metabolically activating drugs and other chemicals. For this reason a(More)
The hepatotoxicity of the herbal plant germander and that of one of its major furanoneoclerodane diterpenes, teucrin A, were investigated in mice. Teucrin A was found to cause the same midzonal hepatic necrosis as observed with extracts of the powedered plant material. Evidence that bioactivation of teucrin A by cytochromes P450 (P450) to a reactive(More)
Chronic hepatic necrosis developed in a man who had been taking 4 g of paracetamol daily for about a year (cumulative dose 1700 g). Liver biopsy done 23 days after the drug was stopped showed prominent diffuse central necrosis and portal changes. Repeat biopsy 5 months later showed chronic active hepatitis. This prompted anti-inflammatory treatment, with(More)
An inhibitor of adrenal steroid biosynthesis, aminoglutethimide, was administered to seven patients with low renin essential hypertension, and the antihypertensive action of the drug was compared with its effects on adrenal steroid production. In all patients aldosterone concentrations in plasma and urine were within normal limits before the study. Mean(More)
The N-methyl analogs of p-hydroxyacetanilide (acetaminophen) and p-ethoxyacetanilide (phenacetin) were prepared and tested for toxicity. N-Methylacetaminophen was found to cause no hepatic necrosis in mice, rats, or hamsters in doses that caused massive hepatic necrosis in the same animals when acetaminophen was administered. Neither acetaminophen nor its(More)