C. E. Seddon

Species differences in the hepatotoxicity of paracetamol are due to differences in the rate of conversion to its cytotoxic metabolite.

A. Boobis, D. Davies, L. Tee, 1987, Biochemical pharmacology.

Quinidine and the identification of drugs whose elimination is impaired in subjects classified as poor metabolizers of debrisoquine.

A. Boobis, D. Davies, C. Speirs, 1986, British journal of clinical pharmacology.

Bufuralol 1'-hydroxylase activity of the rat. Strain differences and the effects of inhibitors.

A. Boobis, D. Davies, C. E. Seddon, 1986, Biochemical pharmacology.

Evidence for a direct role of intracellular calcium in paracetamol toxicity.

A. Boobis, D. Davies, C. E. Seddon, 1990, Biochemical pharmacology.

Comparative activation of paracetamol in the rat, mouse and man.

D. Davies, C. E. Seddon, A. R. Bobois, 1987, Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement.

Quinidine andtheidentification ofdrugs whoseelimination is impaired insubjects classified aspoormetabolizers ofdebriso- quine

S. Murray, A. Boobis, C. Speirs, 1986 .

Cytoprotective effects of 16,16-dimethyl prostaglandin E2 on paracetamol toxicity in isolated hepatocytes

A. Boobis, D. Davies, C. E. Seddon, 1988 .

In vitro studies of induction and inhibition of drug oxidation in man.

A. Boobis, D. Davies, C. E. Seddon, 1987, Pharmacology & therapeutics.