J. Mitchell

发表

Molecular basis for several drug-induced nephropathies.

S. Nelson, J. Mitchell, R. Mcmurtry, 1977, The American journal of medicine.

Acetaminophen-induced hepatic necrosis. I. Role of drug metabolism.

B B Brodie, J R Gillette, B. Brodie, 1973, The Journal of pharmacology and experimental therapeutics.

Isoniazid-associated hepatitis in 114 patients.

K. Ishak, H. Zimmerman, J. Mitchell, 1975, Gastroenterology.

Isoniazid hepatoxicity: the relationship between covalent binding and metabolism in vivo.

J. Timbrell, S. Nelson, S D Nelson, 1980, The Journal of pharmacology and experimental therapeutics.

Pharmacokinetics of the toxic hydrazino metabolites formed from isoniazid in humans.

C. V. Smith, J. Mitchell, B. Lauterburg, 1985, The Journal of pharmacology and experimental therapeutics.

Role of detoxifying enzymes in bromobenzene-induced liver necrosis.

J R Gillette, D. Jollow, D J Jollow, 1973, The Journal of pharmacology and experimental therapeutics.

Bromobenzene-induced liver necrosis. Protective role of glutathione and evidence for 3,4-bromobenzene oxide as the hepatotoxic metabolite.

D. Jollow, J. Mitchell, J. Gillette, 1974, Pharmacology.

Studies on the microsomal formation of arylating metabolites of acetaminophen and phenacetin.

S. Nelson, J. Hinson, J. Mitchell, 1977, Molecular pharmacology.

Acetaminophen-induced hepatic necrosis. II. Role of covalent binding in vivo.

B B Brodie, J R Gillette, B. Brodie, 1973, The Journal of pharmacology and experimental therapeutics.

ACETAMINOPHEN-INDUCED HEPATIC NECROSIS. III. CYTOCHROME P-450-MEDIATED COVALENT BINDING IN VITRO

B. Brodie, W. Potter, D. Jollow, 1973 .

Acetaminophen-induced hepatic necrosis. VI. Metabolic disposition of toxic and nontoxic doses of acetaminophen.

S. Thorgeirsson, W. Potter, D. Jollow, 1974, Pharmacology.

N-hydroxylation of p-chloroacetanilde in hamsters.

D. Jollow, J. Hinson, J. Mitchell, 1976, Biochemical pharmacology.

N-Hydroxylation of phenacetin by hamster liver microsomes.

J. Hinson, J. Mitchell, 1976, Drug metabolism and disposition: the biological fate of chemicals.

The formation of arylating and alkylating metabolites of phenacetin in hamsters and hamster liver microsomes.

Y. Vaishnav, S. Nelson, J. Hinson, 1981, Molecular pharmacology.

A placebo-controlled dose-response study of the reactogenicity and immunogenicity of a cold-adapted recombinant A/Victoria/3/75 (H3N2) live influenza virus candidate vaccine in healthy volunteers.

H. Maassab, F. André, J. Mitchell, 1977, Developments in biological standardization.

Species differences in hepatic glutathione depletion, covalent binding and hepatic necrosis after acetaminophen.

W. Potter, D. Jollow, J. Mitchell, 1974, Life sciences.

Formation of chemically reactive metabolites of phenacetin and acetaminophen.

G. Mulder, L. Pohl, S. Nelson, 1981, Advances in experimental medicine and biology.

Effects of N-acetylcysteine on the disposition and metabolism of acetaminophen in mice.

C. V. Smith, J. Mitchell, W. J. Racz, 1985, The Journal of pharmacology and experimental therapeutics.

Spectrum of dysautonomia in mitral valvular prolapse.

A. A. Taylor, J. Pool, E. Nelson, 1989, The American journal of medicine.

Drug-induced liver injury.

J. Mitchell, B. Lauterburg, 1978, Hospital practice.

Effect of sodium valproate on carbamazepine disposition and psychomotor profile in man.

B. K. Park, G. Macphee, M. Brodie, 1988, British journal of clinical pharmacology.

J. Timbrell, J. Mitchell, 1977, Xenobiotica; the fate of foreign compounds in biological systems.

Effect of aminoglutethimide on blood pressure and steroid secretion in patients with low renin essential hypertension.

A. A. Taylor, J. Gill, R. Franklin, 1978, The Journal of clinical investigation.

The role of biotransformation in chemical-induced liver injury.

J R Gillette, J. Mitchell, J. Gillette, 1976, Environmental health perspectives.

Renal necrosis, glutathione depletion, and covalent binding after acetaminophen.

J. Mitchell, R. Mcmurtry, W. Snodgrass, 1978, Toxicology and applied pharmacology.

Renal and hepatic necrosis after metabolic activation of 2-substituted furans and thiophenes, including furosemide and cephaloridine.

J. Mitchell, R. Mcmurtry, 1977, Toxicology and applied pharmacology.

Drug metabolism as a cause of drug toxicity.

B. Brodie, D. Jollow, J. Mitchell, 1973, Drug metabolism and disposition: the biological fate of chemicals.

Acetaminophen-induced hepatic necrosis. V. Correlation of hepatic necrosis, covalent binding and glutathione depletion in hamsters.

S. Thorgeirsson, W. Potter, D. Jollow, 1974, Pharmacology.

Drug Actions and Interactions: Theoretical Considerations

J. Mitchell, J. Gillette, 1975 .

The possible involvement of cytochrome b5 in the oxidation of lauric acid by microsomes from kidney cortex and liver of rats.

S. Thorgeirsson, J. Mitchell, J. Gillette, 1974, Life sciences.

Propylbutyldopamine: Hemodynamic Effects in Conscious Dogs, Normal Human Volunteers and Patients with Heart Failure

A. A. Taylor, T. Brandon, W. Fennell, 1983, Circulation.

Echocardiographic comparison of black and white hypertensive subjects.

A. A. Taylor, J. Gardin, J. Laragh, 1979, Journal of the National Medical Association.

Activities of enzymes of glycerolipid synthesis in brown adipose tissue after treatment of rats with the adrenergic agonists BRL 26830A and phenylephrine, after exposure to cold and in streptozotocin-diabetes.

E. Saggerson, J. Mitchell, 1991, The Biochemical journal.

High-performance liquid chromatography and gas chromatography-mass spectrometry determination of specific lipid peroxidation products in vivo.

C. V. Smith, E. Horning, J. Mitchell, 1983, Analytical biochemistry.

Quantitation of lipid peroxidation products by gas chromatography-mass spectrometry.

C. V. Smith, J. Mitchell, H. Hughes, 1986, Analytical biochemistry.

Plasma norepinephrine concentrations: no differences among normal volunteers and low, high or normal renin hypertensive patients.

A. A. Taylor, J. Pool, M. Ziegler, 1978, Life sciences.

Renin-aldosterone profiling in hypertension.

A. A. Taylor, J. Pool, D. Rollins, 1977, Annals of internal medicine.

Acetaminophen hepatotoxicity in vivo is not accompanied by oxidant stress.

C. V. Smith, J. Mitchell, C. V. Smith, 1985, Biochemical and biophysical research communications.

Alkylation of the liver plasma membrane and inhibition of the Ca2+ ATPase by acetaminophen.

C. V. Smith, Charles V. Smith, J. Mitchell, 1988, Biochemical pharmacology.

Evidence that acetaminophen and N-hydroxyacetaminophen form a common arylating intermediate, N-acetyl-p-benzoquinoneimine.

Y. Vaishnav, E. Horning, J. Mitchell, 1980, Molecular pharmacology.

ATP-dependent calcium uptake by rat liver plasma membrane vesicles. Effect of alkylating hepatotoxins in vivo.

J. Mitchell, E. Todd, J. O. Tsokos-Kuhn, 1985, Molecular pharmacology.

Liver membrane calcium transport in diquat-induced oxidative stress in vivo.

C. V. Smith, J. Mitchell, H. Hughes, 1988, Molecular pharmacology.

Effects of N-acetylcysteine on acetaminophen covalent binding and hepatic necrosis in mice.

C. V. Smith, J. Mitchell, W. J. Racz, 1985, The Journal of pharmacology and experimental therapeutics.

The effects of age and glutathione depletion on hepatic glutathione turnover in vivo determined by acetaminophen probe analysis.

Y. Vaishnav, W. Stillwell, J. Mitchell, 1980, The Journal of pharmacology and experimental therapeutics.

In vivo regulation of hepatic glutathione synthesis: effects of food deprivation or glutathione depletion by electrophilic compounds.

J. Mitchell, B. Lauterburg, 1981, Advances in experimental medicine and biology.

Regulation of hepatic glutathione turnover in rats in vivo and evidence for kinetic homogeneity of the hepatic glutathione pool.

J. Mitchell, B. Lauterburg, 1981, The Journal of clinical investigation.

Quantitation of leukotriene B4 in human serum by negative ion gas chromatography-mass spectrometry.

S. Gaskell, J. Mitchell, H. Hughes, 1989, Analytical biochemistry.

Evidence for redox cycling of acetaminophen and its reactive metabolite by endogenous microsomal systems.

J. Mitchell, G. Corcoran, 1981, Advances in experimental medicine and biology.

Mechanism of action of N-acetylcysteine in the protection against the hepatotoxicity of acetaminophen in rats in vivo.

J. Mitchell, B. Lauterburg, G. Corcoran, 1983, The Journal of clinical investigation.

Alkylating toxins and the liver plasma membrane calcium pump/calcium atpase.

C. V. Smith, J. Mitchell, H. Hughes, 1988, Advances in experimental medicine and biology.

Ethanol suppresses hepatic glutathione synthesis in rats in vivo.

J. Mitchell, B. Lauterburg, S. Davies, 1984, The Journal of pharmacology and experimental therapeutics.

Biochemical changes after hepatic injury from toxic doses of acetaminophen or furosemide.

S. Thorgeirsson, W. Potter, D. Jollow, 1976, Pharmacology.

IMPORTANCE OF DOSE-THRESHOLD FOR DRUG-INDUCED TISSUE LESIONS

J. Mitchell, 1976 .

Application of chemical ionization mass spectrometry and the twin-ion technique to better define a mechanism in acetylhydrazine toxicity.

S. Nelson, J. Hinson, J. Mitchell, 1976, Biochemical and biophysical research communications.

Reactive oxygen species during ischemia-reflow injury in isolated perfused rat liver.

C. V. Smith, H. Jaeschke, J. Mitchell, 1988, The Journal of clinical investigation.

Cimetidine inhibits the formation of the reactive, toxic metabolite of isoniazid in rats but not in man

C. V. Smith, J. Mitchell, Jerry R. Mitchell, 1985, Hepatology.

DISTRIBUTION OF GUANIDINIUM ANTIHYPERTENSIVES—MECHANISM OF THEIR SELECTIVE ACTION *

J. Oates, D. Shand, J. Mitchell, 1971, Annals of the New York Academy of Sciences.

Metabolic activation: biochemical basis for many drug-induced liver injuries.

S. Thorgeirsson, E. Dybing, S. Nelson, 1976, Progress in liver diseases.

Hypoxic damage generates reactive oxygen species in isolated perfused rat liver.

C. V. Smith, H. Jaeschke, J. Mitchell, 1988, Biochemical and biophysical research communications.

Pilot studies on recombinant cold-adapted live type A and B influenza virus vaccines.

H. Maassab, G. Abrams, J. Mitchell, 1977, The Journal of infectious diseases.

Lipid hydroperoxy and hydroxy derivatives in copper-catalyzed oxidation of low density lipoprotein.

C. V. Smith, A. Gotto, J. Guyton, 1990, Journal of lipid research.

The pathophysiological significance of reactive oxygen formation in rat liver.

C. V. Smith, H. Jaeschke, J. Mitchell, 1991, Advances in experimental medicine and biology.

Mitochondria and xanthine oxidase both generate reactive oxygen species in isolated perfused rat liver after hypoxic injury.

H. Jaeschke, J. Mitchell, Hartmut Jaeschke, 1989, Biochemical and biophysical research communications.

Alkylation and peroxidation injury from chemically reactive metabolites.

C. V. Smith, J. Mitchell, B. Lauterburg, 1981, Advances in experimental medicine and biology.

Oxidation of alpha-methyldopa and other catechols by cytochrome P-450-generated superoxide anion: possible mechanism of methyldopa hepatitis.

E. Dybing, S. Nelson, J. Mitchell, 1976, Molecular pharmacology.

Use of isolated perfused organs in hypoxia and ischemia/reperfusion oxidant stress.

H. Jaeschke, J. Mitchell, 1990, Methods in enzymology.

Diquat hepatotoxicity in the Fischer-344 rat: the role of covalent binding to tissue proteins and lipids.

C. V. Smith, H. Jaeschke, J. Mitchell, 1989, Toxicology and applied pharmacology.

Glutathione disulfide formation and lipid peroxidation during cardiac ischemia and reflow in the dog in vivo.

C. V. Smith, M. Entman, L. Michael, 1989, Biochemical and biophysical research communications.

Chemical nature of reactive intermediates as determinant of toxicologic responses.

C. V. Smith, J. Mitchell, B. Lauterburg, 1982, Drug metabolism reviews.

Acute pulmonary injury in rats by nitrofurantoin and modification by vitamin E, dietary fat, and oxygen.

M. Boyd, J. Mitchell, H. Sasame, 2015, The American review of respiratory disease.

Overview of alkylation and peroxidation mechanisms in acute lethal hepatocellular injury by chemically reactive metabolites.

C. V. Smith, M. Horning, J. Mitchell, 1981, Seminars in liver disease.

The role of cytochrome P-450 in N-hydroxylation of 2-acetylaminofluorene.

S. Thorgeirsson, D. Jollow, J. Mitchell, 1973, Molecular pharmacology.

Enzyme-linked immunosorbent assay with major outer membrane proteins of Brucella melitensis to measure immune response to Brucella species

A. Kaufmann, W. Bibb, J. Mitchell, 1986, Journal of clinical microbiology.

Proliferation of human malignant hematopoietic cells in immunodeficient mice: suppression by antibody to pluripotent K-562 leukemia cells involves direct cytolysis and effector cells.

D. Golde, C. Lozzio, B. Lozzio, 1983, Blood.

Isoniazid liver injury: clinical spectrum, pathology, and probable pathogenesis.

U. Thorgeirsson, K. Ishak, H. Zimmerman, 1976, Annals of internal medicine.

Guanethidine and related agents. 3. Antagonism by drugs which inhibit the norepinephrine pump in man.

J. Oates, J. Cavanaugh, J. Mitchell, 1970, The Journal of clinical investigation.

Acetaminophen-induced hepatic necrosis. IV. Protective role of glutathione.

B B Brodie, J R Gillette, B. Brodie, 1973, The Journal of pharmacology and experimental therapeutics.

The role of cytochrome b5 in cytochrome P-450 enzymes.

S. Thorgeirsson, J. Mitchell, J. Gillette, 1975, Advances in experimental medicine and biology.

Relationship between NADH and NADPH oxidation during drug metabolism.

S. Thorgeirsson, J. Mitchell, J. Gillette, 1973, Drug metabolism and disposition: the biological fate of chemicals.

Bromobenzene metabolism and hepatic necrosis.

B. Brodie, G. Krishna, W. D. Reid, 1971, Pharmacology.

Biochemical changes after hepatic injury by allyl alcohol and N-hydroxy-2-acetylaminofluorene.

S. Thorgeirsson, W. Potter, J. Mitchell, 1976, Chemico-biological interactions.

Acetylation rates and monthly liver function tests during one year of isoniazid preventive therapy.

U. Thorgeirsson, D. Jollow, J. Mitchell, 1975, Chest.

High-performance liquid chromatographic determination of diltiazem and its major metabolites, N-monodemethyldiltiazem and desacetyldiltiazem, in plasma.

D. Abernethy, J. Mitchell, S. Montamat, 1987, Journal of chromatography.

Oxidant stress and hepatic necrosis in rats treated with diquat.

C. V. Smith, J. Mitchell, B. Lauterburg, 1985, The Journal of pharmacology and experimental therapeutics.

Cytochrome P-450-mediated oxidation of 2-hydroxyestrogens to reactive intermediates.

E. Dybing, S. Nelson, J. Mitchell, 1976, Biochemical and biophysical research communications.

Drug metabolism in the production of liver injury.

W. Potter, J. Mitchell, 1975, The Medical clinics of North America.

Immunization Against Ehrlich's Ascites Carcinoma with X-Irradiated Tumor Cells.∗

D. M. Donaldson, J. Mitchell, 1959, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.

Rhesus diploid rabies vaccine (adsorbed): a new rabies vaccine using FRhL-2 cells.

K. Kajiya, D. Brown, J. Mitchell, 1985, The Journal of infectious diseases.

Role of interferon in prophylaxis of rabies after exposure.

T. Merigan, H. Koprowski, J. Mitchell, 1976, The Journal of infectious diseases.

Bromobenzene-induced hepatic necrosis: species differences and protection by SKF 525-A.

B. Brodie, G. Krishna, W. D. Reid, 1971, Research communications in chemical pathology and pharmacology.

Antagonism of the antihypertensive action of guanethidine sulfate by desipramine hydrochloride.

J. Oates, J. Mitchell, L. Arias, 1967, JAMA.

Metabolic activation of furosemide to a chemically reactive, hepatotoxic metabolite.

W. L. Nelson, W. Potter, D. Jollow, 1976, The Journal of pharmacology and experimental therapeutics.

Verapamil and norverapamil determination in human plasma by gas-liquid chromatography using nitrogen-phosphorus detection: application to single-dose pharmacokinetic studies.

D. Abernethy, J. Mitchell, E. Todd, 1984, Pharmacology.

Rhesus diploid rabies vaccine (adsorbed), a new rabies vaccine. II. Results of clinical studies simulating prophylactic therapy for rabies exposure.

J. Mitchell, W. E. Brown, C. Goswick, 1983, JAMA.

Age-dependence of hypertensive-normotensive differences in plasma norepinephrine.

D. Goldstein, I. Kopin, B. Chernow, 1983, Hypertension.

Effects of chronic central nervous system administration of agouti-related protein in pair-fed animals.

S. Bloom, M. Ghatei, K. Murphy, 2001, Diabetes.

Detection of Toxacara canis Antibodies with the Fluorescent Antibody Technique.∗

J. Mitchell, 1964, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.

Propylbutyldopamine. Mechanism of blood pressure lowering in hypertensive patients.

J. Ginos, J. Pool, W. Fennell, 1984, Hypertension.

Activation of peripheral dopamine presynaptic receptors lowers blood pressure and heart rate in dogs.

T. Brandon, J. Ginos, W. Fennell, 1983, Hypertension.

Covalent binding: useful index of the formation of chemically reactive drug metabolites.

J. Mitchell, 1975, Biochemical Society transactions.

Rhesus diploid rabies vaccine (adsorbed), a new rabies vaccine. Results of initial clinical studies of preexposure vaccination.

J. Mitchell, N. Mccullough, W. E. Brown, 1982, JAMA.

Sensitive procedure for detecting residual viable virus in inactivated rabies vaccine.

J. Mitchell, G. R. Anderson, R. E. Everest, 1971, Applied microbiology.

268 – FORMATION OF CHEMICALLY REACTIVE METABOLITES FROM DRUGS

J. Mitchell, 1978 .

Biliary excretion of glutathione and glutathione disulfide in the rat. Regulation and response to oxidative stress.

J. Mitchell, B. Lauterburg, H. Hughes, 1984, The Journal of clinical investigation.

Quantitative determination of the glutathione, cysteine, and N-acetyl cysteine conjugates of acetaminophen by high-pressure liquid chromatography.

S. Nelson, D. Rollins, R. Franklin, 1977, Analytical biochemistry.

Therapeutic doses of acetaminophen stimulate the turnover of cysteine and glutathione in man.

J. Mitchell, B. Lauterburg, 1987, Journal of hepatology.

Proliferation and differentiation of human myeloid leukemic cells in immunodeficient mice: electron microscopy and cytochemistry.

D. Golde, C. Lozzio, B. Lozzio, 1984, Blood.

Absence of morphological, chromosomal and antigenic changes in the K-562 cell line growing as localized or disseminated tumours in nude mice.

C. Lozzio, B. Lozzio, J. Mitchell, 1982, British Journal of Cancer.

Metastasizing mammary tumors. Spontaneous mammary tumors in asplenic mice heterozygous for athymia.

B. Lozzio, P. Coulson, J. Mitchell, 1982, The American journal of pathology.

Arrest and extravasation of neoplastic cells. An electron microscopy study of serial sections at sequential stages.

C. Lozzio, B. Lozzio, J. Mitchell, 1982, Virchows Archiv. A, Pathological anatomy and histology.

Isoniazid and iproniazid: activation of metabolites to toxic intermediates in man and rat.

J. Timbrell, S. Nelson, S D Nelson, 1976, Science.

The response of brown adipose tissue mitochondrial glycerolphosphate acyltransferase to cold-exposure in hypothyroidism, after adrenalectomy and after treatment with cycloheximide.

E. Saggerson, J. Mitchell, 1994, The International journal of biochemistry.

Regulation of expression of the lipoprotein lipase gene in brown adipose tissue.

T. Kirchgessner, M. Schotz, B. Cannon, 1992, The American journal of physiology.

Comparison of antioxidant and nonantioxidant lipoxygenase inhibitors on neutrophil function. Implications for pathogenesis of myocardial reperfusion injury.

C. Smith, D. Anderson, J. Mitchell, 1990, The Journal of pharmacology and experimental therapeutics.

Guanethidine and related agents. I. Mechanism of the selective blockade of adrenergic neurons and its antagonism by drugs.

J. Oates, J. Mitchell, 1970, The Journal of pharmacology and experimental therapeutics.

Progress in hepatology. Metabolic activation of drugs to toxic substances.

J. Mitchell, D. J. Jollows, 1975, Gastroenterology.

An investigation of the cause of accumulation of verapamil during regular dosing in patients.

D. Abernethy, J. Schwartz, J. Mitchell, 1985, British journal of clinical pharmacology.

Effect of Environmental Temperature on the Response of Mice to Whole-Body Roentgen Radiation

J. Mitchell, B. Highman, Willie W. Smith, 1949, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.

Evidence for increased membrane permeability of plasmalemmal vesicles from livers of phenobarbital-induced CCl4-intoxicated rats.

M. Entman, J. Mitchell, C. Tate, 1986, Molecular pharmacology.

Hepatotoxicity and metabolism of iproniazid and isopropylhydrazine.

J. Timbrell, S. Nelson, J. Mitchell, 1978, The Journal of pharmacology and experimental therapeutics.

Isolation of a virus from Burkitt lymphoma cells.

J. Mitchell, C. Bowles, G. R. Anderson, 1967, Lancet.

Deuterium isotope effects on the metabolism and toxicity of phenacetin in hamsters.

Y. Vaishnav, S. Nelson, W. Garland, 1978, Drug metabolism and disposition: the biological fate of chemicals.

Tissue selective toxicity: Introduction

J. Mitchell, 1984 .

Application of Chemical Ionization Ms and the Twin-Ion Technique in the Analysis of Reactive Intermediates in Drug Metabolism

L. Pohl, S. Nelson, J. Mitchell, 1977 .

Plasma glutathione disulfide as an index of oxidant stress in vivo: effects of carbon tetrachloride, dimethylnitrosamine, nitrofurantoin, metronidazole, doxorubicin and diquat.

J. Adams, J. Mitchell, B. Lauterburg, 1984, Research communications in chemical pathology and pharmacology.

Plasma concentrations of propranolol and 4-hydroxypropranolol in man measured by high pressure liquid chromatography.

J. Pool, D. Rollins, A. Taburet, 1979, Life sciences.

Steady state verapamil tissue distribution in the dog: differing tissue accumulation.

D. Abernethy, J. Schwartz, J. Mitchell, 1986, Pharmacology.

A study of glycerolphosphate acyltransferase in rat liver mitochondria-submitochondrial localization and some properties of the solubilized enzyme.

E. Saggerson, J. Mitchell, 1994, The International journal of biochemistry.

No evidence for reactive oxygen damage in ischemia-reflow injury.

M. Entman, H. Jaeschke, L. Michael, 1987, Transactions of the Association of American Physicians.