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Biomedical subjects

D E Brenner

Publications and source records attributed to D E Brenner.

At least 19 recordsLinked to original sources

Augmentation of hepatic doxorubicin extraction with extracorporeal filtration avoids the dose-dependent, nonlinear increase in AUC observed with systemic administration.

PURPOSE: Regional therapy of primary or metastatic liver cancer with low hepatic extraction ratio drugs such as doxorubicin is constrained by development of systemic toxicity. To examine the effect of augmentation of hepatic drug extraction, a swine model of hepatic artery infusion (HAI) with minimally invasive hepatic venous isolation and hepatic venous drug extraction (HVDE) was developed to study the comparative pharmacokinetic profiles of regional and systemically administered doxorubicin. METHODS: Doxorubicin 0.5-9 mg/kg was administered to 31 pigs over 90 min either by HAI with simultaneous HVDE or by standard systemic vein infusion. Systemic artery and hepatic vein plasma samples were collected periodically (0 to 240 min) for determination of doxorubicin concentrations by high-performance liquid chromatography. Pharmacokinetic profiles were modeled with PCNONLIN 4.2. RESULTS: Concentration-time data were best described in all pigs by a two-compartment open model of elimination. Independent of the route of administration, AUC and Cmax values increased with dose. Mean systemic AUC and Cmax values were consistently lower with regional administration, with statistically significant decreases at the 0.5 and 3 mg/kg doses, whereas there was no relationship between hepatic vein parameters and route of administration. There was a linear relationship between mean systemic AUC values and dose in pigs receiving doxorubicin via HAI with HVDE, whereas mean systemic AUC values increased exponentially at doses of 5 mg/kg or above with systemic vein administration. CONCLUSIONS: Administration of doxorubicin by HAI with simultaneous HVDE significantly decreases systemic exposure in comparison with standard systemic vein drug infusion, and may protect against nonlinear increases in exposure at higher doses.

Animals

Suppression of human colorectal mucosal prostaglandins: determining the lowest effective aspirin dose.

BACKGROUND: A variety of studies have supported the finding that regular intake of aspirin (acetylsalicylic acid) or nonsteroidal anti-inflammatory agents can affect colorectal cancer carcinogenesis. These agents inhibit the synthesis of prostaglandins. High levels of prostaglandins are observed in colon cancer tissues. PURPOSE: Experiments were planned to determine the lowest dose of aspirin that can markedly suppress the levels of mucosal prostaglandins E2 and F(2alpha) in colorectal mucosa and to determine whether a relationship exists between these levels and plasma levels of both acetylsalicylic acid and its metabolite, salicylic acid. METHODS: Healthy men and women aged 18 years or older participated in the study. The participants took a single, daily dose of aspirin (40.5, 81, 162, 324, or 648 mg) or a placebo for 14 days. Colorectal biopsy specimens were taken at baseline, 24 hours after the first dose of aspirin, and 24-30 hours and 72-78 hours after the last, i.e., fourteenth, daily dose of aspirin. The biopsy specimens were assayed for prostaglandins E2 and F(2alpha) by use of a competitive enzyme immunoassay. Plasma concentrations of acetylsalicylic acid and salicylic acid were determined by use of high-performance liquid chromatography. All P values are two-sided. RESULTS: A total of 65 subjects (10 receiving placebo, groups of 10 each receiving 40.5, 81, 162, or 324 mg of aspirin, and a group of 15 receiving 648 mg of aspirin) completed the protocol. One subject reported unacceptable drug-induced toxic effects and did not complete the protocol; other subjects reported acceptable side effects. The lowest dose to significantly suppress colorectal mucosal prostaglandin E2 concentrations from baseline at 24 hours after the first dose (by 22.6%; P = .002) and at 24-30 hours after the last dose (by 14.2%; P = .021) was 162 mg. At 72-78 hours after the last dose, there was significant suppression for subjects receiving 81 mg (by 23.7%; P = .008). The lowest dose to significantly suppress colorectal mucosal prostaglandin F(2alpha) concentrations from baseline at 24 hours after the first dose (by 18.3%; P = .032) was 324 mg. The lowest dose causing a marked reduction in the level of prostaglandin F(2alpha) at 24-30 hours (by 15.1%; P = .003) and 72-78 hours (by 23.0%; P = .0002) after the last dose was 40.5 mg. No detectable amounts of acetylsalicylic acid or salicylic acid were present in the plasma at any of the biopsy time points. CONCLUSIONS: The lowest doses of aspirin taken daily for 14 days to significantly suppress concentrations of colorectal mucosal prostaglandins E2 and F(2alpha) were 81 and 40.5 mg, respectively. The suppression occurred without detectable amounts of aspirin or salicylic acid in the plasma at the time points studied. On the basis of these observations, we recommend a single, daily dose of 81 mg of aspirin in future studies of this drug as a chemopreventive agent for colorectal cancer.

Adult

Colon cancer chemoprevention: clinical development of aspirin as a chemopreventive agent.

We have studied aspirin as a potential chemopreventive for colorectal cancer, completing Phase I studies on aspirin pharmacology and potential biomarker assays (prostaglandins, PGE2 and PGF2 alpha and cyclooxygenase modulation) in normal human subjects. These studies have determined the optimal dose of aspirin for future Phase IIa and IIb chemopreventive trials in high-risk cohorts of patients for colon cancer. Aspirin's effects on rectal prostaglandins are prolonged, detectable even after aspirin and its metabolite are removed from the plasma. Aspirin-mediated inhibition of prostaglandin production in the human rectal epithelium may be related to direct suppression of cyclooxygenase transcription and not to enzyme inactivation by acetylation. A systematic method to monitor adherence (self-report, telephone contact, pill count, and microelectronic monitoring) has been established for future trials. Strategies to improve recruitment of high-risk cohorts have been developed. Phase IIa non-randomized studies with aspirin at 81 mg in high-risk cohorts (resected Duke's A colon cancer, Duke's C colon cancer treated with adjuvant therapy and disease-free at 5 years, history of colon adenomas > 1 cm, two or more first-degree relatives with colon cancer, and familial adenomatous polyposis and hereditary non-polyposis colorectal cancer syndromes) are currently being conducted for surrogate end-point biomarker (prostaglandins, cyclooxygenase, cellular mucins, and proliferation) modulation.

Animals

Adherence to single daily dose of aspirin in a chemoprevention trial. An evaluation of self-report and microelectronic monitoring.

A consecutive sample of 64 healthy adults (33 female and 31 male) were recruited at the University of Michigan Medical Center, Ann Arbor. Data were available for analysis on 57 subjects. The participants were asked to take a single daily dose of aspirin ranging from 0 to 640 mg. Adherence to the daily aspirin ingestion was measured by self-report and the Medication Event Monitoring System (MEMS, Aprex Corp, Fremont, Calif); adherence rate for the study population was 35%. The adherence rates for all dosing errors between self-report and Medication Event Monitoring System were significantly different (P = .002). There was no significant gender difference in adherence rates. Adherence to regular aspirin ingestion was poor in healthy, paid subjects despite explicit, written and verbal instructions. Patient self-report alone is not a reliable measure of adherence.

Adult

Chemoprevention of colorectal cancer.

This review summarizes the principles of cancer chemoprevention and discusses the evidence from epidemiologic and experimental studies and preclinical and clinical trials of potential colorectal chemopreventive agents. The putative mechanisms of action of the drugs in chemoprevention and their potential to reduce the incidence and mortality rate of colorectal neoplasms are discussed. The future of colorectal chemoprevention will depend on important new insights into molecular carcinogenesis of colorectal cancer, application of molecular markers as surrogate endpoints, and ultimately on therapeutic targets of prevention in clinical trials.

Animals

Solvent exposure as a risk factor for Alzheimer's disease: a case-control study.

This case-control study investigates whether history of organic solvent exposure is associated with increased risk of Alzheimer's disease. The study base includes about 23,000 persons aged 60 years or more from the local membership of a health maintenance organization in Seattle, Washington, who entered the study between 1987 and 1992. Probable Alzheimer's disease cases (n = 193) who had presented with new dementia symptoms were identified, enrolled, and diagnosed by our Alzheimer's Disease Patient Registry following standardized criteria. Control subjects (n = 243), free of dementia and neurologic disease causing dementia, were selected randomly from the study base and frequency matched to cases for age and sex. Proxy informants provided specific solvent exposure history as well as job descriptions likely to involve solvent use as part of a comprehensive risk factor interview. Kappa statistics indicated substantial agreement for control-control proxy solvent responses. History of exposure to one or more solvent groups (benzene and toluene; phenols and alcohols; ketones; other solvents) yielded an adjusted Alzheimer's disease odds ratio of 2.3 (95 percent confidence interval 1.1-4.7); among males only, it increased to 6.0 (95% confidence interval 2.1-17.2). Thus, past exposure to organic solvents may be associated with onset of Alzheimer's disease.

Age Factors

Surrogate endpoint biomarkers for cervical cancer chemopreventive trials.

Cervical intraepithelial neoplasia (CIN) represents a spectrum of epithelial changes that provide an excellent model for developing chemopreventive interventions for cervical cancer. Possible drug effect surrogate endpoint biomarkers are dependent on the agent under investigation. Published and preliminary clinical reports suggest retinoids and carotenoids are effective chemopreventive agents for CIN. Determination of plasma and tissue pharmacology of these agents and their metabolites could serve as drug effect intermediate endpoints. In addition, retinoic acid receptors could serve a both drug and biological effect intermediate endpoints. Possible biological effect surrogate endpoint biomarkers include cytomorphological parameters, proliferation markers, genomic markers, regulatory markers, and differentiation. Given the demonstrated causality of human papillomavirus (HPV) for cervical cancer, establishing the relationship to HPV will be an essential component of any biological intermediate endpoint biomarker. The pathologic effect surrogate endpoint biomarker for cervical cancer is CIN, used clinically for years. The desired effect for chemopreventive trials is complete regression or prevention progression. In planning chemoprevention trials, investigators need to consider spontaneous regression rates, the subjective nature of detecting CIN, and the impact of biopsy on regression. If intermediate endpoint biomarkers that met the above criteria were available for cervical cancer, then new chemopreventive agents could be rapidly explored. The efficacy of these new agents could be determined with a moderate number of subjects exposed to minimal risk over an acceptable amount of time. The impacts on health care for women would be significant.

Anticarcinogenic Agents

Pharmacokinetic evaluation of percutaneous hepatic venous isolation for administration of regional chemotherapy.

Hepatic artery infusion (HAI) chemotherapy has been used to treat patients with unresectable liver tumours. We report a preclinical study of the pharmacokinetics of HAI combined with hepatic venous drug extraction (HVDE) for regional administration of doxorubicin. HVDE was aided by a double balloon catheter inserted via femoral vein cutdown into the inferior vena cava to collect all hepatic vein blood. Pigs received doxorubicin 0.5-9.0 mg kg-1 over 90 min via HAI or systemic infusion (SYSI). HVDE was performed for 240 min. SYSI pigs underwent hepatic venous isolation without drug filtration. Doxorubicin levels were assayed using high-pressure liquid chromatography (HPLC). HAI/HVDE reduced systemic exposure to doxorubicin with equivalent hepatic exposure at all doses. Pharmacokinetic enhancement ranged from 7.0 to 22.3 for peak concentration, 8.8-23.2 for the area under the curve and 2.9-4.2 for tissue concentration. HAI/HVDE also prevented the mortality which was observed with SYSI administration of high-dose (5.0 and 9.0 mg kg-1) doxorubicin. We conclude that HAI/HVDE reduces systemic exposure to doxorubicin as compared with SYSI of equivalent doses. Pharmacokinetic enhancement indices suggest that HAI/HVDE may allow equivalent hepatic drug exposure with reduced systemic exposure. This method may be applicable to other drugs and to other anatomic settings in which enhanced regional drug delivery is desirable.

Animals

An evaluation of hepatic extraction and clearance of doxorubicin.

A swine model was developed to study quantitatively the pharmacokinetics of hepatic extraction and clearance of doxorubicin (DOX). Systemic and hepatic artery infusions of DOX (0.5-9 mg kg-1) were administered to 34 pigs. Pharmacokinetic analysis was simplified by use of a double-balloon catheter in the inferior vena cava to collect hepatic venous effluent. During hepatic artery infusion only, DOX in hepatic venous blood was extracted using activated carbon filters to prevent drug recirculation. Hepatic extraction and clearance of DOX were independent of dose and route of administration. Extraction ratios varied from 0.75 to 0.91 during hepatic artery infusion and from 0.50 to 0.72 during systemic infusion. Clearance results were analogous. After cessation of drug infusions, hepatic extraction and clearance of DOX was negative, suggesting that the liver serves as a drug reservoir during DOX infusion and subsequently is a net source of unmetabolised drug. Liver extraction and clearance of DOX in pigs are substantial. During either systemic or hepatic artery infusion of DOX, the liver serves as a drug reservoir. Subsequent mobilisation of this hepatic pool of DOX may cause prolonged systemic exposure to drug.

Animals

History of depression as a risk factor for Alzheimer's disease.

Research regarding the possible association between Alzheimer's disease and a history of depression has been inconclusive. Using a case-control design, we assessed the strength of the association between reported history of depression and onset of Alzheimer's disease. We enrolled probable Alzheimer's disease cases (N = 294), who were ascertained and diagnosed by our Alzheimer's Disease Patient Registry, and randomly selected nondemented controls (N = 300) of similar age and gender from the same base population. The mean age (for cases) was 78.5 years. Informants provided data regarding history of depression. "Treated depression" was defined as depression for which a physician/psychologist consultation, medication, or hospitalization had occurred. Restricting treated depression to exclude primary loss or grief reactions, we found a modest association with Alzheimer's disease [odds ratio (OR) = 1.8; 95% confidence interval (CI) = 0.9-3.5] after adjusting for gender, age, education, and type of informant. When these data were stratified by depression onset year, we observed an odds ratio of 2.0 (95% CI = 0.9-4.6) for depression occurring more than 10 years before the onset of dementia symptoms, and an OR of 0.9 (95% CI = 0.2-3.0) for depression onset within 10 years of the onset of dementia symptoms. Thus, depressive episodes occurring well before dementia symptom onset appear to increase the risk of Alzheimer's disease.

Age Distribution

Postmenopausal estrogen replacement therapy and the risk of Alzheimer's disease: a population-based case-control study.

Preliminary animal and human data suggest that estrogens may be protective against Alzheimer's disease in women. In a population-based case-control study at Group Health Cooperative of Puget Sound, Seattle, Washington, the authors compared the exposure of estrogen replacement therapy of 107 female Alzheimer's disease cases with 120 age- and sex-matched controls by using computerized pharmacy data. The cases were obtained from the Alzheimer's Disease Patient Registry of the University of Washington, Seattle, Washington, which is based on the enumerated health plan population from 1987 to 1992. Newly recognized cases of probable Alzheimer's disease according to standardized diagnostic criteria were ascertained, evaluated, and enrolled in the Registry. The controls were selected from the same defined population by stratified random sampling. When the authors applied logistic regression, ever use of estrogens did not show an association with Alzheimer's disease (adjusted odds ratio = 1.1, 95 percent confidence interval 0.6-1.8). Oral and vaginal estrogens yielded similar results. In conclusion, this study provides no evidence that estrogen replacement therapy has an impact on the risk of Alzheimer's disease in women.

Administration, Intravaginal

Hepatic artery infusion of doxorubicin with hepatic venous drug extraction.

Hepatic artery infusion (HAI) has been used to take advantage of the steep dose-response relationship characteristic of chemotherapeutic agents. Systemic toxicity, however, remains the dose limiting factor for HAI of low hepatic extraction drugs. This investigation compared the pharmacokinetics of doxorubicin administered using a system that combines HAI and hepatic venous drug extraction (HVDE) versus systemic administration without HVDE. HAI was accomplished by transfemoral cannulation of the hepatic artery. HVDE was aided by use of a double-balloon catheter inserted fluoroscopically via femoral vein cutdown into the inferior vena cava. Inflation of the balloons above and below the hepatic veins allowed collection of hepatic venous effluent. Hepatic venous blood was pumped through the double-balloon catheter into an extracorporeal circuit with activated carbon filters to extract drug prior to return to the systemic circulation. Domestic female swine (25-35 kg) received 3 mg/kg doxorubicin over 90 min via HAI. HVDE was performed for 240 min following initiation of HAI (Time 0-240 min). Control swine underwent hepatic venous isolation using the double-balloon catheter without drug filtration and received 3 mg/kg doxorubicin over 90 min via systemic vein (SYSI). Serum and myocardial doxorubicin and doxorubicinol levels were assayed using HPLC. Blood was serially sampled from hepatic vein blood, from the extracorporeal circuit after filtration, and from a systemic artery. Area under the curve (AUC) was integrated from time-concentration plots over Time 0-180 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Causes of death associated with Alzheimer disease: variation by level of cognitive impairment before death.

OBJECTIVE: To describe causes of death for patients with Alzheimer disease (AD) and other dementing illnesses enrolled in a population-based Alzheimer disease patient registry (ADPR) and to describe the variation in causes by the level of cognitive impairment before death in probable AD cases. SETTING: The ADPR enrolls and diagnoses newly recognized potential dementia cases occurring in a large, stable health maintenance organization. To date, 654 cases have been enrolled and followed annually to monitor cognitive decline and verify initial diagnosis. DESIGN: Longitudinal descriptive study. PATIENTS: ADPR enrollees who have died. MEASUREMENTS: Death certificates were obtained for all who died (total n = 104, probable AD = 55); reported causes of death were reviewed by a physician to determine the underlying cause. AD patients were categorized according to their Mini-Mental State Exam score (cognitive impairment) within 12 months of death as (a) mildly (21+), (b) moderately (15-20), or (c) severely (0-14) impaired, and underlying cause and all reported causes of death for each group were tabulated. MAIN RESULTS: Among probable AD patients, pneumonia and AD were most often recorded on death certificates when cognitive impairment within the year prior to death had reached the severe level; heart disease, stroke, and other common causes of death predominated in AD patients who were less cognitively impaired. CONCLUSIONS: When AD cases were followed from first diagnosis to death, the causes of death varied by level of cognitive impairment. Illnesses potentially amenable to treatment caused death at all levels of disease, but more so early in the course of AD. Cognitive impairment may make patients less able to recognize and report symptoms of medical problems, thereby complicating efforts to intervene.

Aged

Initial clinical (phase I) trial of TLC D-99 (doxorubicin encapsulated in liposomes).

A liposome-encapsulated form of doxorubicin (TLC D-99), which was shown in preclinical toxicology to be less toxic to the gastrointestinal tract and myocardium than free doxorubicin, was administered by constant infusion (1.00-1.80 h) to 38 patients in single doses of 20, 30, 45, 60, 75, and 90 mg/m2 every 3 weeks and daily for 3 days at doses of 20, 25, and 30 mg/m2/day. The dose-limiting toxicity was leucopenia: the maximum tolerated doses were one at 90 mg/m2 and three at 25 mg/m2/day. Nausea, vomiting, and stomatitis were minimal or absent at each dose; alopecia was minor. Fever and chills were noted at most of the doses, and malaise was seen in some patients, especially at the higher doses. No hepatic, renal, or other organ toxicities were observed. Clinical cardiac toxicity was not observed in any patient; however, the cumulative doxorubicin dose was greater than 400 mg/m2 in only one patient. There was large variation among patients in estimated pharmacokinetic parameters and profiles. Higher plasma levels and dose intensities were achieved with TLC D-99 than were predicted for free doxorubicin. Liposome-encapsulated doxorubicin was well tolerated and produced less nausea, vomiting, and stomatitis than would be expected with free doxorubicin administered at equally myelosuppressive doses.

Adult

Selection criteria for breast cancer chemoprevention subjects.

Early phase chemoprevention trials differ from standard therapeutic clinical trials because asymptomatic, healthy people are treated with a potentially toxic intervention for a prolonged period of time. Current subject selection protocols have relied upon epidemiological methods to identify high-risk individuals. Most available data provide risk estimates for various individual risk factors, but few have reported risk estimates for combinations of risk factors. Selection criteria for the large tamoxifen intervention trial (NSABP P1) were developed from the work of Gail et al. [1]. The Gail model takes into account non-genetic factors (e.g., nulliparity, age at menarche, preexisting pathological conditions) and genetic factors (family history). Using a lifetime risk of 10% of developing breast cancer as a standard to intervene, NSABP P1 uses the Gail algorithm to select pre- and postmenopausal women for a primary intervention trial. This approach has been criticized for being insufficiently selective (i.e., all women > or = 60 yrs), but appears to be the best available method to select subjects for a chemoprevention trial. Other approaches have been based on identification of very high-risk women with acknowledged pathologic conditions [lobular carcinoma in situ, ductal carcinoma in situ (DCIS)]. Attempting to use these proliferative lesions as pathologic endpoints for drug effect has not been attempted. DCIS as a risk factor for tamoxifen intervention was excluded because of controversies over its management and because of frequent difficulties in distinguishing microinvasive from non-invasive lesions. Women treated for early stage breast cancer (Stage I) may be subjects for early stage chemopreventive interventions.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors

Adherence to oral tamoxifen: a comparison of patient self-report, pill counts, and microelectronic monitoring.

PURPOSE: Recent innovations allow the integration of microelectronics into drug packaging, providing a continuous record of the interactions of the patient with the drug package. We hypothesized that adherence to oral tamoxifen, as measured by a pressure-activated microelectronic monitoring device, would be significantly discrepant from traditional measures of patient adherence, ie, patient self-report (SR) and pill counts (PCs). PATIENTS AND METHODS: Twenty-six patients receiving oral tamoxifen therapy were assessed by patient SR, PCs, and Medication Event Monitoring System (MEMS; Aprex Corp, Fremont, CA) microelectronic monitoring. A microprocessor in the MEMS cap recorded each opening as a presumptive dose, listing the date, time, and duration of opening for later retrieval on a microcomputer. Patients were not informed that their adherence was to be monitored electronically or that PCs would be performed. RESULTS: A total of 2,102 days (70.1 months) of tamoxifen therapy were monitored; patients were monitored for a mean of 2.92 months of tamoxifen therapy. SR adherence to oral tamoxifen was significantly higher than that suggested by either PCs (SR missed doses only v PC, P = .008) or MEMS adherence monitoring (SR missed doses only v MEMS missed doses only, P = .005; SR dosing-interval errors only v MEMS dosing-interval errors only, P < .0001; SR all dosing errors v MEMS all dosing errors, P < .0005). PC data also suggested significantly higher adherence rates than MEMS monitoring. CONCLUSION: Microelectronic adherence monitoring provides both confirmatory and complimentary data regarding adherence behavior, while also allowing for the evaluation of patterns of nonadherence. Patient SRs and PCs likely overestimate the degree to which patients adhere to their tamoxifen regimen.

Administration, Oral

Relationship between cigarette smoking and Alzheimer's disease in a population-based case-control study.

We investigated whether cigarette smoking is negatively associated with Alzheimer's disease (AD) in a population-based, frequency-matched, case-control study of 152 AD patients and 180 controls. Ever having smoked was associated with lower risk of AD (adjusted odds ratio = 0.61; 95% confidence interval: 0.37-0.99). Additional multivariate analyses demonstrated that education and history of hypertension modified this association. The direction of the modification was for higher education level and history of hypertension to further reduce the risk. The "dose-response" pattern showed the greatest risk reduction among those who smoked least and suggests a biologic mechanism of a dose-dependent up-regulation of nicotinic (cholinergic) brain receptors. These data, although consistent with current opinion about pathophysiology of AD, do not suggest smoking should be used as a preventive strategy for AD.

Aged

DNA damage and cytotoxicity induced by metabolites of anthracycline antibiotics, doxorubicin and idarubicin.

This study assessed the ability of major metabolites of two types of anthracycline antibiotics, doxorubicin and idarubicin (4-demethoxydaunorubicin) to damage DNA in mouse fibrosarcoma 935.1 cells. Since DNA lesions by anthracyclines may be mediated by topoisomerase II, we also characterized the ability of the drugs to inhibit this enzyme. The C-13 alcohol and aglycone metabolites of doxorubicin and idarubicin were compared to the parent drugs in terms of induction of DNA single strand breaks measured by filter elution. In whole cells, the maximal DNA strand breakage induced by the C-13 alcohol metabolites was similar to that of their respective parent drugs. In isolated nuclei, however, the alcohol metabolites were two times more potent than the parent drugs. The aglycone metabolites produced very little damage in either whole cells or nuclei. The doxorubicin compounds differed markedly from idarubicin drugs in the way their ability to induce DNA breaks was related to cytotoxic activity. Doxorubicin and doxorubicinol cytotoxic effects (50% cell growth inhibition at 0.2 and 4 microM, respectively) coincided (in terms of drug concentrations) with the induction of significant breakage of cellular DNA. In contrast, the concentrations of idarubicin and idarubicinol needed to produce 50% growth inhibition (0.005 and 0.006 microM, respectively) were about 20 times lower than drug levels that induced significant DNA damage. All six compounds inhibited the catalytic activity of isolated topoisomerase II. While the alcohol metabolites produced this inhibition at concentrations similar to those of their parent drugs (5-10 microM), the aglycones were again much less active.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals