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Biomedical subjects

F Maffei

Publications and source records attributed to F Maffei.

At least 19 recordsLinked to original sources
PubMed2006

Incorrect use of thromboprophylaxis for venous thromboembolism in medical and surgical patients: results of a multicentric, observational and cross-sectional study in Brazil.

OBJECTIVES: Although effective strategies for the prevention of venous thromboembolism (VTE) are widely available, a significant number of patients still develop VTE because appropriate thromboprophylaxis is not correctly prescribed. We conducted this study to estimate the risk profile for VTE and the employment of adequate thromboprophylaxis procedures in patients admitted to hospitals in the state of São Paulo, Brazil. METHODS: Four hospitals were included in this study. Data on risk factors for VTE and prescription of pharmacological and non-pharmacological thromboprophylaxis were collected from 1454 randomly chosen patients (589 surgical and 865 clinical). Case report forms were filled according to medical and nursing records. Physicians were unaware of the survey. Three risk assessment models were used: American College of Chest Physicians (ACCP) Guidelines, Caprini score, and the International Union of Angiololy Consensus Statement (IUAS). The ACCP score classifies VTE risk in surgical patients and the others classify VTE risk in surgical and clinical patients. Contingency tables were built presenting the joined distribution of the risk score and the prescription of any pharmacological and non-pharmacological thromboprophylaxis (yes or no). RESULTS: According to the Caprini score, 29% of the patients with the highest risk for VTE were not prescribed any thromboprophylaxis. Considering the patients under moderate, high or highest risk who should be receiving prophylaxis, 37% and 29% were not prescribed thromboprophylaxis according to ACCP (surgical patients) and IUAS risk scores, respectively. In contrast, 27% and 42% of the patients at low risk of VTE, according to Caprini and IUAS scores, respectively, had thromboprophylaxis prescribed. CONCLUSION: Despite the existence of several guidelines, this study demonstrates that adequate thromboprophylaxis is not correctly prescribed: high-risk patients are under-treated and low-risk patients are over-treated. This condition must be changed to insure that patients receive adequate treatment for the prevention of thromboembolism.

Anticoagulants↗
PubMed2002

Mutagenic and clastogenic activity of gastric juice in human gastric diseases.

To investigate whether subjects with low-acid states are exposed to increased genetic risk with respect to controls, we evaluated mutagenicity and presence of clastogenic factors (CF) in the gastric juice of chronic atrophic gastritis and omeprazole-treated patients. Mutagenic gastric juice was found in 8/15 (53%) chronic atrophic gastritis patients, 8/11 (73%) omeprazole-treated patients, and 2/13 (15%) healthy control subjects. The mean mutagenicity ratio of omeprazole-treated patients (1.52+/-0.48/0.1 ml gastric juice) was significantly higher than those of either controls (1.07+/-0.15; P<0.01) or chronic atrophic gastritis patients (1.16+/-0.21; P<0.05). Only chronic atrophic gastritis patients showed an increased clastogenic index with respect to healthy controls (2.67+/-2.13 versus 0.38+/-0.51; P<0.001). These findings expand our knowledge of gastric disease risk factors, and indicate that there may well be a risk of mucosal DNA damage arising from the presence of mutagenic and CF in the gastric juice.

Adult↗
PubMed2000

Increased cytogenetic damage detected by FISH analysis on micronuclei in peripheral lymphocytes from alcoholics.

Alcohol abuse greatly increases the risk of various malignancies, including cancer of the liver and digestive tract. Although it is thought that this may be due, at least partially, to the mutagenic properties of ethanol, little is known about the genotoxic effects of ethanol in humans. We investigated the chromosomal damage in lymphocytes from 20 alcoholics and 20 controls using the micronucleus (MN) assay combined with fluorescence in situ hybridization (FISH) with a pancentromeric DNA probe capable of differentiating centromere positive (C+) from centromere negative (C-) MN. The frequency of MN in binucleate lymphocytes was significantly higher in alcoholics than in controls (12.0 +/- 5.4 and 7.6 +/- 1.6, respectively; P: < 0.05). FISH revealed significantly higher frequencies of C+ MN in alcoholics than in controls (8.2 +/- 4.8 and 3.4 +/- 1.4, respectively; P: < 0.05). In the alcoholics, no association was found between years of alcohol abuse and frequency of MN or C+ MN. However, age influenced MN and C+ MN frequency both in alcoholics and controls. These results indicate that alcohol abuse may well induce chromosome loss in humans, suggesting a possible aneugenic mechanism of alcohol. This effect could contribute to the health hazards related to alcoholism such as cancer risk.

Adult↗
PubMed2000

Treatment of shigellosis with cefixime: two days vs. five days.

BACKGROUND: Although the recommended standard course of therapy for shigellosis is 5 days of oral ampicillin or trimethoprim-sulfamethoxazole therapy, successful outcome has been reported in adults treated with abbreviated courses of antibiotics. The purpose of this study was to compare short course (2-day) vs. 5-day therapy with cefixime for treatment of diarrheal disease caused by Shigella sonnei in children. METHODS: This was a prospective, randomized, double blind, placebo-controlled study. Patients were eligible if they were at least 6 months of age and presented to the Children's Hospital of Pittsburgh during an outbreak of diarrhea caused by S. sonnei, with (1) a history of fever and diarrhea (at least three loose or watery stools per day), (2) bloody diarrhea or (3) diarrhea and known exposure to an individual with documented shigellosis. Patients were randomized to receive either 2 days of cefixime (8 mg/kg(day) given once daily followed by 3 days of placebo or 5 days of cefixime. Telephone follow-up was performed on Days 3, 7 and 14 after enrollment. Follow-up stool cultures were obtained on Day 7 to assess bacteriologic cure. There were standardized definitions for cure, improvement, failure and relapse. RESULTS: Forty-seven patients were enrolled. Eleven were eliminated from analysis because their stool cultures were not positive for S. sonnei. There were 36 evaluable patients, 21 in the 2-day group and 15 in the 5-day group. Patients ranged in age from 6 months to 17 years. Forty-four percent of the subjects were male. Symptoms were improved or had resolved by Day 3 of therapy in all patients. There were 8 patients who experienced a clinical relapse: 5 of 21 (24%) patients in the 2-day treatment group and 3 of 15 (20%) in the 5-day group. There were 13 patients who experienced a bacteriologic failure (defined as the occurrence of a positive culture at the Day 7 follow-up visit), 11 of 20 (55%) in the 2-day group and 2 of 14 (14%) in the 5-day group (P < 0.02). CONCLUSION: Two- and 5-day treatment courses with cefixime for treatment of diarrheal disease caused by S. sonnei result in similar rates of clinical cure and clinical relapses; however, there was a higher rate of bacteriologic failure with shorter course therapy.

Cefixime↗
PubMed1999

Bromodeoxyuridine labelling as an alternative method to identify 6-thioguanine-resistant mutant lymphocytes in humans.

6-Thioguanine-resistant (TGR) mutant lymphocytes in human blood are usually enumerated by the cloning assay which allows the molecular characterisation of the HPRT mutations to be detected. A "short-term" alternative approach is provided by the anti-bromodeoxyuridine (anti-BrdU) technique in which TGR lymphocytes are identified immunocytochemically by their ability to synthesise DNA in the presence of 6-thioguanine (TG). We have evaluated the influence of various experimental factors that could affect the frequency of TGR lymphocytes. A standard protocol is proposed, based on 24-h cold storage of isolated lymphocytes at 4 degrees C and 40-h culture with and without TG, the last 16 h with BrdU. The harvested cells are treated with hypotonic (0.075 M) KCl, fixed with methanol:acetic acid (3:1) and put on microscopic slides. For the TG cultures, all cells are prepared on the slides, while slides from the control cultures are made by a 1/50 dilution. DNA is denatured by formamide, and the BrdU label is identified by anti-BrdU antibody detected by immunoperoxidase staining using a peroxidase-conjugated secondary antibody with diaminobenzidine as substrate. In 10 donors, the frequency of TGR lymphocytes (variant frequency, Vf) detected by this protocol ranged from 69.65 x 10(-6) to 83.45 x 10(-6), and split measurements showed a relatively small intra-assay variation in Vf values of each donor. BrdU in DNA was also detected by immunofluorescence using a fluorescein-conjugated anti-BrdU monoclonal antibody. This method, facilitating easy identification of positive cells and rapid microscopic scoring, may serve as a basis for an automated analysis of TGR lymphocytes. Vf values detected by the anti-BrdU assay are higher than mutant frequencies obtained by the cloning assay, which has been assigned to the presence of non-mutant phenocopies considered to represent spontaneously cycling lymphocytes. Although the anti-BrdU assay is rapid and easy and has been shown to respond to genotoxic exposures, its true value could be evaluated only when it can be ascertained that phenocopies do not significantly contribute to the Vf values obtained.

Bromodeoxyuridine↗
PubMed1999

Influence of nitroreductase and O-acetyltransferase on the mutagenicity of substituted nitrobenzothiophenamines in Salmonella typhimurium.

The mutagenic activity of 17 substituted (aryl)(2-nitrobenzo[b]thiophen-3yl)amines has been evaluated in the Ames test with different isogenic strains of Salmonella typhimurium, that varied in their expression of nitroreductase and O-acetyltransferase. Active derivatives induced frameshift mutations in TA98 strain, and differences in the chemical structure resulted in up to 15-fold changes in mutagenic activity. The non-mutagenic compounds are the unsubstituted parent compound and derivatives with para-chloro, para-fluoro, para-diethylamino, meta-bromo and para-dimethylamino groups. They do not show any activity even in strains with higher level of nitroreductase or O-acetyltransferase. The addition of S9 fraction decreases the mutagenic potential or gives comparable results to those obtained without metabolic activation. For electron-donating substituents, the meta-isomers display the greatest mutagenic potency, whereas the transfer of the group to the para-position leads to less active or unactive molecules. All active nitrobenzothiophenes are substrates for bacterial nitroreductase and O-acetyltransferase, as shown by the reduced mutagenicity in the deficient strains and increased mutagenicity in the corresponding overproducing bacteria. Previous reports have pointed out interest in nitrothiophene analogues with para-chloro and para-fluoro substituents as promising anti-inflammatory drugs. The present study further enhances the putative interest in these derivatives, based on absence of mutagenicity.

Acetyltransferases↗
PubMed1998

Synthesis, metabolism and structure-mutagenicity relationships of novel 4-nitro-(imidazoles and pyrazoles) in Salmonella typhimurium.

A new series of 4-nitro-(imidazoles and pyrazoles) were synthesized as novel antimycotics and tested for their activation to mutagenic forms using Salmonella typhimurium TA98 and TA100, in the presence and in the absence of metabolic activation. TA100NR, TA100/1,8-DNP6, YG1026 and YG1029 strains were employed to identify a specific metabolic reaction which governs the mutagenic potency. Derivatives in the pyrazole group were generally found to be non mutagenic and active imidazoles were weak-direct-acting mutagens. For most of the compounds the mutagenic responses in TA98 were absent or 12- to 22-fold lower compared to TA100. The presence of a methyl or a benzylic group on the imidazole ring and substituents on the N1 and N3 positions were determinant for mutagenicity. Metabolism by bacterial enzyme systems was important to the expression of genotoxicity. Active compounds showed no mutagenicity toward the strain defective in classical nitroreductase and increased mutagenicity, from 2- to 7-fold depending on the test compound, toward the corresponding overproducing bacteria. On the other hand, compounds displayed reduced mutagenicity to the O-acetyltransferase strain without having increased activity in the corresponding overproducing bacteria, YG1029.

Imidazoles↗
PubMed1998

Hemodynamic support in fluid-refractory pediatric septic shock.

OBJECTIVE: Assess outcome in children treated with inotrope, vasopressor, and/or vasodilator therapy for reversal of fluid-refractory and persistent septic shock. DESIGN: Survey; case series. SETTING: Three pediatric hospitals. PATIENTS: Fifty consecutive patients with fluid-refractory septic shock with a pulmonary artery catheter within 6 hours of resuscitation. INTERVENTIONS: Patients were categorized according to hemodynamic state and use of inotrope, vasopressor, and/or vasodilator therapy to maintain cardiac index (CI) >3.3 L/min/m2 and systemic vascular resistance >800 dyne-sec/cm/m to reverse shock. OUTCOME MEASURES: Hemodynamic state, response to class of cardiovascular therapy, and mortality. RESULTS: After fluid resuscitation, 58% of the children had a low CI and responded to inotropic therapy with or without a vasodilator (group I), 20% had a high CI and low systemic vascular resistance and responded to vasopressor therapy alone (group II), and 22% had both vascular and cardiac dysfunction and responded to combined vasopressor and inotropic therapy (group III). Shock persisted in 36% of the children. Of the children in group I, 50% needed the addition of a vasodilator, and in group II, 50% of children needed the addition of an inotrope for evolving myocardial dysfunction. Four children showed a complete change in hemodynamic state and responded to a switch from inotrope to vasopressor therapy or vice versa. The overall 28-day survival rate was 80% (group I, 72%; group II, 90%; group III, 91%). CONCLUSIONS: Unlike adults, children with fluid-refractory shock are frequently hypodynamic and respond to inotrope and vasodilator therapy. Because hemodynamic states are heterogeneous and change with time, an incorrect cardiovascular therapeutic regimen should be suspected in any child with persistent shock. Outcome can be improved compared with historical literature.

Adolescent↗
PubMed1998

The frequency of 844ins68 mutation in the cystathionine beta-synthase gene is not increased in patients with venous thrombosis.

BACKGROUND AND OBJECTIVES: A frequent mutation in the cystathionine beta-synthase (CBS) gene (844ins68, a 68-bp insertion in the coding region of exon 8) was recently discovered. In the present study we investigated this mutation as a candidate risk factor for venous thrombosis. DESIGN AND METHODS: The prevalence of the 844ins68 CBS mutation was determined in 101 patients with objectively diagnosed deep venous thrombosis and in 101 healthy controls matched for age, sex and race. PCR amplification of a DNA fragment containing exon 8 of the CBS gene was employed to determine the genotypes. Additionally, Bsrl restriction enzyme digestion of the PCR products was performed in all samples from carriers of the insertion, to test for concurrent presence of a second mutation (T833C) in the CBS gene. RESULTS: The insertion was found in 21 out of 101 patients (20.8%; allele frequency 0.109) and in 20 out of 101 controls (19.8%; allele frequency 0.114), yielding a relative risk for venous thrombosis related to the 844ins68 CBS mutation close to 1.0. In addition, the T833C CBS mutation was detected in all alleles carrying the 844ins68 CBS insertion, confirming the co-inheritance of the two mutations. INTERPRETATION AND CONCLUSIONS: Our findings do not support the hypothesis that the 844ins68 mutation in the CBS gene is a genetic risk factor for venous thrombosis.

Adolescent↗
PubMed1997

Toxicological assessment of liquorice: biliary excretion in rats.

Glycyrrhizin (G) and its aglycone, glycyrrhetic acid (GA) have been prescribed for several therapeutic purposes. However, side effects have pointed out the problem of the toxicity of G. On the contrary, it was recently shown that the pure aqueous liquorice extract (LE), which also contains G, produces reduced adverse effects in rat and human, as compared to pure G, this is likely be related to differences in G bioavailability and the resulting pharmacokinetics of G and GA. Using a sensitive HPLC procedure for the determination of G and GA in rat bile, pharmacokinetics of G and GA in bile have been determined. The results of the analysis showed significantly lower concentrations of G in bile samples from rats treated with LE compared to pure G. Furthermore, LE presented a significant choleretic effect after both oral and i.v. administration, which increases the excretion rate of G. In case of GA, all the concentrations were very low, often below the detection limit. The results prompted us to assess the risk associated with liquorice intake and to determine the daily amount of pure liquorice root extract that can be safely consumed.

Administration, Oral↗
PubMed1997

Potentiating effect of EDTA-Tris on the activity of antibiotics against resistant bacteria associated with otitis, dermatitis and cystitis.

Possible synergistic effects of the combination of EDTA-tromethamine (EDTA-Tris) and three antimicrobial agents (cephaloridine, kanendomycin and enrofloxacin) against resistant Gram-positive and Gram-negative bacteria are reported. Bacteria were isolated from eight cases of chronic otitis externa, five cases of chronic dermatitis and four cases of recurrent cystitis in dogs which had previously been treated with one of the three antibiotics without success. Animals exposed to EDTA-tromethamine plus the antibiotic recovered completely within 10 days, and were controlled clinically and bacteriologically for 180 days. Local irrigation with EDTA-tromethamine solution was well tolerated and no side effects were recorded.

Animals↗
PubMed1996

Cytogenetic effects of Metalaxyl on human and animal chromosomes.

The purpose of this study was to assess the cytogenetic effects in vitro and in vivo of a commonly used fungicide, Metalaxyl. Chromosome damage in vitro, quantified by cultured human peripheral blood lymphocytes, demonstrated dose-related effects not associated with mitotic inhibition or cell death. Significant induction of chromosomal aberrations was observed with between 300 and 1000 micrograms/ml Metalaxyl in the absence of microsomal activation. Incubation in the presence of S9 mix produced less cytogenetic damage. Single i.p. injections of 75-300 mg/kg Metalaxyl had no effect on the frequency of micronuclei, detected in murine polychromatic erythrocytes. Micronuclei results were not compromised by direct evidence of cytotoxicity in the bone marrow of treated animals. The results in the present study indicated that genotoxicity of Metalaxyl was detected only in vitro and not in vivo. Available data reported that Metalaxyl was non-carcinogenic and gave negative results in a battery of genotoxicity tests. So, clastogenicity of Metalaxyl may not be evidence for DNA reactivity, but it may indicate alterations in cell homeostasis which are well implicated in the process of carcinogenesis.

Alanine↗
PubMed1996

Genetic and non-genetic biomarkers related to carcinogenesis in evaluating toxicological risk from Fenarimol.

A multibiomarker approach based on the study of toxicity mechanisms at both genetic and metabolic levels has been applied to Fenarimol. With regard to genotoxicity, particular attention was given to assays for chromosomal aberration and micronuclei; clastogenic potential was assessed in human peripheral blood lymphocytes in vitro, while the induction of micronuclei was studied in male CD1 mouse bone marrow polychromatic erythrocytes (PCE). Fenarimol did not induce any significant dose-related increase in micronucleated PCEs, up to 4-fold above the control level at a single dose of 75 mg/kg b.w., was observed 24 h after treatment. Using selective biochemical markers of effect Fenarimol was found to induce CYP 2B1 isoforms in liver, kidney and lung microsomes of Swiss Albino CD1 male and female mice, as shown by the significant increase in specific 2B1-probe pentoxyresorufin O-dealkylase activity. On the contrary, CYP 3A, probed by N-demethylation of aminopyrine, were only induced in the liver. Results were corroborated by means of Western immunoblotting using rabbit polyclonal antibodies anti-CYP 2B1 and 3A. Northern blotting analysis with CYP 2B1 and 3A cDNA biotinylated probes showed that the expression of such isoforms is regulated at mRNA level. Taken as a whole, these data indicate the possible (mutagenic) cotoxic/cocarcinogenic and promoting potential of this fungicide.

Animals↗
PubMed1996

The genetic and non-genetic toxicity of the fungicide Vinclozolin.

The mutagenic/cocarcinogenic potential of the fungicide Vinclozolin was assessed by a comprehensive examination of toxicity mechanisms at both the genetic and the metabolic level. Vinclozolin did not induce any significant increase in chromosomal aberrations in human pheripheral blood lymphocytes cultured in vitro, both in the presence and in the absence of metabolic activation. However, significant dose-related increases in micronucleated erythrocytes (up to 4-fold over the control) were found in the bone marrow cells of mice 24 h after treatment with the fungicide over a range of concentrations from 312.5 to 1250 mg/kg. The morphology and the size of micronuclei induced was suggestive of a predominantly clastogenic mode of action. Several cytochrome P450 (CYP)-dependent reactions have been monitored in liver, kidney and lung microsomes of male and female Swiss Albino CD1 mice in order to ascertain certain toxic non-genetic properties (related to carcinogenesis) of Vinclozolin. It was found to be a selective inducer towards CYP 3A (liver, kidney) and 2E1 (liver), as exemplified by the significant increases of the demethylation of aminopyrine (APND, up to 2.3-fold, female liver), and hydroxylation of p-nitrophenol (pNPH, up to 5.6-fold, male liver). In general, however, Vinclozolin has a complex pattern of induction and suppression of CYP-dependent enzymes, as shown from the reduced expression of various monooxygenases depending upon dose, sex or organ considered. For example, pNPH activity was suppressed in kidney (up to 48% loss, averaged between male and female), whereas ethoxycoumarin O-deethylase was reduced in lung up to 53% in male (at the highest dose). These data were sustained by means of Western immunoblotting using rabbit polyclonal antibodies anti-CYP 3A and 2E1. Northern blotting analysis using CYP 3A1/2 and 2E1 cDNA biotinylated probes showed that the expression of such isozymes is regulated at the mRNA level. Taken together, the findings indicate the clastogenic activity and the possible cotoxic, cocarcinogenic and promoting potential of Vinclozolin.

Animals↗
PubMed1995

Analysis of metabolism and genotoxicity of 5-nitro-3-thiophenecarboxanilides in bacterial, mammalian and human cells.

5-nitro-3-thiophenecarboxanilide (NTCA3) was clearly mutagenic in Salmonella typhimurium strains TA98, YG1021 (the strain with elevated nitroreductase) and YG1024 (the strain with elevated O-acetyltransferase) and only slightly mutagenic at the gpt locus in AS52 cells. Clastogenic activity in human lymphocytes was dependent on the length of exposure: detectable chromosome aberrations were observed following a 24 h treatment period, but not after 3 h exposure. S9 increased genotoxicity in both mammalian cells and human lymphocytes. Metabolites formed by incubation of NTCA3 with the different cell systems were examined. A time-course study in cell whole extracts showed that bacterial and mammalian cells can acetylate NTCA3 forming 5-acetylamino-3-thiophene-carboxanilide. The formation of this metabolite in human lymphocyte extracts was not confirmed. These data support the conclusions that: (i) both bacterial and mammalian activation pathways play a role in mutations by NTCA3; (ii) the N-acetylated derivative is generated by acyl-transferase after reduction and is the end product of the metabolism in both bacterial and mammalian cells; and (iii) different levels of reductase and acetyltransferase activity may contribute to the differential sensitivity of the different cellular species to the genotoxicity of NTCA3. The fact that NTCA3 serves as substrate for enzymatic activities of importance also in human metabolism needs consideration in assessing the potential risk posed by NTCAs.

Acetylesterase↗
PubMed1994

Genetic safety evaluation of pesticides in different short-term tests.

Cyanazine, cyhexatin, dicamba and DNOC are pesticides commonly and broadly used in agriculture pest control. However, there is little information on their toxicity and mutagenicity in human cells and in whole animals. Therefore, UDS assay and SCE assay in human peripheral lymphocytes, and chromosome aberration analysis in bone marrow of rats have been used to assess the DNA-damaging activity of the above pesticides. Cyanazine proved non-genotoxic in all the test systems. Cyhexatin showed only weakly positive results for SCE induction in human lymphocytes, providing no concern for genotoxicological hazard. While dicamba did not show clastogenic effects in rodents, DNOC gave significant dose-related increases of structural chromosome aberrations in rat bone marrow cells. Female animals showed increased sensitivity to the toxic effects by DNOC at the highest dose. The results provide further information on the intrinsic genotoxic activity of the tested pesticides, which may contribute to the toxicological assessment of the risk associated with human exposure.

Animals↗
PubMed1994

Interactive effects between trichloroethylene and pesticides at metabolic and genetic level in mice.

A combined cytogeneticurine metabolite analysis approach was used to assess potential interactive effects between Fenarimol (FN), a fungicide, and trichloroethylene (TRI), a halogenated solvent. FN was demonstrated to selectively induce P450-2B1 isoforms in different organs of treated mice. Since the rate of metabolism and the stereospecificity of metabolism are dependent on the types and amount of P450s available, FN might drastically alter the metabolic activation of a precarcinogen, such as TRI, and its toxicological consequences. Male CD1 mice were divided into untreated, vehicle control, and experimental groups. Animals of the latter groups were treated ip with 150 mg/kg bw FN in corn oil, 457 mg/kg bw TRI in corn oil, TRI plus FN separated by different time intervals. Bone marrow cells were harvested for determination of micronuclei (MN) frequencies in polychromatic erythrocytes (PCE). The presence of the known metabolite of TRI, trichloroethanol (TCE), was quantitated in collected urine by gas chromatography using an electron-capture detector. Linear regression analysis shows that MN frequency by TRI is correlated with TCE concentration in urine. Observed potentiation of genotoxicity of TRI by FN pretreatment (1 hr before TRI treatment) apparently reflects changes in the spectra of enzymes involved in TRI metabolism, and altered toxicokinetic, as witnessed by the 20% difference in TCE excretion from combined treated mice. However, no increased genetic or metabolic effects were observed when FN was administered 3 hr before TRI. No significant interactive effects were observed at a genetic level when FN was administered 1 hr and 3 hr after TRI whereas a 33 to 47% loss in TCE excretion was recorded.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗