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Biomedical subjects

W Lee

Publications and source records attributed to W Lee.

At least 199 records · Page 11Linked to original sources
PubMed1997

Enhanced ocular hypotensive response to epinephrine in rabbits with prior dexamethasone treatment.

The purpose of this study was to determine glucocorticoid modulation of ocular pressure to epinephrine applied topically to rabbit eyes that were pretreated with dexamethasone. Rabbit eyes were pretreated with five applications of topical 0.07% dexamethasone (0.1% dexamethasone phosphate) or saline drops, administered at ten minute intervals. The eyes were then treated with epinephrine bitartrate drops at concentrations of free base epinephrine of 1.1%, 0.27%, 0.05%, 0.027%, 0.005% or 0.0005%. An additional group of rabbits received dexamethasone pretreatment only. Intraocular pressure (IOP) was measured for the next four hours. Enhanced lowering of intraocular pressure was observed with dexamethasone pretreatment. Rabbits receiving the smaller dose of epinephrine with dexamethasone had the largest decrease in IOP at 135 minutes after instillation of the epinephrine drops (0.005% epinephrine, mean difference +/- standard error of mean = 5.4 +/- 1.1 mmHg). Similarly, the duration of significant decrease of the IOP was prolonged in the groups receiving the lower concentrations of epinephrine (0.005% epinephrine, 255 minutes after administration of epinephrine). The synergism between glucocorticoids and adrenergic agonists in lowering IOP may be potentially useful in the therapy of ocular hypertension and glaucoma.

Administration, Topical↗
PubMed1997

Large-scale sequencing in human chromosome 12p13: experimental and computational gene structure determination.

The detailed genomic organization of a gene-dense region at human chromosome 12p13, spanning 223 kb of contiguous sequence, was determined. This region is composed of 20 genes and several other expressed sequences. Experimental tools including RT-PCR and cDNA sequencing, combined with gene prediction programs, were utilized in the analysis of the sequence. Various computer software programs were employed for sequence similarity searches and functional predictions. The high number of genes with diverse functions and complex transcriptional patterns make this region ideal for addressing challenges of gene discovery and genomic characterization amenable to large-scale sequence analysis.

Alternative Splicing↗
PubMed1997

Molecular Delivery System for Antisense Oligonucleotides: Enhanced Effectiveness of Antisense Oligonucleotides by HVJ-liposome Mediated Transfer.

BACKGROUND: The effectiveness of antisense oligodeoxynucleotides for in vitro and in vivo studies is limited by a low efficiency of cellular uptake and instability due to degradation by nucleases. To overcome some of these problems, we recently developed a transfer method that utilizes inactivated Sendai virus (hemagglutinating virus of Japan [HVJ]) complexed with liposomes to deliver antisense oligodeoxynucleotides. In this study, we compared the effectiveness of the HVJ-liposome method versus a cationic liposome method versus passive uptake to deliver antisense oligodeoxynucleotides against basic fibroblast growth factor on angiotensin (Ang) II-induced rat vascular smooth muscle cell growth. METHODS AND RESULTS: Twenty to twenty-eight hours after transfection, antisense fibroblast growth factor oligodeoxynucleotides introduced by passive uptake and HVJ-liposome method decreased basal DNA synthesis significantly as compared to the sense, control, and scrambled oligodeoxynucleotides groups; however, 60-68 hours after transfection, only antisense fibroblast growth factor oligodeoxynucleotides transduced by the HVJ-liposome method resulted in a significant inhibition of DNA synthesis under basal and Ang II-(10(-;6)M) stimulated conditions. The IC(25) of oligodeoxynucleotides assessed by the inhibition of thymidine incorporation was significantly lower using the HVJ-liposome method than those using the other transfer methods. To clarify the mechanisms of cellular uptake of oligodeoxynucleotides with the HVJ-liposome method, we studied the cellular fate of fluorescein isothiocyanate (FITC)-labeled oligodeoxynucleotides FITC-oligodeoxynucleotides was localized in nuclei at 5 minutes after transfection with the HVJ-liposome method. In contrast, FITC-oligodeoxynucleotides introduced by passive uptake was detected in nonnuclear cellular compartments, possibly endosomes, but not the nuclei. Cellular fluorescence of oligodeoxynucleotides introduced by passive uptake disappeared within 24 hours, while that introduced by the HVJ-liposome method could be observed up to 72 hours. CONCLUSION: These results demonstrate that the HVJ-liposome transfer enhanced the effectiveness of AS-fibroblast growth factor via its specific molecular mechanisms of transfer.

Journal Article↗
PubMed1997

Birthweight prediction by three-dimensional ultrasonographic volumes of the fetal thigh and abdomen.

Our validation study examined a three-dimensional ultrasonographic phantom that contained irregularly shaped volume targets ranging from 0.5 to 76.1 milliliters. Four different examiners made blinded measurements from volume datasets that were acquired by 4 and 7 MHz transducers. Birthweight predictions using abdominal and thigh volumes from 18 term fetuses also were compared with two-dimensional ultrasonographic methods. In vitro volume measurements were accurate, precise, and repeatable despite a small systematic overestimation with increasing object size. Mean systematic error and precision for birthweight predictions by three-dimensional ultrasonography (-0.03% +/- 6.1%) were not significantly different from those by two-dimensional ultrasonography (-0.60% +/- 8.8%). Conventional prediction methods yielded three birthweights with greater than 15% error. By comparison, except for one infant whose birthweight indicated an 11% error, all predictions based on fetal volume parameters were within 10% of true values. Accurate birthweight predictions by fetal volume parameters appear to be technically feasible at term gestation although their practical clinical application requires further investigation. Birthweight predictions in this manner may allow remote consultants to evaluate the fetus over wide-area computer networks despite the physical absence of the patient.

Abdomen↗
PubMed1997

Ascorbic acid determination with an automated enzymatic procedure.

Given the widespread interest in antioxidant nutrients, we have developed a new procedure that will permit the automated determination of plasma ascorbic acid (AA) concentration with a Roche Fara centrifugal analyzer. After the deproteinization of plasma with metaphosphoric acid, AA is oxidized to dehydroascorbic acid by AA oxidase. The product is coupled to o-phenylenediamine to produce a chromophore for which the absorbance is measured at 340 nm. The procedure allows much faster throughput than conventional HPLC methods while yielding results that correlate well and provide improved precision. Linearity extends beyond the reference range of 26.1-84.6 micromol/L, and severe hemolysis is the only interference identified.

Adult↗
PubMed1997

Optimization of the MGH repair using an algorithm for tenorrhaphy evaluation.

Previous investigations have demonstrated the superior strength and toughness of the MGH four-strand tendon repair technique and shown that it neither weakens during maximum tendon softening nor interferes with healing in an in vivo rabbit model. In the current study, the biomechanical performance of the modified Becker (MGH) and the modified Kessler repairs were compared in situ using a dynamic human cadaveric model to evaluate strength, toughness, glide efficiency, and operator variability. Three different surgeons performed a total of 42 zone II flexor digitorum profundus repairs in 14 fresh human cadaver hands. The modified Becker (MGH) repairs were stronger (79 +/- 3 versus 64 +/- 4 N; p < 0.01) and tougher (0.092 +/- 0.002 versus 0.078 +/- 0.003 J; p < 0.01) than the Kessler repairs while allowing equally efficient glide (32 +/- 6 versus 33 +/- 4 percent; p > 0.9). Strength was operator-dependent only for the modified Kessler repair (p < 0.005). We then established the optimal configuration of the MGH tenorrhaphy (number of preloaded crosses on either side of the tendon transection) by examining gap resistance ex vivo. Fifty-one MGH flexor tendon repairs were performed on explanted fresh human cadaver tendons. The experimental groups were randomly assigned to receive 0, 1, 2, 3, or 4 crosses on each side of the tenorrhaphy. Strength and toughness to gap formation and to ultimate failure were assessed tensiometrically. The MGH two-cross configuration was most resistant to gap formation (peak load 39 +/- 3 N; p < 0.05), establishing this configuration as the optimal design of this four-strand crisscrossing repair technique. The augmented Becker (MGH) repair is significantly stronger and tougher than the modified Kessler repair and demonstrates no operator dependence. It is a superior technique for zone II tenorrhaphy in the human hand. An algorithm is presented as a systematic approach that includes the important elements necessary for the rigorous biomechanical evaluation of any tendon repair technique.

Algorithms↗
PubMed1997

Relapse of polymyositis after prolonged remission.

We describe the case of a patient with polymyositis and anti-Jo-1 antibodies who experienced a relapse of his inflammatory muscle disease after 7 years of clinical remission. Our review of the literature shows that remission is achieved in 25-68% of patients treated with high dose corticosteroids as part of their initial therapy. Relapse rates after complete remission vary from 6 to 43% in the few studies where this information is available. Late relapses after initial remission appear to be unusual, but may be more frequent in patients like this one with antisynthetase syndrome.

Antibodies, Antinuclear↗
PubMed1996

Interaction of nonylphenol and hepatic CYP1A in rats.

Both estradiol and nonylphenol (NP) inhibited hepatic microsomal 7-ethoxyresorufin O-deethylase (EROD) activity of beta-naphthoflavone-treated rats. Enzyme kinetic analyses (Lineweaver-Burk plots) using different estradiol and NP concentrations with graded increases in the concentrations of the substrate, ethoxyresorufin, showed that the inhibition was of a competitive nature at all concentrations of estradiol or NP used. Thus, the mechanism by which NP inhibits EROD activity is similar to that of estradiol. NP, however, was much less potent than estradiol. Young rats treated in vivo with 80 mg/kg body weight of NP demonstrated a slight but significant decrease in their hepatic microsomal EROD activity and CYP1A protein as measured by western blot analysis. In addition, treatment with NP led to a decrease in the steady-state levels of hepatic CYP1A mRNA in rats, suggesting that NP acted at the pre-translational level. The competitive nature of inhibition by NP on hepatic microsomal EROD activity indirectly suggests that this compound is a possible substrate of the CYP1A enzyme. Furthermore, NP had a moderate modulating effect on the expression of CYP1A in rat liver.

Animals↗
PubMed1996

Inhibition of the expression of inducible cyclooxygenase and proinflammatory cytokines by sesquiterpene lactones in macrophages correlates with the inhibition of MAP kinases.

In our previous studies (Refs. 1 and 2), it was shown that protein tyrosine kinase (PTK) inhibitors, radicicol and herbimycin A, inhibit the expression of the mitogen-inducible cyclooxygenase (COX-2) and proinflammatory cytokines. Radicicol and herbimycin A possess polarized double bonds which can conjugate sulphydryl groups of proteins. Parthenolide, the predominant sesquiterpene lactone in European feverfew (Tanacetum parthenium), contains alpha-methylene-gamma-lactone (MGL) and an epoxide in its structure. These moieties can interact with biological nucleophiles such as a sulfhydryl group. Parthenolide inhibited the expression of COX-2 and proinflammatory cytokines (TNF alpha and IL-1) in lipopolysaccharide (LPS)-stimulated macrophages. The structure-function relationship indicates that the MGL moiety confers the inhibitory effect. Parthenolide suppressed LPS-stimulated protein tyrosine phosphorylation in the murine macrophage cell line (RAW 264.7). This suppression was correlated with its inhibitory effect on the expression of COX-2 and the cytokines. Among tyrosine phosphorylated proteins, mitogen-activated protein kinases (MAPKs) exhibited the most dramatic inhibition.

Animals↗
PubMed1996

TNF-alpha inactivation of collagen receptors: implications for fibroblast function and fibrosis.

TNF-alpha inhibits collagen synthesis and at high concentrations stimulates collagenase synthesis in fibroblasts. As fluid from chronic inflammatory lesions contains significant levels of TNF-alpha, it is puzzling why these lesions exhibit dense accumulations of disorganized collagen. In this study we determined if low concentrations of TNF-alpha may inhibit the collagen phagocytic pathway in fibroblasts and thereby contribute to fibrosis. Collagen phagocytosis was measured by flow cytometric assessment of internalized, fluorescent collagen beads. TNF-alpha induced a dose-dependent reduction (optimal dose: 40% at 10 ng/ml; p<0.001) in the proportion of phagocytic cells and a twofold reduction of the number of internalized beads per cell but did not alter the total number of vital cells. TNF-alpha reduced by twofold the degradation of collagen films. Fluid flow shear-force assays demonstrated that TNF-alpha caused a 72% reduction (p < 0.05) in strong binding of collagen-coated beads to cells indicating that TNF-alpha may inactivate receptors and inhibit collagen binding. Furthermore, TNF-alpha reduced cell contact area with collagen substrates by threefold and inhibited reattachment of trypsinized cells by fourfold. Although levels of collagen receptors were increased by TNF-alpha (53% increase in alpha(2) (beta)1 integrin; p<0.001, 20% increase in alpha(1)beta(1)), the receptors were inactivated by the cytokine. The reduced phagocytic activity of TNF-alpha-treated cells was restored to control levels by treatment with the integrin-activating Abs A16G6 and JBS2. TNF-alpha inhibited focal adhesion formation and phosphotyrosine staining in focal adhesions. These effects were replicated by the tyrosine kinase inhibitor genistein, which also inhibited phagocytosis. Collectively, these data indicate that TNF-alpha inhibits adherence and phagocytosis of collagen. These effects are mediated by a reduction in the strength of alpha(2)beta(1) integrin binding to collagen, possibly through tyrosine kinases in focal adhesions. At low concentrations of TNF-alpha (10 ng/ml) that are found in the periphery of chronic inflammatory lesions, we suggest that inhibition of the collagen phagocytic pathway may contribute to fibrosis.

Actins↗
PubMed1996

Regulation of phosphatidylcholine synthesis in maturing type II cells: increased mRNA stability of CTP:phosphocholine cytidylyltransferase.

Pulmonary surfactant phosphatidylcholine synthesis increases in fetal lung type II cells with advancing gestation. This increase is accompanied by an increase in gene and protein expression of CTP:phosphocholine cytidylyltransferase (CT; EC 2.7.7.15), which catalyses a regulatory step in de novo phosphatidylcholine synthesis by fetal type II cells. In the present study we investigated the role of transcriptional and post-transcriptional mechanisms in the developmental induction of CT mRNA in maturing type II cells. We found that CT mRNA increased 2-fold from days 18 to 21 of fetal rat gestation (term 22 d). This increase in CT mRNA was not accompanied by a developmental increase in CT gene transcription. However, CT mRNA was more stable on day 21 (t1/2 48 h) compared with that on day 18 (t1/2 17 h). Glucocorticoids have been shown to enhance surfactant phosphatidylcholine synthesis in fetal type II cells. Therefore we also examined the effect of maternal glucocorticoid administration to pregnant rats at 19 d of gestation on CT mRNA expression in fetal type II cells isolated 24 h later. Glucocorticoid treatment did not increase type II cell CT mRNA. As reported previously, however, glucocorticoids increased CT activity in the microsomal membrane fraction of fetal type II cells, whereas no differences in cytosolic CT activity were observed. We conclude that the developmental increase in CT mRNA in fetal type II cells is due to a decreased breakdown of the CT transcript and that glucocorticoids regulate fetal type II cell CT activity at a post-translational level.

Animals↗
PubMed1996

Immunocytochemistry and flow cytometry evaluation of human megakaryocytes in fresh samples and cultures of CD34+ cells.

Adhering platelets on the cell surface can give misleading results when doing flow cytometry analysis of platelet/megakaryocyte-specific glycoprotein (GP) antigens to enumerate megakaryocytes (MK) in mobilized peripheral blood (PB), apheresis products, or normal bone marrow (BM). For adequate quantification and characterization of human MK, we examined samples with parallel flow cytometry and immunocytochemistry. MK expression of GP IIb/IIIa (CD41a), GP Ib (CD42b), GP IIIa (CD61), CD45, CD33, and CD11b, and their light scatter properties were evaluated. Fresh samples of low density mononuclear cells (MNC) or purified CD34+ cells contained 10-45% of platelet-coated cells. Platelet-coated cells decreased dramatically after several days of incubation in a serum-free medium supplemented with stem cell factor, IL-3, IL-6, and/or GM-CSF. Between d 9-12, flow cytometry detected a distinct CD41a+ MK population, 8.3 +/- 1.3% in BM CD34 cell cultures (n = 7) and 13.1 +/- 2.1% in PB CD34 cell cultures (n = 14), comparable to immunocytochemistry data (7.8 +/- 1.9% and 16.4 +/- 2.6%, respectively). CD41a stained a higher proportion of MK than CD42b or CD61, while CD42b+ or CD61+ cells contained more morphologically mature MK than CD41a+ cells in cultures containing aplastic serum. When fluorescence emission of CD41a was plotted against forward-light scatter (FSC), subpopulations of small and large MK were observed. Such subpopulations overlapped in CD41a intensity and side-light scatter (SSC) property. Most MK co-expressed CD45 (98.8% positive) but not CD33 (80.7% negative) or CD11b (88.9% negative). Our data indicate that flow cytometry can be used effectively to identify MK. However, caution should be taken with samples containing adherent platelets.

Adult↗
PubMed1996

GLUT1 transmembrane glucose pathway. Affinity labeling with a transportable D-glucose diazirine.

We synthesized a transportable diazirine derivative of D-glucose,3-deoxy-3,3-azi-D-glucopyranose (3-DAG), and studied its interaction with purified human erythrocyte facilitative glucose transporter, GLUT1. 3-DAG was rapidly transported into human erythrocytes and their resealed ghosts in the dark via a mercuric chloride-inhibitable mechanism and with a speed comparable with that of 3-O-methyl-D-glucose (3-OMG). The rate of 3-DAG transport in resealed ghosts was a saturable function of 3-DAG concentration with an apparent Km of 3.2 mM and the Vmax of 3.2 micromol/s/ml. D-Glucose inhibited the 3-DAG flux competitively with an apparent KI of 11 mM. Cytochalasin B inhibited this 3-DAG flux in a dose-dependent manner with an estimated KI of 2.4 x 10(-7) M. Cytochalasin E had no effect. These findings clearly establish that 3-DAG is a good substrate of GLUT1. UV irradiation of purified GLUT1 in liposomes in the presence of 3-DAG produced a significant covalent incorporation of 3-DAG into glut1, and 200 mM D-glucose abolished this 3-dag incorporation. Analyses of trypsin and endoproteinase Lys-C digestion of 3-DAG-photolabeled GLUT1 revealed that the cleavage products corresponding to the residues 115 183, 256 300, and 301 451 of the GLUT1 sequence were labeled by 3-DAG, demonstrating that not only the C-terminal half but also the N-terminal half of the transmembrane domain participate in the putative substrate channel formation. 3-DAG may be useful in further identification of the amino acid residues that form the substrate channel of this and other members of the facilitative glucose transporter family.

Affinity Labels↗
PubMed1996

Identification of a human erythroid progenitor cell population which expresses the CD34 antigen and binds the plant lectin Ulex europaeus I.

Two and three color flow cytometry of normal human bone marrow was used to identify CD34+ progenitor cells and examine their binding to the plant lectin Ulex europaeus I (Ulex). In normal bone marrow, 48.48 +/- 17.4% of the CD34+ cells bind to Ulex. Two color flow cytometry was used to sort CD34 + cells, and subsets of CD34+ cells, CD34+ Ulex+ and CD34+ Ulex-. These populations were sorted into colony assays to assess myeloid (CFU-GM) and erythroid (BFU-E) progenitors. The CD34+ Ulex+ subset was 84 +/- 14% BFU-E colonies (mean +/- S.D.) and had the highest cloning efficiency of 28 +/- 13%. Three color analysis of CD34+ Ulex+ cells showed staining with other erythroid (CD71, GlyA) antibodies and lack of stain. ing with myeloid (CD13, CD45RA) antibodies. These studies confirmed the erythroid characteristics of this subpopulation.

Antibodies↗
PubMed1996

Role of integrins in regulation of collagen phagocytosis by human fibroblasts.

Phagocytosis of collagen fibrils by fibroblasts is an important pathway for degradation of extracellular matrix in mature connective tissues. To study regulatory mechanisms in phagocytosis, 2-microns fluorescent beads coated with either collagen (COL) or bovine serum albumin (BSA) were incubated with human gingival fibroblasts in vitro. For these studies single cell suspensions were prepared by trypsinization, and bead internalization and collagen receptor expression were assessed by flow cytometry. After 3-h incubations, up to 8-fold more cells internalized COL beads than BSA-coated beads. Increased collagen coating concentration was associated with elevated proportions of cells that internalized COL beads, and was observed also in the presence of competing fibronectin-coated beads. The number of beads per cell and the percent of phagocytic cells increased proportionally with higher bead loadings. At > 4 beads per cell a maximum of approximately 80% of cells were phagocytic. Cells reacted with mAbs against the alpha 1, alpha 2, and alpha 3 integrin subunits were, respectively, 5%, 98% and 93% positively stained above background controls. All cells that internalized COL beads exhibited alpha 2 staining but there were large proportions of phagocytic cells that were not stained for alpha 1. In unfixed cells, bead internalization caused an immediate reduction of surface staining of membrane-bound alpha 2 by approximately 55% which returned to control levels within 3 h, indicating that cell-surface alpha 2 was internalized by phagocytosis. Preincubation of cells with up to 8 COL beads per cell reduced the proportion of phagocytic cells and the number of internalized beads after a second COL bead incubation 4 h later. To assess the relationship between the percent of phagocytic cells and alpha 2 integrin levels, serum starvation and cycloheximide experiments were conducted. Compared to controls, serum starvation for 24 h induced a 3.2-fold increase of cells internalizing COL beads but did not alter alpha 2 staining levels. In contrast, 3 h cycloheximide treatment reduced alpha 2 staining to 60% of control levels and this treatment also inhibited COL bead internalization. GRGDTP peptide as well as mAbs against the alpha 1 and alpha 2 subunits significantly reduced internalization of COL beads by 1.8 to 2.6-fold, whereas GRGESP peptide and alpha 3 mAb exerted no effect. Internalization of BSA beads was not affected by any of these treatments. Collectively, these data indicate that the alpha 2 integrin, along with other, as yet unidentified components, is likely involved in COL bead internalization. The alpha 2 integrin subunit is rapidly recycled or synthesized following a phagocytic load. In contrast, the alpha 1 integrin is not directly required for phagocytosis but may regulate the internalization step.

Amino Acid Sequence↗
PubMed1996

Variable gene expression within human tyrosinemia type 1 liver may reflect region-specific dysplasia.

Patients with hereditary tyrosinemia type 1 have a deficiency of fumarylacetoacetate hydrolase (FAH) and develop progressive hepatocellular dysfunction with a high risk of malignant transformation. Serum alpha-fetoprotein levels are frequently elevated in these patients; therefore, this commonly used marker of tumorigenesis is inadequate. To date, no literature exists describing the hepatic gene alterations in patients with this disease. We analyzed the expression of a panel of proliferation associated and liver-specific genes in the liver of a 33 month-old girl at the time of orthotopic liver transplantation. This study provides information that may be useful in developing markers for malignancy and understanding the pathogenesis of this disease. Gene expression patterns of two regenerating nodules and total liver from the patient with FAH deficiency were compared with control donor liver. Liver-specific and growth-induced genes with altered expression in the tyrosinemic liver included several functional classes: structural proteins (actin, thrombospondin), transcription factors (c-fos, egr-1, C/EBPalpha), liver-specific enzymes (glucose-6-phosphatase [G6Phase], and secreted factors (insulin-like growth factor binding protein 1 [GFBP-1]. Isolated macronodules demonstrated varied patterns of expression, suggesting that they do not form a homogeneous cellular environment. In the tyrosinemic liver, IGFBP-1 messenger RNA expression was high and G6Phase messenger RNA was not detectable. Although G6Phase and IGFBP-1 are coexpressed in regenerating liver, immunohistochemistry in the tyrosinemic liver demonstrated a mutually exclusive distribution for the two proteins in a tissue section with features of dysplasia. We propose that cells in these areas may have an aberrant transcription factor and growth factor "milieu" that leads to altered gene and protein expression. These molecular alterations are reflected in dysplastic histologic changes and may ultimately predispose to the development of malignancy.

Amino Acid Metabolism, Inborn Errors↗
PubMed1996

Effect of selenium on 1,2-dimethylhydrazine-induced intestinal cancer in rats.

PURPOSE: This study was designed to determine the cancer prevention and therapeutic effects of selenium on rats treated with 1,2-dimethylhydrazine (DMH). METHODS: One hundred sixty Spraque-Dawley male rats were divided into seven groups and received 20 mg/kg/week DMH, subcutaneously for 20 weeks. Two different dosages of selenium (8 and 4 ppm) were administered to the rats through drinking water during DMH treatment (B and C groups) or one month before and during DMH treatment (D and E groups). The rats of Groups A (control group), B, C, D, and E were killed immediately after the last DMH injection. The incidence of intestinal cancer in each group was compared. Eight ppm selenium was also administered to rats after DMH treatment (Group F), and survival times were observed and compared with Group G (treated with DMH only). RESULTS: Rats of Groups B and D received 8 ppm selenium and had a significantly decreased incidence of intestinal cancer (from 65.8 percent (Group A) to 33.3 percent (Group B) and 27.8 percent (Group D); P = 0.0225 and 0.0038). Rats receiving 4 ppm selenium had a relatively decreased incidence of intestinal cancer (from 65.8 percent (Group A) to 44.4 percent (Group C) and 47.1 percent (Group E) but P > 0.05). Survival time of Groups F and G showed no difference. CONCLUSIONS: Eight ppm selenium provided via drinking water has a significant intestinal cancer prevention effect in the presence of a high dose of DMH (20 mg/kg x 20 weeks), and the cancer therapeutic effect of selenium is doubtful in this animal model.

1,2-Dimethylhydrazine↗