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PubMed2002

Inhibitory effect of tumor cell proliferation and induction of G2/M cell cycle arrest by panaxytriol.

Panaxytriol, a polyacetylenic compound, isolated from red ginseng (Panax ginseng C.A. Meyer), was studied to determine its effects on the growth and cell cycle of tumor cell lines. The compound showed both significant cytotoxicity and inhibition of DNA syntheses in various tumor cells tested. For P388D1, a mouse lymphoma cell line, IC50 values for cytotoxicity and inhibition of DNA synthesis were 3.1 and 0.7 microg/ml, respectively. The cytotoxic effect of panaxytriol was both time- and dose-dependent. It also induced the cell cycle arrest of P388D1 at the G2/M phase, which was measured through flow cytometry. Particularly, the proportion of cells in the G2/M phase of the cell cycle increased from 9 % to 26 and 48 %, respectively, after 24 and 36 h exposure to panaxytriol at 5 microg/ml. There were corresponding decreases in the proportion of cells at the G0/G1 phase. The S phase also decreased during the 36-h treatment.

3T3 Cells↗

PubMed1992

Growth modulatory effects of some 6-methylenic steroids on human and hamster pancreatic adenocarcinoma cells in vitro.

Similarities between pancreatic, prostate and mammary tumors in possession of steroidal receptors and enzymes led to investigation of the responsiveness of pancreatic cancer to steroids with potential for tumor inhibition. The compounds were tested in vitro against human (HPAF and PANC-1) and hamster (HP-1) pancreatic ductal tumor cell lines using a colorimetric enzyme-based assay (MTT) to assess both cytotoxic and cytostatic effects and the 3H-thymidine uptake assay for cytostatic effects. Only certain 6-methylenic steroidal 3-ketones and the anti-estrogen tamoxifen citrate exerted appreciable anti-tumor effects. Marked cytotoxic and cytostatic activity was shown by some 6-methylenic congeners of progesterone, testosterone and its acetate, and 4-androstene-3,17-dione on both human and hamster pancreatic tumor cell lines. In contrast to prostate cancer, testosterone, but not 5 alpha-dihydrotestosterone, enhanced growth of the well differentiated HPAF cell line as well as the poorly differentiated PANC-1 cell line. It is therefore surprising that the 6-methylene derivative of testosterone acetate, which is both a potent androgen and 5 alpha-reductase inhibitor, is a very active tumor inhibitor in our assay.

Animals↗

PubMed1997

Differanisole A, a novel antitumor antibiotic, enhances growth inhibition and differentiation of human myeloid leukemia cells induced by 9-cis retinoic acid.

Differanisole A, 3,5-dichloro-2-hydroxy-4-methoxy-6-n-propylbenzoic acid, inhibited growth of human myeloid leukemia cells. The compound induced G1 arrest and granulocytic differentiation of HL-60 cells, although the differentiation-inducing effect was modest. Differanisole A and 9-cis retinoic acid (9cisRA) synergistically inhibited the growth and induced functional and morphologic differentiation of HL-60 and NB4 cells, whereas the combined treatment with differanisole A and all-trans retinoic acid or 1alpha,25-dihydroxyvitamin D3 was less effective. Similar results were obtained in primary culture of leukemia cells from a patient with acute promyelocytic leukemia. The synergistic effect on growth inhibition and induction of differentiation required simultaneous treatment with differanisole A and 9cisRA. Differanisole A and an RXR-specific ligand (Ro47-5944) cooperatively inhibited the cell growth, while the combined effect of differanisole A and an RAR-specific ligand Am80 was just additive. Differanisole A in combination with 9cisRA may have implications for therapy of acute promyelocytic leukemia patients.

Alitretinoin↗

PubMed2004

Cell activating capacity of 50 Hz magnetic fields to release reactive oxygen intermediates in human umbilical cord blood-derived monocytes and in Mono Mac 6 cells.

The aim of this study was to investigate the mechanism of cell activation induced by extremely low frequency magnetic fields (ELF-MF) (50 Hz) in human cells. We examined the production of free radicals in human umbilical cord blood-derived monocytes and in human Mono Mac 6 cells. The release of superoxide radical anions was analyzed using nitroblue tetrazolium chloride and the total of reactive oxygen species (ROS) was detected using dihydrorhodamine 123. Our results show a significant increase of superoxide radical anion production up-to 1.4 fold as well as an increase in ROS release up-to 1.2 fold upon exposure of monocytes to 1 mT ELF-MF (45 min). Mono Mac 6 cells exhibit higher superoxide radical anion and ROS production up-to 1.4 and 1.5 fold, respectively. These results indicate that Mono Mac 6 cells are more sensitive to ELF-MF than monocytes. Using diphenyleneiodonium chloride (DPI) a specific inhibitor for the NADPH oxidase, the MF-effect was not inhibited in Mono Mac 6 cells. Therefore, we suggest that ELF-MF exposure induces the activation of NADH oxidase in these cells. However, the MF-effect was inhibited by DPI in monocytes, indicating the activation of the NADPH oxidase after exposure to ELF-MF.

Cell Line↗

PubMed1999

A comparative study of the effects of two nitric oxide synthase inhibitors and two nitric oxide donors on temporary focal cerebral ischemia in the Wistar rat.

OBJECT: A critical review of the literature indicates that the effects of nitric oxide synthase (NOS) inhibitors on focal cerebral ischemia are contradictory. In this experiment the authors methodically examined the dose-dependent effects of two NOS inhibitors and two NO donors on cortical infarction volume in an animal model of temporary focal cerebral ischemia simulating potential ischemia during neurovascular interventions. METHODS: Ninety-two Wistar rats underwent 3 hours of combined left middle cerebral artery and bilateral common carotid artery occlusion after having been anesthetized with 1% halothane. A nonselective NOS inhibitor, N(G)-nitro-L-arginine-methyl-ester (L-NAME), and two NO donors, 3-morpholinosydnonimine hydrochloride and NOC-18, DETA/NO, (Z)-1-[2(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-i um-1,2-diolate, were administered intravenously 30 minutes before ischemia was induced. A selective neuronal NOS inhibitor, 7-nitroindazole (7-NI), was administered intraperitoneally in dimethyl sulfoxide (DMSO) 60 minutes before ischemia was induced. Two ischemic control groups, to which either saline or DMSO was administered, were also included in this study. Seventy-two hours after flow restoration, the animals were perfused with tetrazolium chloride for histological evaluation. Cortical infarction volume was significantly reduced by 71% in the group treated with 1 mg/kg L-NAME when compared with the saline-treated ischemic control group (27.1+/-37 mm3 compared with 92.5+/-26 mm3, p < 0.05). The NOS inhibitor 7-NI significantly reduced cortical infarction volume by 70% and by 92% at doses of 10 and 100 mg/kg: 35.2+/-32 mm3 (p < 0.05) and 9+/-13 mm3 (p < 0.005), respectively, when compared with the DMSO-treated ischemic control group (119+/-43 mm3). There was no significant difference between the saline-treated and DMSO-treated ischemic control groups. Treatment with NO donors did not significantly alter cortical infarction volume. CONCLUSIONS: These results support an important role for NO in ischemic neurotoxicity and indicate that neuronal NOS inhibition may be valuable in reducing cortical injury in patients suffering temporary focal cerebral ischemia during neurovascular procedures.

Animals↗

PubMed2002

Photo-induced cytotoxicity of malonic acid [C(60)]fullerene derivatives and its mechanism.

The biological activities of fullerenes have attracted extensive attention in recent years. The aim of this paper is to study the relation of the photo-induced cytotoxicity of fullerene derivatives to their chemical structures as well as the possible cellular mechanism involved in the photocytotoxicity. Three C(60) derivatives with two to four malonic acid groups (DMA C(60), TMA C(60) and QMA C(60)) were prepared and the cytotoxicity of these compounds against HeLa cells was determined by MTT. Cell cycle was measured by flow cytometry. The results showed that the cytotoxicity of the malonic acid C(60) derivatives was irradiation- and dose-dependent. The sequence of their photo-induced growth inhibition was DMA C(60)>TMA C(60)>QMA C(60). Hydroxyl radical quencher mannitol (10mM) was not able to prevent cells from the damage induced by irradiated DMA C(60). DMA C(60), together with irradiation, was found to have an ability of inducing a decrease in the number of G(1) cells from 63 to 42% and a rise in that of G(2)+M cells from 6 to 26%. These data indicated that the number of malonic acid molecules added to C(60) played an important role in the phototoxicity, and the blockage of cell cycle might be a mechanism of this activity.

Carbon↗

PubMedDate not supplied

The use of genomics technology to investigate gene expression changes in cultured human liver cells.

The field of genomics has great potential in toxicology; however, the technology is still in its infancy and there are many questions that need to be addressed. In this study we focus on the use of toxicogenomics for the determination of gene expression changes associated with hepatotoxicity. The human hepatoma cell line HepG2 was used to assess the toxic effects of two well-studied hepatotoxins, carbon tetrachloride (CCl(4)) and ethanol (EtOH). Replicate dishes of HepG2 cells were exposed to two concentrations of CCl(4) and EtOH--doses which caused 20% and 50% cell death (as determined by the MTT assay) were chosen [0.18% and 0.4% (v/v) CCl(4); 2.5% and 5% (v/v) EtOH] and the cells exposed for periods of 2 and 24 h. mRNA was extracted and used to probe Atlas Human Toxicology II arrays (Clontech). Preliminary data revealed that following a 2-h exposure at the low doses of both compounds, few changes in gene expression were detected. However, after 24-h exposure of the cells to the same low concentration of both compounds, multiple changes in gene expression were observed, many of which were specific to the individual hepatotoxins, presumably reflecting their different mechanisms of action. CCl(4) treatment of HepG2 cells gave rise to treatment specific up-regulation of genes involved in extracellular transport and cell signalling, whereas EtOH treatment gave rise predominantly to down-regulation of genes involved in stress response and metabolism. In addition, changes in regulation of certain genes (involved in stress response and cell cycle) were common to both treatments. Exposure of HepG2 cells to higher doses of the hepatotoxins gave rise to more changes in gene expression at lower exposure times. These results strongly suggest that different mechanisms of hepatotoxicity may be associated with specific patterns of gene expression, while some genes associated with common cellular responses may be useful as early markers of toxicity.

Animal Testing Alternatives↗

PubMed2003

Boswellic acid acetate induces differentiation and apoptosis in highly metastatic melanoma and fibrosarcoma cells.

The aim of the study was to investigate the antitumor and/or preventive effect of BC-4, an isomeric compound isolated from the plant Boswellia carteri Birdw. containing alpha- and beta-boswellic acid acetate in 1:1, MW 498.3. We used the MTT (3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide) assay to study the growth inhibition activity of BC-4. Tumor cells migration within a three-dimensional collagen matrix was recorded by time-lapse videomicroscopy and computer-assisted cell tracking. Topoisomerase II was isolated from mouse melanoma B16F10 cells and its activity was determined by its ability to cut plasmid pBR322 DNA. The secretion and activity of matrix metalloproteinases (MMPs) from human fibrosarcoma HT-1080 cells were determined by gelatin zymography. BC-4 was a cytostatic compound and could induce the differentiation of B16F10 mouse melanoma cells, blocked the cell population in G1 phase and inhibited topoisomerase II activity. The G1 phase population of B16F10 cells was increased from 57.4 to 87.7%, while S phase population was reduced from 33.3 to 5.9% after treatment with BC-4 at 25 microM concentration for 48 h. BC-4 also inhibited the migration activity of B16F10. BC-4 could induce apoptosis of HT-1080 cells, as proved by acridine orange fluorescence staining, Wright-Giemsa staining, electromicroscopy, DNA fragmentation and flow cytometry. BC-4 inhibited the secretion of MMPs from HT-1080 cells, too. In conclusion, if it turns out that BC-4 is a well tolerated substance, exhibiting no significant toxicity or side effects, being evaluated currently in China, BC-4 is a good candidate for the prevention of primary tumor, invasion and metastasis.

Animals↗

PubMed2005

Effects of coumarin and 7OH-coumarin on bcl-2 and Bax expression in two human lung cancer cell lines in vitro.

Coumarin and its derivative 7-hydroxycoumarin (7-OHC) have antitumor and antimetastatic properties. The purpose of this study was to investigate the possible effects of these compounds on expression of the bcl-2 and Bax oncoproteins in two human lung cancer cell lines, A427 and Calu-1. The cells were cultured in vitro for 24 h in RPMI 1640 with 1.5% (v/v) ethanol, 1.0 mM ethanolic coumarin or 1.0 mM ethanolic 7-OHC. Viability was determined in each cell line by an MTT assay. Total protein was extracted from cell lysates and the bcl-2 and Bax oncoproteins were identified. Western blotting showed a decrease in bcl-2 and an increase in Bax in A427 cells cultured with coumarin or 7-OHC. Neither drug changed bcl-2 expression in Calu-1 cells compared to solvent controls, and Bax expression was only slightly increased by coumarin. We conclude that 7-OHC is a more potent inhibitor of cell proliferation than coumarin and has more marked effects on oncoprotein expression. Also, the A427 cell line was more sensitive to the drugs than Calu-1.

Adenocarcinoma↗

PubMed2004

New platinum(IV) complex with adamantylamine ligand as a promising anti-cancer drug: comparison of in vitro cytotoxic potential towards A2780/cisR cisplatin-resistant cell line within homologous series of platinum(IV) complexes.

The aim of this study was to compare anti-tumor potency of platinum(IV) complexes with increasing hydrophobicity of their ligands. Cytotoxic potential of the new platinum(IV) complex, coded as LA-12 [(OC-6-43)-bis(acetato)(1-adamantylamine)amminedichloroplatinum(IV)], was compared within the series of complexes of the general formula (OC-6-43)-bis(acetato)(alkylamine)amminedichloroplatinum(IV). Alkylamine ligands with increasing hydrophobicity were: isopropylamine, cyclohexylamine, 1-adamantylamine and 3,5-dimethyl-1-adamantylamine. Particular platinum(IV) complexes were coded as LA-4, LA-2 (known as JM-216), LA-12 and LA-15, respectively. Cytotoxicity was tested with the microplate tetrazolium (MTT) assay on the panel of cancer cell lines and the results were verified by microscopy. HPLC was used to measure hydrophobicity, stability of complexes in various buffers and velocity constants for their reactivity with glutathione. Platinum(IV) complexes with bulky hydrophobic ligands (LA-12 and LA-15) demonstrated about one order higher velocity constant for pseudo-first-order reaction with glutathione in comparison to cisplatin, LA-4 and LA-2, whose velocity constants were close to those measured for cisplatin and related platinum(II) complexes. Cytotoxicities of LA-12 and LA-15 towards cisplatin-resistant epithelial carcinoma A2780/cisR were superior to cisplatin, LA-4 and LA-2 in both 24- and 72-h continuous exposure MTT tests. Rapid induction of apoptosis in the treated cancer cell lines and no cisplatin cross-resistance were found for LA-12, which is a candidate for clinical testing.

Amantadine↗

PubMed2001

Effect of melatonin on cell growth, metabolic activity, and cell cycle distribution.

We have recently demonstrated that the pineal secretory product melatonin inhibits the key transcriptional regulator nuclear factor-kappa B (NF-kappa B). As the activation of NF-kappa B is known to regulate the expression of cellular genes associated with cell cycle progression, cell growth, and differentiation, we investigated the effect of melatonin treatment on several cellular processes. These include cell viability, metabolic activity, and cell cycle phase distribution. Human embryonic kidney (293S) cells were treated with melatonin at concentrations of 0.02, 0.2, or 2 mM. When cell viability was measured 24, 48, and 72 hr after continuous exposure to melatonin using the trypan blue dye exclusion method, no significant cell death was observed. Even after exposure to 2 mM melatonin for 72 hr, cell viability remained at 98%. In contrast, another antioxidant compound, pyrrolidine dithiocarbomate (PDTC), at a 2 mM concentration reduced cell viability to 80.7+/-2.1% as early as 24 hr compared with untreated controls (P<0.05). When the metabolic activity was determined at 24, 48, and 72 hr using the colorimetric MTT assay, no significant changes in metabolic activity were observed. Even if the cells were treated with 10 mM melatonin for 72 hr, the metabolic activity was similar to that of the control cells. When cell cycle analysis was performed by flow cytometry, no marked difference in cell cycle distribution was observed. Melatonin at a concentration of 2 mM, however, did slightly alter the cell cycle (percentage of S phase cells) at 48 hr. This study revealed that when 293S cells are treated with concentrations of melatonin up to 2 mM, no significant alterations in three important cellular functions occurred. Exogenously added melatonin appeared to have a limited influence on the normal functioning of the cells even when the exposure continued for 72 hr.

Adjuvants, Immunologic↗

PubMed1989

A kinetic model of superoxide production from single pulmonary alveolar macrophages.

A kinetic model was developed to describe the production of superoxide (O2-) by single pulmonary alveolar macrophages (PAM). Model predictions were compared with experimental results obtained from single rat PAM. The O2- was quantified by measuring the reduction of nitro blue tetrazolium (NBT) to a diformazan precipitate (NBTH2) from video-recorded images of individual cells. The kinetic model considered three reactions: 1) the production of extracellular O2- from the reduction of oxygen by NADPH oxidase using intracellular NADPH as the substrate, 2) the subsequent dismutation of O2- to form H2O2, and 3) the reaction of O2- and NBT to form diformazan. NBT specificity for O2- was analyzed by comparing results in the presence and absence of superoxide dismutase (SOD) that catalyzes the dismutation of O2- to H2O2. Measured PAM heterogeneity was accounted for by varying the concentration of intracellular NADPH, its rate of depletion, and the concentration of intracellular NADPH oxidase in the kinetic model. Model predictions compared favorably with experimental results except when SOD was present. This discrepancy may be due to diffusional limitations because NBT is a relatively small molecule (818 mol wt) compared with SOD (34,000 mol wt). In addition, the cell surface is both ruffled and negatively charged, which may introduce steric hindrances and/or electrostatic effects, since SOD is also negatively charged, whereas NBT is positively charged.

Animals↗

PubMed1995

Myocardial technetium-99m-teboroxime activity in acute coronary artery occlusion and reperfusion: relation to myocardial blood flow and viability.

UNLABELLED: The purpose of this study was to test the hypothesis that 99mTc-teboroxime retention within the heart depends at least in part on the presence of viable myocytes. METHODS: We used a porcine model of acute myocardial infarction with reperfusion and compared the myocardial uptake of labeled microspheres at 1 hr of reperfusion with that of 99mTc-teboroxime. Eleven domestic swine had measurements of hemodynamics and regional myocardial blood flow (microspheres) at baseline, at 10 and 50 min of left anterior descending (LAD) coronary artery occlusion and at 10 and 60 min of LAD reperfusion. Technetium-99m-teboroxime was injected intravenously at 60 min of reperfusion and the animal was killed 5-7 min later. The heart was then perfused with triphenyl tetrazolium chloride to identify infarcted and jeopardized myocardium in the occlusion zone and with Evans blue dye to mark normally perfused myocardium. After imaging, tissue sections were digested and colored microspheres were extracted and counted to determine myocardial blood flow. RESULTS: After coronary occlusion, infarct zone (MIZ) to normal zone (NZ) blood flow ratios declined from 0.95 +/- 0.27 (pre-occlusion) to 0.18 +/- 0.15 at 10 min and 0.25 +/- 0.35 at 50 min of occlusion (both p < 0.05). The MIZ:NZ count ratio at 60 min of reperfusion was less than the MIZ:NZ blood flow ratio in every animal and over the entire range of flow ratios (0.55-3.64). CONCLUSION: Technetium-99m-teboroxime requires viable myocytes for retention within the heart and is not exclusively a tracer of myocardial blood flow when imaged 5-7 min after injection. Additional in vivo imaging studies are required to determine the extent to which reduced retention of the tracer by reperfused but nonviable myocardium influences the appearance of clinical scans.

Animals↗

PubMed2003

RS-4252 inhibits amyloid beta-induced cytotoxicity in HeLa cells.

Progressive deposition of amyloid beta peptide in the senile plaques is a principal event in the neurodegenerative process of Alzheimer's disease. Several reports have demonstrated that amyloid beta is cytotoxic using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) as an indicator of viability in cells. With the MTT assay, we screened an in-house library to find compounds which suppress amyloid beta-induced inhibition of MTT reduction. We have previously reported that 6-ethyl-N,N'-bis(3-hydroxyphenyl)[1,3,5]triazine-2,4-diamine (named RS-0466), found in an in-house library, was capable of significantly inhibiting amyloid beta-induced cytotoxicity in HeLa cells. From further screening hits, we newly focused on 4-(7-hydroxy-2,2,4-trimethyl-chroman-4-yl)benzene-1,3-diol (named RS-4252), which show comparable potency to RS-0466 to ameliorate amyloid beta-induced cytotoxicity. Furthermore, RS-4252 reversed the decrease in phosphorylated Akt by amyloid beta. These results imply that RS-4252 or one of its derivatives has the potential to be a therapeutic for Alzheimer's disease patients, and that activation of Akt is at least in part involved in the effect.

Amyloid beta-Peptides↗

PubMed1998

Infarct size reduction by AT1-receptor blockade through a signal cascade of AT2-receptor activation, bradykinin and prostaglandins in pigs.

OBJECTIVE: We studied the effect of the angiotensin II type 1 (AT1)-receptor antagonist candesartan on infarct size resulting from regional myocardial ischemia in pigs. BACKGROUND: The effects of AT1-receptor blockade on infarct size in different species remain controversial and its potential cardioprotective mechanisms are still unclear. In pigs, infarct development closely resembles that observed in humans. METHODS: A total of 62 enflurane-anesthetized pigs underwent a protocol of 90-min low-flow ischemia and 120-min reperfusion. Systemic hemodynamics (micromanometer), regional myocardial function (sonomicrometry), regional myocardial blood flow (microspheres) and infarct size (TTC [triphenyl tetrazolium chloride]-staining) were determined. RESULTS: Left ventricular peak pressure decreased with candesartan (1 mg/kg i.v.) from 97+/-2 standard error of the mean (SEM) to 86+/-5 mm Hg and was then readjusted by aortic banding. In placebo pigs (n=9), infarct size was 21.8+/-4.8% of the area at risk. Candesartan (n=7) reduced infarct size to 9.7+/-2.5% (p < 0.05). Pretreatment with the AT2-receptor antagonist PD123319 (3 microg/kg/min intracoronarily [i.c.]; n=8), the bradykinin B2-receptor antagonist HOE140 (0.01 microg/kg/min i.c.; n=8) or the cyclooxygenase inhibitor indomethacin (10 mg/kg i.v.; n= 8) per se did not affect infarct size but did abolish the reduction of infarct size achieved by candesartan (PD123319 + candesartan (n=7): 23.2+/-4.7%; HOE140 + candesartan (n=7): 18.2+/-4.0%; indomethacin + candesartan (n=8): 21.1+/-5.2%). Hemodynamics, regional myocardial blood flow during ischemia and the area at risk were comparable among all groups of pigs. CONCLUSIONS: Reduction of infarct size by the AT1-receptor antagonist candesartan in pigs involves angiotensin II type 2 receptor (AT2) activation, bradykinin and prostaglandins.

Angiotensin Receptor Antagonists↗

PubMed2001

Oxidative stress and lipid retention in vascular grafts: comparison between venous and arterial conduits.

BACKGROUND: Because saphenous vein grafts (SVGs) exhibit greater cellular heterogeneity and worse clinical outcomes than arterial grafts (AGs), we examined oxidative stress and lipid retention in different vascular conduits. METHODS AND RESULTS: In a porcine model of graft interposition into carotid artery, superoxide anion (.O(2)(-)) was measured at 2 weeks after surgery. SVGs demonstrated increased.O(2)(-) production compared with AGs (SOD-inhibitable nitro blue tetrazolium reduction, P<0.01). The NAD(P)H oxidase inhibitor diphenyleneiodonium (P<0.01) abolished SVG-derived.O(2)(-), whereas the inhibitors of other pro-oxidant enzymes were ineffective. The change in oxidative stress was also reflected by lower activity of the endogenous antioxidant superoxide dismutase in SVGs than in AGs (P<0.001). SVG remodeling was associated with increased synthesis of sulfated glycosaminoglycans and augmented expression of a core protein, versican. These changes were accompanied by SVGs retaining significantly more (125)I-labeled LDL than AGs ex vivo (P<0.001). In hyperlipemic animals, lipid accumulation and oxidized epitopes were preferentially noted in the intima of SVGs at 1 month after surgery. CONCLUSIONS: This study demonstrated significant differences in the biology of SVGs and AGS: SVGs exhibited higher oxidative stress, LDL accumulation, and the presence of oxidized epitopes. These findings suggest that proatherogenic changes in SVGs may commence early after surgical revascularization.

Animals↗

PubMed2006

Cellular toxicity of mineral trioxide aggregate mixed with an alternative delivery vehicle.

OBJECTIVE: Mineral trioxide aggregate (MTA) mixed with water has a short working time, delayed setting, and poor consistency. A preliminary study suggested that substituting KY Jelly as a mixing vehicle improves the working properties of MTA. The present study compared the biocompatibility of white MTA mixed with water or with KY Jelly to that of Fuji II cement and of silver amalgam. STUDY DESIGN: Periodontal ligament (PDL) cells were cultured using standard laboratory procedures. Cells were plated in wells at a density of 10,000 cells/well. The test materials were mixed and eluate placed in contact with the PDL cells. Cell viability was determined by measuring mitochondrial enzyme activity using the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenytl)-2H-tetrazolium inner salt assay. Cytotoxicity was also measured in terms of cell lysis using the lactate dehydrogenase assay. The assays were completed in triplicate after time intervals of 24, 48, and 72 h. Mean cell counts were calculated and converted to a percentage of control results. A 2-way analysis of variance and Tukey honestly significant difference post-hoc test were performed to determine statistical significance. RESULTS: Eluate extractions from all materials caused significantly less cell viability and more cell death than control eluate (medium only) at all eluate time points tested. However, at 72 h the MTA/water, MTA/KY, and amalgam eluate extractions led to significantly better cell viability than the Fuji II eluates. However, there was significantly greater cell lysis for all eluates from the tested materials at 72 h than at 24 h. CONCLUSIONS: Within the limitations of this in vitro study, we conclude that MTA/KY, MTA/water, and amalgam have similar biocompatibility regarding effects of their eluates on human PDL cells, and eluates from all 3 materials demonstrate better biocompatibility than eluates derived from a resin-modified glass ionomer cement.

Aluminum Compounds↗

PubMed1999

Induction of apoptosis by selenite and selenodiglutathione in HL-60 cells: correlation with cytotoxicity.

Effects of selenite and selenodiglutathione, an initial metabolite of selenite, on the induction of apoptosis and cytotoxicity were investigated in human promyelocytic leukemia HL-60 cells. Treatment of selenite or selenodiglutathione resulted in concentration-dependent cytotoxicity, measured by lactate dehydrogenase leakage assay, and by tetrazolium salt reduction assay. Selenodiglutathione has been shown to exert more cytotoxic effect than selenite in both assay systems. Time-course study of cellular selenium uptake suggests that the higher cytotoxicity of selenodiglutathione be largely due to faster and greater selenium uptake rate. Treatment with selenite or selenodiglutathione also induced apoptosis in a dose-dependent manner, as detected by enzyme-linked immunosorbent assay and by DNA fragmentation assay. The dose-response data of apoptosis induced by selenite or selenodiglutathione were similar to those of cytotoxicity, implicating a relationship between the induction of apoptosis and cytotoxicity. Zn, which is a well-known inhibitor of apoptosis, dose-dependently blocked not only the induction of apoptosis, but also the membrane damage induced by selenium, corroborating this hypothesis. It was noted that the inhibition of apoptosis by Zn exerted little protective effect on cytotoxicity at higher concentrations of selenium, compared with a perfect protective effect at low concentration of selenium. These results suggest that cytotoxicity induced by selenium may be partially correlated with apoptosis.

Apoptosis↗