Effects of (-)-Menthol on Arylamine N-Acetyltransferase Activity in Human Liver Tumor Cells

2001 ◽  
Vol 29 (02) ◽  
pp. 321-329 ◽  
Author(s):  
Jing-Pin Lin ◽  
Yuh-Ching Li ◽  
Weng-Chuan Lin ◽  
Ching-Liang Hsieh ◽  
Jing-Gung Chung
Keyword(s):  
Tumor Cells ◽  
Liver Tumor ◽  
Human Liver ◽  
High Performance ◽  
Time Course ◽  
Tumor Cell Line ◽  
Intact Cells ◽  
Steady State Kinetic ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition

To evaluate whether or not (-)-menthol affects arylamine N-acetyltransferase (NAT) activity, we selected human liver tumor cell line (J 5) for examination. By using high performance liquid chromatography, NAT activity for acetylation of 2-aminofluorene (AF) was determined. (-)-Menthol displayed a dose-dependent inhibition to cytosolic NAT activity. Time-course experiments showed that NAT activity measured from intact human liver tumor cells was inhibited by (-)-menthol for up to 24 hrs. But in human liver tumor intact cells, the low doses (0.0032 and 0.032 mM) of (-)-menthol inhibited NAT activity andthe 0.32 mM (-)-menthol did not show any significant differences between control and (-)-menthol treated groups. Using standard steady-state kinetic analysis, it was demonstrated that (-)-menthol was a possible uncompetitive inhibitor (decrease Km and Vmax) to NAT activity in cytosols. This report is the first demonstration which showed (-)-menthol affect on human liver tumor cells NAT activity.

Sodium cromoglycate: evidence of tachykinin antagonist activity in the human skin

1993 ◽  
Vol 75 (1) ◽  
pp. 167-172 ◽  
Author(s):  
D. C. Crossman ◽  
M. R. Dashwood ◽  
G. W. Taylor ◽  
R. Wellings ◽  
R. W. Fuller
Keyword(s):  
Sodium Cromoglycate ◽  
Human Skin ◽  
High Performance ◽  
Gel Filtration ◽  
Inhibitory Effect ◽  
Intradermal Injection ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent

The mechanism of action of the antiasthmatic drug sodium cromoglycate (SCG) is unclear. One possibility is that SCG antagonizes the effects of the tachykinin substance P (SP), an agent known to cause airway edema. However, when SP is inhaled by humans, it has no demonstrable effect on airway function; therefore, the possibility that SCG prevents SP-induced changes in microvascular permeability was examined in human skin in vivo where potent edema-producing effects are seen. SCG (5–500 nmol) caused significant (P < 0.05) dose-dependent inhibition of SP-induced edema (wheal) formation when coadministered by intradermal injection. There was no effect on the nonreceptor-mediated flare response. SCG also significantly (P < 0.05) inhibited the wheal response to the related tachykinin neurokinin B but had no inhibitory effect on the cutaneous responses to histamine and prostaglandin E2. In addition, SCG (0.1–10 mM) caused dose-dependent inhibition of binding of SP labeled with 125I-labeled Bolton-Hunter to a number of tissues known to contain SP binding sites, as assessed by autoradiography. These concentrations were equivalent to the final concentrations of SCG found to inhibit the wheal response in the skin. The possibility that SCG interacted with SP was investigated both by gel filtration and high-performance liquid chromatography. No strong interaction was demonstrated with an 8,000 M excess of SCG under both hydrophobic and hydrophilic conditions. These results raise the possibility that SCG may have tachykinin antagonist properties.

Simultaneous Determination of Eight Flavonoids in the Flowers of Matricaria chamomilla by High Performance Liquid Chromatography

2014 ◽  
Vol 97 (3) ◽  
pp. 778-783 ◽  
Author(s):  
Xiao-Yu Xie ◽  
Fang-Fang Chen ◽  
Yan-Ping Shi
Keyword(s):  
Simultaneous Determination ◽  
High Performance ◽  
Antioxidant Activities ◽  
Hplc Method ◽  
Matricaria Chamomilla ◽  
Extract Solution ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Stability And Accuracy

Abstract An HPLC method was developed for simultaneous determination of five flavones (apigenin, three apigenin 7-O-glucoside acylated derivatives, and luteolin) and three methoxylated flavonols in Matricaria chamomilla. Full validation of the assay was carried out including linearity, LODs, LOQs, precision, repeatability, stability, and accuracy. The results demonstrated that the method developed was simple, accurate, and reliable. Five batches of M. chamomilla samples were determined using the developed method, and total contents of the eight flavonoids ranged from 1.843 to 2.134 mg/g. Among them, the content of apigenin was the highest with values of 0.538 to 0.618 mg/g. In addition, the extract solution from M. chamomilla exhibited a significant dose-dependent inhibition of 2,2-diphenyl-1-picrylhydrazyl (DPPH) activity, with a 50% inhibition (SC50) at a concentration of 3.06 ± 0.09 mg/mL, and the flavonoids apigenin-7-O-(6″-acetyl)-glucoside, luteolin, apigenin, eupatolitin, and chrysosplenol D played an important role in the antioxidant activities of the extract solution from M.chamomilla.

Eicosanoids are modulators of larval settlement in the barnacle, Balanus amphitrite

1999 ◽  
Vol 80 (1) ◽  
pp. 113-117 ◽  
Author(s):  
John Knight ◽  
Andrew F. Rowley ◽  
Mizue Yamazaki ◽  
Anthony S. Clare
Keyword(s):  
High Performance ◽  
Larval Settlement ◽  
Nordihydroguaiaretic Acid ◽  
Balanus Amphitrite ◽  
Lipoxygenase Inhibitors ◽  
Lipoxygenase Products ◽  
Dependent Inhibition ◽  
Generating Capacity ◽  
Dose Dependent Inhibition ◽  
Dose Dependent

Eicosanoids are oxygenated derivatives of C20 polyunsaturated fatty acids known to play key roles in many physiological events in both invertebrates and vertebrates. The eicosanoid generating capacity of cypris larvae of the barnacle, Balanus amphitrite, was examined using enzyme immunoassay and high-performance liquid chromatography. These larvae generated the lipoxygenase products, 12-hydroxyeicosapentaenoic acid (HEPE), 8-HEPE and 8,15-diHEPE, together with the cyclooxygenase products, prostaglandin (PG) E, PGF and thromboxane (TX) B. Indomethacin, a selective cyclooxygenase inhibitor, caused a dose-dependent inhibition of PGE generation by B. amphitrite larvae, while esculetin and nordihydroguaiaretic acid (lipoxygenase inhibitors) also strongly inhibited the generation of 8-HEPE, 12-HEPE and 8,15-diHEPE. PGE2, PGE3 and 16,16-dimethyl PGE2 caused a dose-dependent inhibition of settlement of B. amphitrite larvae while indomethacin (25–100 μM) stimulated this process. Lipoxygenase products (8-HEPE, 12-HEPE and 8,15-diHEPE) as well as esculetin and nordihydroguaiaretic acid (10–100 μM) had no effect on the attachment of larvae.

Mitochondrial injury: an early event in cisplatin toxicity to renal proximal tubules

1990 ◽  
Vol 258 (5) ◽  
pp. F1181-F1187 ◽  
Author(s):  
H. R. Brady ◽  
B. C. Kone ◽  
M. E. Stromski ◽  
M. L. Zeidel ◽  
G. Giebisch ◽  
...  
Keyword(s):  
Atpase Activity ◽  
Proximal Tubule ◽  
Threshold Concentration ◽  
Early Event ◽  
Intact Cells ◽  
Mitochondrial Injury ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Early Effects ◽  
K Transport

Oxygen consumption (QO2) and net K+ transport were studied in rabbit proximal tubule suspensions to define the early effects of cisplatin on proximal tubule function. Cisplatin caused dose-dependent inhibition of QO2, which was delayed in onset. The concentration of cisplatin required for inhibition decreased as the duration of exposure was increased [40-min exposure, threshold concentration of 10(-4) M, inhibitor constant (Ki) of 10(-3) M; 4-h exposure, threshold concentration of 3 X 10(-5) M, Ki of 10(-4) M]. Both ouabain-sensitive and ouabain-insensitive QO2 were reduced, indicating inhibition of all adenosinetriphosphatases, including Na(+)- K(+)-ATPase activity. There was a parallel fall in ouabain-sensitive net K+ transport and cytosolic K+ content, confirming the latter observation. Na(+)-K(+)-ATPase activity was unchanged in cell membranes prepared by hypotonic lysis from cisplatin-treated tubules, indicating an indirect cytosol-dependent mechanism of enzyme inhibition. Nystatin-stimulated QO2 was reduced in cisplatin-treated tubules, excluding inhibition of Na+ entry as the mechanism of injury and suggesting mitochondrial injury. The latter was confirmed by measurement of carbonylcyanide-m-chlorophenylhydrazone (CCCP)-uncoupled QO2 in intact cells and ADP-stimulated (state 3) QO2 in digitonin-permeabilized tubules. Furthermore, by maximally stimulating mitochondrial respiration with CCCP and nystatin, it was possible to demonstrate mitochondrial injury at a time when basal QO2 and K+ transport were apparently normal. These data suggest that mitochondrial injury is a central event in cisplatin toxicity to the proximal tubule.

Autocrine inhibition of chemotherapy response in human liver tumor cells by insulin-like growth factor-II

2004 ◽  
Vol 206 (1) ◽  
pp. 85-96 ◽  
Author(s):  
Per Lund ◽  
Dominic Schubert ◽  
Fataneh Niketeghad ◽  
Peter Schirmacher
Keyword(s):  
Growth Factor ◽  
Tumor Cells ◽  
Liver Tumor ◽  
Human Liver ◽  
Chemotherapy Response ◽  
Insulin Like Growth Factor ◽  
Factor Ii

Induction of Necrosis in Human Liver Tumor Cells by α-Phellandrene

2014 ◽  
Vol 66 (6) ◽  
pp. 970-979 ◽  
Author(s):  
Shu-Ling Hsieh ◽  
Yi-Chen Li ◽  
Weng-Cheng Chang ◽  
Jing-Gung Chung ◽  
Lan-Chi Hsieh ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Liver Tumor ◽  
Human Liver

scholarly journals Novel combination of Celecoxib and proteasome inhibitor MG132 provides synergistic antiproliferative and proapoptotic effects in human liver tumor cells

Cell Cycle ◽  
2010 ◽  
Vol 9 (7) ◽  
pp. 1399-1410 ◽  
Author(s):  
Antonella Cusimano ◽  
Antonina Azzolina ◽  
Juan L. Iovanna ◽  
Dimcho Bachvarov ◽  
James A. McCubrey ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Liver Tumor ◽  
Proteasome Inhibitor ◽  
Human Liver ◽  
Proteasome Inhibitor Mg132

Induction of α-Phellandrene on Autophagy in Human Liver Tumor Cells

2015 ◽  
Vol 43 (01) ◽  
pp. 121-136 ◽  
Author(s):  
Lan-Chi Hsieh ◽  
Shu-Ling Hsieh ◽  
Chi-Tsai Chen ◽  
Jing-Gung Chung ◽  
Jyu-Jye Wang ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Liver Tumor ◽  
Human Liver ◽  
Binding Activity ◽  
Control Group ◽  
Autophagosome Formation ◽  
P53 Expression ◽  
Protein Levels ◽  
Dna Binding Activity ◽  
P53 Signaling

α-Phellandrene (α-PA) is a cyclic monoterpene. To investigate the induction of autophagy by α-PA and its mechanism, human liver tumor cells (J5) were incubated with α-PA and analyzed for cell viability and the molecular regulation of pre-autophagosome origination and autophagosome formation. According to the results, PI3K-I, mTOR, and Akt protein levels were decreased after α-PA treatment compared to those of the control group (p < 0.05). The phosphorylation of Bcl-2, and PI3K-III, LC3-II and Beclin-1 protein levels in J5 cells were increased after α-PA treatment (p < 0.05). In addition, α-PA up-regulated nuclear p53 and down-regulated cytoplasmic p53 expression in J5 cells. The NF-κB pathway was activated, as indicated by increase in cytosolic phosphorylated IκB, nuclear NF-κB levels, and the DNA-binding activity of NF-κB after α-PA treatment in J5 cells (p < 0.05). These results suggest that α-PA can induce J5 cell autophagy by regulating mTOR and LC-3II expression, p53 signaling, and NF-κB activation in J5 cells.

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