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Biomedical subjects

T Y Liu

Publications and source records attributed to T Y Liu.

At least 19 recordsLinked to original sources
PubMed1997

Seroprevalences of hepatitis B and C viruses and Helicobacter pylori infection in a small, isolated population at high risk of gastric and liver cancer.

The objective of this study was to examine the seroprevalences of chronic infection with hepatitis B and C viruses and Helicobacter pylori in Matzu, a group of small islets with 5,566 civilian residents who have extremely high mortality from cancers of the stomach and liver. The standardized mortality ratios (SMR) of all cancer sites combined, liver cancer and stomach cancer in 1984-1993 were calculated using the general population in Taiwan as the referent (SMR = 100). The SMRs (95% confidence interval) for all cancer sites combined, liver cancer and stomach cancer were 160 (131-195), 252 (170-360) and 351 (229-516), respectively, in Matzu. A health survey was carried out with 1,485 civilian residents aged 30 years or more, giving a response rate of 69% among those who were eligible. Serum samples were tested for antibodies against Helicobacter pylori (anti-HP) by enzyme-linked immunosorbent assay and hepatitis B surface antigen (HBsAg) and antibodies against hepatitis C virus (anti-HCV) by enzyme immunoassay. The seroprevalence was 61% for anti-HP, 24.7% for HBsAg and 1.8% for anti-HCV in Matzu. While mortality rates of liver and stomach cancers were significantly higher in Matzu than in Taiwan, the seroprevalences of anti-HP, HBsAg and anti-HCV in Matzu were similar to or even lower than those in Taiwan. These findings suggest the existence of risk factors other than microbial agents involved in the development of stomach and liver cancers.

Adult↗
PubMed1996

Modification of mitomycin C-induced clastogenicity by Terminalia catappa L. in vitro and in vivo.

The water extract of the leaves of Terminalia catappa L. was tested for inhibition of mitomycin C-induced micronuclei in CHO-K1 cells. The simultaneous and pre-treatment of CHO-K1 cells with T. catappa extract (75 and 150 micrograms/ml) significantly (P < 0.05) suppressed mitomycin C-induced micronuclei. Furthermore, gastric intubation of T. catappa extract (4.8 and 24 mg/animal per day) to male ICR mice for 8 days significantly (P < 0.01) reduced mitomycin C-induced micronuclei in peripheral blood. In addition, T. catappa dose dependently inhibited lipid peroxidation in vitro and TPA-induced hydrogen peroxide formation in human mononuclear leukocytes. The anticlastogenic effects of T. catappa in vitro and in vivo may be attributed to its antioxidative potential.

Animals↗
PubMed1996

Paclitaxel-induced apoptosis in human gastric carcinoma cell lines.

BACKGROUND: Gastric cancer is one of the most common cancers in Asia. Chemotherapy and radiation therapy have had limited success. Recently, paclitaxel has been found to be effective against a variety of cancers, including lung, breast, ovary, melanoma, and prostate. Whether paclitaxel is effective in the treatment of gastric cancer is not known and is worthy of investigation. METHODS: Human gastric carcinoma cell lines NUGC-3 and SC-M1 were examined for response to paclitaxel treatment. Cancer cells were treated with paclitaxel (0.001, 0.01, 0.1, and 1 microM) for 1-3 days. Cell number was counted by hemocytometer and cell viability was determined by the trypan blue exclusion method. Cell cycle progression and expression of proliferating cell nuclear antigen (PCNA) were examined by flow cytometry. The percentage of apoptotic cells was determined after staining with hematoxylin and eosin. RESULTS: Paclitaxel was cytotoxic to the two human gastric carcinoma cell lines examined. The growth-inhibiting dose was 0.01 microM. Paclitaxel-treated gastric carcinoma cells were arrested mainly in G2/M phases before apoptosis. However, treatment with 0.01 microM of paclitaxel resulted in a decrease of cells at G0/G1 phases without an increase of cells at G2/M phase indicating that paclitaxel was also cytotoxic to gastric carcinoma cells at G0/G1 phases. In addition, the expression of PCNA was significantly increased in 0.1 and 1 microM paclitaxel-treated cells, suggesting that DNA repair was increased in these cells. CONCLUSIONS: Paclitaxel is effective in growth inhibition of gastric carcinoma cell lines in clinically attainable concentrations. Our results suggest that paclitaxel is a potential chemotherapeutic drug for gastric carcinoma.

Antineoplastic Agents, Phytogenic↗
PubMed1996

Oxidative damage to DNA induced by areca nut extract.

In Taiwan, people chew betel quid which contains tender areca nut with husk. In other countries, people prefer ripe and dried areca nut without husk. In this study, we compared the reactive oxygen species-induced oxidative DNA damage in isolated DNA and CHO-K1 cells between treatments with tender areca nut extract (ANE) and ripe ANE. Incubation of these two ANE preparations with isolated DNA generated 8-hydroxy-2'-deoxyguanosine (8-OH-dG) in an alkaline environment in a dose-dependent manner. Ripe ANE generated higher levels of 8-OH-dG compared to tender ANE. The addition of iron(II) (100 microM) resulted in 1.4- and 3.1-fold increases of 8-OH-dG when incubated with 1 mg/ml each of tender and ripe ANE. In testing the effect of ANE to cellular DNA, CHO-K1 cells were used for its documented sensitivity to reactive oxygen species. In CHO-K1 cells, ripe ANE was more cytotoxic than tender ANE following an 18-h incubation. The cytotoxicity to CHO-K1 cells was positively correlated with the formation of 8-OH-dG following tender (r=0.97) and ripe (r=0.91) ANE treatment. Addition of the iron chelating agent o-phenanthroline (10 and 20 microM) to cells prior to ri ANE exposure significantly increased (p<0.05) the survival of CHO-K1 cells. In addition, ripe ANE induced dichlorofluorescein-mediated fluorescence which indicated the formation of hydrogen peroxide in CHO-K1 cells. In conclusion, this study demonstrated that ANE-induced oxidative damage to isolated and cellular DNA which may result from the generation of hydrogen peroxide, and iron may serve as a catalyst in this process. Furthermore, ripe ANE generated higher oxidative DNA damage levels compared to tender ANE.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1996

Induction of 8-hydroxydeoxyguanosine in DNA by chromium(III) plus hydrogen peroxide and its prevention by scavengers.

The capability of Cr(III) to induce DNA lesions generated by oxidative damage was investigated in this study by examining the formation of 8-hydroxydeoxyguanosine (8-OHdG) in calf thymus DNA by CrCl3 and/or H2O2 in 10 mM phosphate buffer. In the presence of 0.5 mM H2O2, the formation of 8-OHdG markedly increased with increasing CrCl3 concentration. In contrast, H2O2 or CrCl3 alone did not cause any increase in 8-OHdG level above background. The amount of 8-OHdG induced by CrCl3 plus H2O2 was time dependent; its generation increased linearly over an incubation period of 90 min. The formation of 8-OHdG was unfavorable in an acidic solution (pH < 6); the highest level of 8-OHdG was observed at pH 7-8. Scavengers of reactive oxygen species markedly inhibited the formation of 8-OHdG by CrCl3 plus H2O2; the inhibition effect was sodium azide > D-mannitol > Tris-HCl at an equal concentration. The induction of 8-OHdG by CrCl3 plus H2O2 remained unchanged in D2O. Moreover, an addition of catalase (2.2 U/ml) to the reaction mixture completely inhibited the formation of 8-OHdG by CrCl3/H2O2, whereas only 22% of that formation was inhibited by superoxide dismutase (11 U/ml). A large amount of bovine serum albumin (1.1 mg/ml) could reduce the formation of 8-OHdG by CrCl3 plus H2O2, thereby implying that Cr(III)-mediated DNA-protein crosslinks are unfavorable for 8-OHdG formation. Furthermore, ascorbate could prevent the formation of 8-OHdG by CrCl3 plus H2O2; the extent of prevention increased with increasing ascorbate concentration (10 microM-3 mM). Thus, ascorbate acts as a free radical scavenger in the CrCl3/H2O2 system. The above findings suggest that Cr(III)/H2O2 could generate oxidative damage to DNA, possibly through a Fenton-like reaction, i.e. Cr(III)+H2O2-->Cr(IV)+.OH+OH-. This study also indicates that Cr(III), previously considered as the ultimate kinetically stable species of Cr(VI) metabolites, is capable of inducing carcinogenic lesions through interaction with a cellular oxygen species.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1996

Role of oxidative DNA damage in hydroxychavicol-induced genotoxicity.

Chewing betel quid has been linked to the development of oral cancer. In Taiwan, fresh Piper betle inflorescence is uniquely added to betel quid, and hydroxychavicol is the major phenolic components of P.betle inflorescence. In this study, we tested the mutagenic potential of hydroxychavicol in Salmonella typhimurium TA97, TA98, TA100 and TA102 with and without Aroclor-1254 induced S9 fraction. The results showed that hydroxychavicol was positive in S.typhimurium TA102 without metabolic activation. This increase in revertants was partially inhibited by catalase and superoxide dismutase. In Chinese hamster ovary (CHO-K1) cells, hydroxychavicol induced chromosome aberrations in a dose-dependent manner (10-50 microM) and the majority were chromosome-type aberrations. Hydroxychavicol also significantly increased the frequency of micronuclei in CHO-K1 cells up to 3-fold at a concentration of 40 microM. In addition, hydroxychavicol dose-dependently (0.1-20 microM) induced copper-dependent strand breaks in plasmid DNA. We further tested the oxidative DNA damage potential of hydroxychavicol by measuring 8-hydroxydeoxyguanosine (8-OH-dG) formation in CHO-K1 cells following an 18-h incubation and found that hydroxychavicol (6.25-100 microM) induced 8-OH-dG levels dose-dependently. The increase of 8-OH-dG formation was positively correlated (r = 0.79) with the hydroxychavicol-induced cytotoxicity. In conclusion, hydroxychavicol may exert its genotoxic potential through oxidative DNA damage.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1996

Epsilon 4 allele of apolipoprotein E increases risk of Alzheimer's disease in a Chinese population.

We examined the apolipoprotein E genotype in 56 Chinese patients with late-onset sporadic Alzheimer's disease (AD) and 57 Chinese control subjects of similar age. The frequency of epsilon 4 in the AD group was significantly higher than that in the control group (23.2% versus 7.9%, p = 0.003). The odds ratio for AD in individuals with either one or two epsilon 4 was 2.96 (95% CI 1.11 to 8.03). The linear trend for AD in proportion to alleles of epsilon 4 was also significant (chi 2 = 8.2, p = 0.004). Our results support the association between epsilon 4 and AD in the Chinese.

Age of Onset↗
PubMed1995

Heterologous desensitization of opioid-stimulated Ca2+ increase by bradykinin or ATP in NG108-15 cells.

Leucine-enkephalin (Leu-EK) dose-dependently elicited an increase in cytosolic Ca2+ concentration ([Ca2+]i) with an EC50 of 1.2 microM via the phosphoinositide cascade in NG108-15 cells. Chronic treatment of cells with [D-Ala2,D-Leu5]enkephalin caused time-dependent homologous desensitization. In the presence of extracellular Ca2+, ATP as well as bradykinin stimulated significantly higher increases in inositol 1,4,5-trisphosphate (IP3) generation than did Leu-EK; however, the magnitude of intracellular Ca2+ pools increased after ATP stimulation, whereas bradykinin depleted intracellular pools. Hence, cells lost their [Ca2+]i response to Leu-EK if bradykinin was first added to induce a [Ca2+]i increase, whereas the response was unchanged if Leu-EK was added after addition of ATP. When Leu-EK was added simultaneously with bradykinin or ATP, an additive response was observed in IP3 generation; however, the rise in [Ca2+]i reached the same level as that induced by bradykinin or ATP alone. In the absence of extracellular Ca2+ in which the replenishment of intracellular pools was not possible, ATP displayed an inhibitory effect similar to that of bradykinin on the Leu-EK-induced [Ca2+]i increase. Prior treatment of cells with Leu-EK slightly heterologously desensitized the action of bradykinin, but had no effect on the ATP response. Our results suggest that a shared intracellular Ca2+ pool is sensitive to the opioid, bradykinin and P2-purinoceptor agonists; however, a defined pool of phosphatidylinositol 4,5-bisphosphate or a specific phospholipase C is responsible for each receptor.

Adenosine Triphosphate↗
PubMed1995

Mechanistic study of the inhibition of aflatoxin b1-induced hepatotoxicity by dimethyl 4,4'-dimethoxy-5,6,5',6'-dimethylenedioxy biphenyl-2, 2'-dicarboxylate.

The mechanism of DDB (dimethyl 4,4'-dimethoxy-5,6,5',6'-dimethylenedioxy biphenyl-2,2'-dicarboxylate) prevention of aflatoxin B1 (AFB1)-induced hepatotoxicity in rats has been investigated. Pretreatment of DDB (200 mg/kg) daily for 4 days significantly suppressed (P < 0.05) the AFB1-induced hepatic damage as evidenced by the increase of serum marker enzymes. DDB induced rat hepatic cytochrome P450IA1, IIB1 and glutathione S-transferase activities. The hepatic microsomes derived from DDB treated rats increased the mutation frequency of AFB1 and enhanced the binding of AFB1 to DNA. However, the hepatic S9 fraction from DDB treated rats showed a protective effect against AFB1-induced damage. It is concluded that the protective effect of DDB against AFB1-induced damage might be mediated by the induced glutathione S-transferase activity and not from the accelerated hepatic cytochrome P450 detoxification pathway of AFB1 which was previously believed.

Aflatoxin B1↗
PubMed1995

Establishment of in vivo hepatoma models in rat and mouse from rodent hepatoma cell lines.

BACKGROUND: Hepatoma is one of the most common cancers in Southeast Asia and African countries. In Taiwan, it is the leading cause of death in male cancer patients. In order to examine the effect of various factors on the growth of hepatoma, in vivo hepatoma models such as carcinogen-induced hepatoma and subcutaneous implantation of hepatoma in nude mice have been used. However, there are disadvantages in these models. METHODS: Rats and mice were anesthetized by ketamine or ether, respectively. After a midline incision was made, N1S1 rat hepatoma cells were injected intrasplenically to partially hepatectomized or sham-operated rats, while BALB/c mice received intrasplenic injection of ML-2 and ML-3 mouse hepatoma cells. For direct tumor implantation, a 1mm3 N1S1 tumor piece was implanted in liver of Sprague-Dawley (SD) rat using a trocar. Animals were sacrificed at specific times after tumor implantation. Tumor incidence and the number of tumor nodules on the liver surface were recorded. Tumor samples were fixed and embedded for histological examination. RESULTS: After intrasplenic implantation of ML-2 cells, no tumor was observed on the liver in any of the 10 mice 40 days later. In comparison, rapid growth of hepatic ML-3 tumors was observed in all animals. Rat hepatoma cells RH-35, McA-RH7777 and McA-RH8994 cells did not form tumors in SD rats. The tumorigenicity of N1S1 cells in SD rats was dose-dependent on implanted tumor cells. In addition, hepatic N1S1 tumors could be obtained within a few weeks by homograft. CONCLUSIONS: We have successfully established in vivo hepatoma models in both the rat and the mouse. The murine ML-3 cells generated hepatoma in syngeneic BALB/c mice while the tumorigenicity of N1S1 cells in partially hepatectomized SD rats was dose-dependent on implanted tumor cells. These in vivo rodent models will be valuable tools for future studies of hepatoma.

Animals↗
PubMed1995

Carbachol but not bradykinin blocks the enkephalin-induced calcium transient in human neuroblastoma SK-N-SH cells.

Carbachol stimulated significantly higher increase in inositol 1,4,5-trisphosphate (IP3) generation than did leucine-enkephalin (leu-EK) and bradykinin in SK-N-SH cells. When leu-EK was concomitantly added with carbachol, an additive effect was observed in IP3 generation. However, the rise in cytosolic Ca2+ concentration ([Ca2+]i) reached the same level as that induced by carbachol alone. On the other hand, additive effects were observed in both [Ca2+]i rise and IP3 generation when leu-EK was simultaneously added with bradykinin. Furthermore, cells lost their [Ca2+]i response to leu-EK if carbachol was first added to induce a [Ca2+]i increase whereas the response was unchanged if leu-EK was added after addition of bradykinin. Our results suggest that a shared intracellular Ca2+ pool is sensitive to the opioid, bradykinin and muscarinic receptor agonists; however, a specific phospholipase C might be responsible for each receptor activation.

Bradykinin↗
PubMed1994

A phospholipase A2 inhibitor from the plasma of the South American rattlesnake (Crotalus durissus terrificus). Protein structure, genomic structure, and mechanism of action.

The lethal toxicity of the South American rattlesnake (Crotalus durissus terrificus) venom can be attributed mainly to the presence of a pre-synaptic neurotoxin, crotoxin, with phospholipase A2 activity. Crotoxin is a heterodimer of an acidic protein (CA) and a basic phospholipase A2 (CB). An anti-toxic protein of subunit molecular mass 23.6 kDa that neutralizes both lethal and PLA2 activity of crotalid venom and crotoxin has been previously purified from the plasma of this snake (Fortes-Dias, C., Fonseca, B. C. B., Kochva, E., and Diniz, C. R. (1991) Toxicon 29, 997-1008). The protein has been named CNF for Crotalus neutralizing factor. In the present study, we have shown that CNF exists as an oligomeric aggregate of (CNF)n, where n = 6-8, and when it interacts with crotoxin, it replaces the acidic protein CA of crotoxin to form a stable near stoichiometric complex of CNF.CB. The CNF.CB complex no longer exhibits PLA2 activity and is inert in vivo. Thus, the exchange reaction between CA.CB of crotoxin and CNF to form CNF.CB and free CA is reminiscent of the interaction of crotoxin with its target receptor at the neuromuscular transmission site in the presynaptic cells. A cDNA encoding CNF has been isolated from a liver cDNA library using an appropriate nucleotide probe. The nucleotide sequence codes for a 19-residue signal peptide, followed by a 181-residue protein of which 16 are half-cystines. Calculated molecular mass is 20.06 kDa, and there is a putative N-linked carbohydrate site at Asn157.

Amino Acid Sequence↗
PubMed1994

C-reactive proteins, limunectin, lipopolysaccharide-binding protein, and coagulin. Molecules with lectin and agglutinin activities from Limulus polyphemus.

In 1964, Levin and Bang discovered that gram-negative bacterial endotoxin could rapidly induce gelation of Limulus amebocyte lysate. This observation has led to the development of the most sensitive and specific method for the detection of bacterial endotoxin in pharmaceuticals and drugs intended for human use. Over 10 years ago, Bang injected endotoxin into young horseshoe crabs and observed a time and dose-dependent coagulation of the whole hemolymph. Limunectin, LEBP-PI, and Limulus CRP are found together with coagulin as part of the hemolymph clot at the time of endotoxin-induced exocytosis of amebocytes. In this manner, these molecules with agglutinin/lectin activities could work in concert to assist in the recognition and eventual removal of invading microorganisms from the circulating system. Although the mechanism of endotoxin-induced clot formation is to a large extent understood, the mechanism of clot dissolution and removal in the Limulus hemolymph remains to be clarified.

Acute-Phase Proteins↗
PubMed1994

Bacterial mutagenicity, metabolism, and DNA adduct formation by binary mixtures of benzo[a]pyrene and 1-nitropyrene.

Air pollutants are a complex mixture containing polycyclic organic compounds. Among these are 1-NP and B[a]P, which are important contributors to the mutagenicity of diesel exhaust and airborne particulate matters. To investigate the interaction of a complex mixture of airborne mutagens, the mutagenicity of 1-NP was examined with S. typhimurium TA98 and TA98NR in the presence and absence of B[aP. B[a]P exhibited a more antagonistic effect on the mutagenicity of 1-NP in strain TA98 than in strain TA98NR. Also studied were (1) the inhibitory effects of B[a]P on the nitroreductive metabolism of 1-NP and (2) DNA adduct formation by 1-NP. Nitroreductase was associated with the metabolism of 1-NP, and was reduced in a dose-dependent manner in a binary mixture of 1-NP and B[a]P. HPLC analysis showed that the amounts of 1-AP and NAAP, the metabolites of 1-NP, were significantly decreased by the addition of B[a]P in mixtures. The results indicate that the antagonistic effect of B[a]P on the mutagenicity of 1-NP is mediated through altering its nitroreductive metabolism.

Air Pollutants↗
PubMed1994

Flowcytometric analysis of the effect of berberine on the expression of glucocorticoid receptors in human hepatoma HepG2 cells.

Berberine is an alkaloid found in many plants, including the Coptis chinensis and Arcangelisia flava. Berberine has been reported to have cytostatic effect on tumor growth. Previously, we have found that the level of glucocorticoid receptors (GR) was significantly higher in hepatoma than in adjacent liver tissues. Using human HepG2 hepatoma cells, we have found that GR were expressed not only in G0-G1 phases, but also in S and G2+M phases. The objective of the present study was to examine the effect of berberine on the expression of GR and its relation to cell cycle progression of HepG2 cells. Continuous exposure of HepG2 cells to various concentrations (1-50 microM) of berberine resulted in growth inhibition in a dose dependent manner. The viability of berberine-treated HepG2 cells was greater than 90% in all treatment groups. Flowcytometric analysis of berberine-treated HepG2 cells showed that the S phase fraction was significantly reduced. GR levels were higher in berberine-treated HepG2 cells than in vehicle (DMSO)-treated cells. In addition, the secretion of alpha-fetoprotein by HepG2 cells was inhibited by berberine. Finally, the berberine induced cell growth arrest was partially reversible in HepG2 cells.

Analysis of Variance↗
PubMed1993

Aromatic DNA adducts in brain tumors by 32P-postlabeling analysis.

DNA from human brain tumor samples was analysed by the 32P-postlabeling technique for the presence of aromatic DNA adducts. Thirteen out of 16 samples showed low levels of adducts at 0.14-3.53 adducts per 10(9) nucleotides. Inter-individual variations in the patterns of these aromatic adducts were observed. On the other hand, none of 5 brain samples from epilepsy patients revealed any evidence of such adducts. The data demonstrated the presence of low level, large molecule aromatic DNA adducts in malignant brain tissues and these adducts may either result from environmental exposure to an undetermined genotoxic agent or from the aging process.

Adenoma↗
PubMed1993

Isolation and characterization of C-reactive protein (CRP) cDNA and genomic DNA from Xenopus laevis. A species representing an intermediate stage in CRP evolution.

C-reactive protein (CRP) is a prototypic acute phase protein in human and rabbit. Although it is structurally and functionally conserved from invertebrate to human, there are species-specific differences in patterns of expression and putative function. To further investigate the biological significance, regulation, and evolution of CRP, we isolated Xenopus CRP and subsequently derived and sequenced corresponding cDNA and the genomic clones. The structure and expression of Xenopus CRP were also compared to those of the other CRPs. Analyses of the amino acid sequence and the nucleotide sequence reveal that the mature Xenopus CRP is a 222-amino acid protein preceded by a 16-residue signal peptide. During development, Xenopus CRP is expressed, only when the liver appears, and therefore is not likely to play a role in early embryonic development. Compared to other species, Xenopus CRP is present at an intermediate low level of < 1 microgram/ml in the normal serum. Unlike human and rabbit CRP, Xenopus CRP is not induced by turpentine or heatshock treatment. The heatshock consensus sequence (Woo, P., Korenberg, J. R., and Whitehead, A. S. (1985) J. Biol. Chem. 265, 4136-4142) are not present in the Xenopus CRP gene. It is suggested that Xenopus CRP represents a transitional period in CRP evolution when host defenses switched from primitive innate immunity to a much more complex immune system. The constitutive functions of CRP gradually became less essential as the result of the development of a complex immune system.

Amino Acid Sequence↗