PubMed Health⌕ Search

Biomedical subjects

M H Kang

Publications and source records attributed to M H Kang.

At least 19 recordsLinked to original sources
PubMed2002

Implantation of penile prosthesis in a patient with severe corporeal fibrosis induced by cavernosal injection therapy.

Implantation of a penile prosthesis in men with complicated fibrosis of corpus cavernosum is very difficult and even impossible. Cavernosal dilation requires sharp intracavernosal dissection to implant prosthesis, however complete removal of the fibrotic tissue is often impossible. We introduce a new technique using electric resection and electrovaporization of fibrotic tissue for implantation of penile prosthesis in a patient with severe corporeal fibrosis.

Fibrosis↗
PubMed2001

Vascular effects of estrogen in type II diabetic postmenopausal women.

OBJECTIVES: We assessed the effects of estrogen on vascular dilatory and other homeostatic functions potentially affected by nitric oxide (NO)-potentiating properties in type II diabetic postmenopausal women. BACKGROUND: There is a higher cardiovascular risk in diabetic women than in nondiabetic women. This would suggest that women with diabetes do not have the cardioprotection associated with estrogen. METHODS: We administered placebo or conjugated equine estrogen, 0.625 mg/day for 8 weeks, to 20 type II diabetic postmenopausal women in a randomized, double-blinded, placebo-controlled, cross-over design. RESULTS: Compared with placebo, estrogen tended to lower low-density lipoprotein (LDL) cholesterol levels by 15 +/- 23% (p = 0.007) and increase high-density lipoprotein (HDL) cholesterol levels by 8 +/- 16% (p = 0.034). Thus, the ratio of LDL to HDL cholesterol levels significantly decreased with estrogen, by 20 +/- 24%, as compared with placebo (p = 0.001). Compared with placebo, estrogen tended to increase triglyceride levels by 16 +/- 48% and lower glycosylated hemoglobin levels by 3 +/- 13% (p = 0.295 and p = 0.199, respectively). However, estrogen did not significantly improve the percent flow-mediated dilatory response to hyperemia (17 +/- 75% vs. placebo; p = 0.501). The statistical power to accept our observation was 81.5%. Compared with placebo, estrogen did not significantly change E-selectin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 or matrix metalloproteinase-9 levels. Compared with placebo, estrogen tended to decrease tissue factor antigen and increase tissue factor activity levels by 7 +/- 46% and 5 +/- 34%, respectively (p = 0.321 and p = 0.117, respectively) and lower plasminogen activator inhibitor-1 levels by 16 +/- 31% (p = 0.043). CONCLUSIONS: The effects of estrogen on endothelial, vascular dilatory and other homeostatic functions were less apparent in type II diabetic postmenopausal women, despite the beneficial effects of estrogen on lipoprotein levels.

Brachial Artery↗
PubMed2001

Vascular effects of synthetic or natural progestagen combined with conjugated equine estrogen in healthy postmenopausal women.

BACKGROUND: Synthetic, not natural, progestagen may negate the favorable effects of estrogen. Nonetheless, observational studies report no differences in risk for clinical cardiovascular events between users of unopposed estrogen and users of estrogen combined with synthetic progestin. METHODS AND RESULTS: In a double-blind study, we randomly assigned 20 healthy postmenopausal women to micronized progesterone (MP) 200 mg or medroxyprogesterone acetate (MPA) 10 mg for 10 days with conjugated equine estrogen (CEE) 0.625 mg for 25 days and the remaining 5 days off cyclically during 2 months, followed by crossover to the alternate therapy. CEE+MP and CEE+MPA significantly improved the percent flow-mediated dilator response to hyperemia relative to baseline measurements (P=0.004 by ANOVA) by a similar degree (P=0.863). Both therapies significantly decreased E-selectin, intercellular adhesion molecule (ICAM)-1, and vascular cell adhesion molecule (VCAM)-1 levels from baseline values (P<0.001, P=0.048, and P=0.016 by ANOVA, respectively) by a similar degree (P=0.977 for ICAM-1 and P=0.541 for VCAM-1, respectively). CEE+MPA decreased E-selectin levels more than CEE+MP did (P=0.040). Both therapies significantly decreased monocyte chemoattractant protein-1 levels from baseline values (P<0.005 by ANOVA) by a similar degree (P=0.194). Both therapies significantly decreased tissue factor antigen and increased tissue factor activity levels from baseline values (P=0.003 and P<0.001 by ANOVA, respectively) by a similar degree (P=0.652 for antigen and P=0.173 for activity). Both therapies significantly lowered plasma plasminogen activator inhibitor-1 levels from baseline values (P<0.001 by ANOVA) by a similar degree (P=0.533). CONCLUSIONS: CEE+MP and CEE+MPA provide similar improvement in endothelium-dependent vasodilator responsiveness and effects on markers of inflammation, hemostasis, and fibrinolysis inhibition in healthy postmenopausal women.

Chemokine CCL2↗
PubMed2001

Phase I study of infusional paclitaxel in combination with the P-glycoprotein antagonist PSC 833.

PURPOSE: PSC 833 (valspodar) is a second-generation P-glycoprotein (Pgp) antagonist developed to reverse multidrug resistance. We conducted a phase I study of a 7-day oral administration of PSC 833 in combination with paclitaxel, administered as a 96-hour continuous infusion. PATIENTS AND METHODS: Fifty patients with advanced cancer were enrolled onto the trial. PSC 833 was administered orally for 7 days, beginning 72 hours before the start of the paclitaxel infusion. Paclitaxel dose reductions were planned because of the pharmacokinetic interactions known to occur with PSC 833. RESULTS: In combination with PSC 833, maximum-tolerated doses were defined as paclitaxel 13.1 mg/m(2)/d continuous intravenous infusion (CIVI) for 4 days without filgrastim, and paclitaxel 17.5 mg/m(2)/d CIVI for 4 days with filgrastim support. Dose-limiting toxicity for the combination was neutropenia. Statistical analysis of cohorts revealed similar mean steady-state concentrations (C(pss)) and areas under the concentration-versus-time curve (AUCs) when patients received paclitaxel doses of 13.1 or 17.5 mg/m(2)/d for 4 days with PSC 833, as when they received a paclitaxel dose of 35 mg/m(2)/d for 4 days without PSC 833. However, the effect of PSC 833 on paclitaxel pharmacokinetics varied greatly among individual patients, although a surrogate assay using CD56+ cells suggested inhibition of Pgp was complete or nearly complete at low concentrations of PSC 833. Responses occurred in three of four patients with non-small-cell lung cancer, and clinical benefit occurred in five of 10 patients with ovarian carcinoma. CONCLUSION: PSC 833 in combination with paclitaxel can be administered safely to patients provided the paclitaxel dose is reduced to compensate for the pharmacokinetic interaction. Surrogate studies with CD56+ cells indicate that the maximum-tolerated dose for PSC 833 gives serum levels much higher than those required to block Pgp. The variability in paclitaxel pharmacokinetics, despite complete inhibition of Pgp in the surrogate assay, suggests that other mechanisms, most likely related to P450, contribute to the pharmacokinetic interaction. Future development of combinations such as this should include strategies to predict pharmacokinetics of the chemotherapeutic agent. This in turn will facilitate dosing to achieve comparable CPss and AUCs.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2001

The P-glycoprotein antagonist PSC 833 increases the plasma concentrations of 6alpha-hydroxypaclitaxel, a major metabolite of paclitaxel.

PURPOSE: Overexpression of P-glycoprotein (Pgp) is one mechanism of drug resistance in cancer chemotherapy. A Phase I trial was conducted using PSC 833, a Pgp antagonist, in combination with paclitaxel in patients with refractory cancer. The objective of this study was to assess the effect of PSC 833 on the metabolism of paclitaxel and characterize the differences in 6alpha-hydroxypaclitaxel pharmacokinetics. In addition, we examined the possibility of enhanced cytotoxicity of paclitaxel by the coexistence of 6alpha-hydroxypaclitaxel. EXPERIMENTAL DESIGN: Patients received paclitaxel 35 mg/m(2)/day by continuous intravenous infusion (CIVI) x 4 days without PSC 833 in cycle 1 and escalating doses of paclitaxel (13.1, 17.5, or 21.3 mg/m(2)/day CIVI x 4 days) with 5 mg/kg PSC 833 by mouth every 6 h x 7 days in cycle 2. Plasma samples were analyzed for both paclitaxel and its major metabolite with high-performance liquid chromatography methods. Using human liver microsomes, we studied the effect of PSC 833 on the metabolism of paclitaxel. In addition, the in vitro cytotoxicity of 6alpha-hydroxypaclitaxel alone and in combination with paclitaxel was evaluated. RESULTS: Twenty-one of 22 patients had a metabolite peak (6alpha-hydroxypaclitaxel) observed in the chromatogram of plasma samples from cycle 2 when they received paclitaxel in combination with PSC 833. This metabolite was not detectable in plasma obtained during the first cycle when they received paclitaxel without PSC 833. During cycle 2, the mean concentrations of 6alpha-hydroxypaclitaxel and paclitaxel were 0.10 +/- 0.074 and 0.079 +/- 0.041 microg/ml, respectively. A moderate association was observed between total bilirubin and 6alpha-hydroxypaclitaxel concentrations (P = 0.015, r = 0.52; n = 21). Human liver microsome experiments showed that a PSC 833 concentration as high as 10 microM did not affect the production of 6alpha-hydroxypaclitaxel. Paclitaxel cytotoxicity in HL60 and K562 human leukemia cells was increased in the presence of noncytotoxic concentrations of 6alpha-hydroxypaclitaxel. CONCLUSIONS: PSC 833 increases the plasma concentration of 6alpha-hydroxypaclitaxel during paclitaxel therapy. Inhibition of cytochrome P-450 3A4 by PSC 833 may explain this in part, although other mechanisms cannot be excluded.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2000

Liquid chromatographic resolution of 2-hydroxycarboxylic acids on a new chiral stationary phase derived from (S)-leucine.

Enantiomers of racemic 2-hydroxycarboxylic acids have been resolved as their O-ethoxycarbonyl pi-basic anilide derivatives on a new chiral stationary phase (CSP) derived from N-(3,5-dinitrobenzoyl)leucine N-phenyl N-alkylamide and the resolution results have been compared with those on various commercial pi-acidic CSPs. The resolution results demonstrate that the new CSP derived from N-(3,5-dinitrobenzoyl)leucine N-phenyl N-alkylamide is most effective among the five CSPs tested for the resolution of 2-hydroxycarboxylic acid derivatives. In order to elucidate the chiral recognition mechanism exerted by the new CSP, the resolution of slightly differently modified derivatives of 2-hydroxycarboxylic acids on the new CSP has been investigated. Based on the resolution results, a chiral recognition mechanism utilizing three simultaneous interactions such as the face to face pi-pi interaction and the two hydrogen bonding interactions between the CSP and the more retained enantiomer of the analyte has been proposed.

Chemical Phenomena↗
PubMed2000

Mode of action of sesame lignans in protecting low-density lipoprotein against oxidative damage in vitro.

We investigated the antioxidant properties of sesaminol, a major component of sesame oil, on the oxidative modification of human low-density lipoprotein (LDL) in vitro. Sesaminol inhibited the Cu2+-induced lipid peroxidation in LDL in a concentration-dependent manner with an IC50 36.0 +/- 10.0 nM. Sesaminol was a more effective scavenger than either alpha-tocopherol or probucol in reducing the peroxyl radicals derived from 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH) in aqueous solution. In addition, as determined by the secondary products of lipid peroxidation identified by using immunochemical methods, sesaminol completely inhibited the formation of 4-hydroxy-nonenal (4-HNE)- and malondialdehyde (MDA)-adducts in a concentration-dependent manner. Probucol and alpha-tocopherol at the same concentration exhibited a lesser inhibitory effect. Our findings suggest that sesaminol is a potentially effective antioxidant that can protect LDL against the oxidation.

Antioxidants↗
PubMed2000

NMDA-Receptor-dependent synaptic activation of voltage-dependent calcium channels in basolateral amygdala.

Afferent stimulation of pyramidal cells in the basolateral amygdala produced mixed excitatory postsynaptic potentials (EPSPs) mediated by N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors during whole cell current-clamp recordings. In the presence of GABA(A) receptor blockade, the mixed EPSPs recruited a large "all-or-none" depolarizing event. This recruited event was voltage dependent and had a distinct activation threshold. An analogous phenomenon elicited by exogenous glutamate in the presence of tetrodotoxin (TTX) was blocked by Cd(2+), suggesting that the event was a Ca(2+) spike. Selective glutamatergic blockade revealed that these Ca(2+) spikes were recruited readily by single afferent stimulus pulses that elicited NMDA EPSPs. In contrast, non-NMDA EPSPs induced by single stimuli failed to elicit the Ca(2+) spike even at maximal stimulus intensities although these non-NMDA EPSPs depolarized the soma more effectively than mixed EPSPs. Elongation of non-NMDA EPSPs by cyclothiazide or brief trains of stimulation were also unable to elicit the Ca(2+) spike. Blockade of K(+) channels with intracellular Cs(+) enabled single non-NMDA EPSPs to activate the Ca(2+) spike. The finding that voltage-dependent calcium channels are activated preferentially by NMDA-receptor-mediated EPSPs provides a mechanism for NMDA-receptor-dependent plasticity independent of Ca(2+) influx through the NMDA receptor.

2-Amino-5-phosphonovalerate↗
PubMed1999

Status of lipidsoluble antioxidants and TRAP in patients with Crohn's disease and healthy controls.

OBJECTIVE: To assess the status of lipidsoluble antioxidants (carotenoids, tocopherols, ubiquinone), retinol and their correlation with TRAP (total radical-trapping antioxidant potential) in patients with Crohn's disease. DESIGN: Prospective case-control study. SETTING: Clinic of Internal Medicine IV/Department of Gastroenterology and Hepatology, University of Vienna Medical School. SUBJECTS/METHODS: Plasma antioxidant concentrations were determined in patients with Crohn's disease (n = 24) to evaluate the antioxidant capacity compared to healthy controls (n = 33). Additionally, plasma TRAP (total radical-trapping antioxidant potential) was measured in 13 patients and 22 controls. RESULTS: All investigated carotenoids (alpha-carotene, beta-carotene and cryptoxanthin) were significantly decreased in patients with Crohn's disease (10.2 +/- 9.3, 16.2 +/- 12.4 and 7.8 +/- 5.5 microg/dl) compared to controls (13.3 +/- 5.1, 34.7 +/- 18.8 and 48.5 +/- 38.4 microg/dl respectively), whereas gamma-tocopherol and ubiquinone were significantly elevated in patients (0.14 +/- 0.07 microg/dl and 82.3 +/- 41.5 microg/dl, controls: 0.09 +/- 0.04 microg/dl and 60.8 +/- 30.0 microg/dl, respectively). Retinol and alpha-tocopherol did not significantly differ from controls. The total radical-trapping antioxidant potential (TRAP) was significantly lower in patients (1.11 +/- 0.28 micromol/l) compared to controls (1.34 +/- 0.26 micromol/l). Antioxidants were neither related to duration or severity of disease nor to disease activity. CONCLUSIONS: In patients with Crohn's disease several plasma antioxidant parameters are altered and the total radical-trapping antioxidant potential is decreased.

Adult↗
PubMed1999

Dietary defatted sesame flour decreases susceptibility to oxidative stress in hypercholesterolemic rabbits.

Plant glucosides possess antioxidative properties due to their ability to scavenge free radicals. Sesame seeds contain a class of these compounds, the sesaminol glucosides. To evaluate their antioxidative activity in vivo, we fed rabbits diets containing 1% cholesterol (Chol) with or without 10% defatted sesame flour (DSF) (containing 1% sesaminol glucosides) for 90 d. We determined the susceptibility of their tissues to oxidation ex vivo as well as serum total cholesterol (TC), phospholipid (PL), triglyceride (TG) and HDL cholesterol (HDL-C) concentrations. Serum TC, HDL-C, PL and TG levels were unaffected by the addition of DSF. The HDL-C in the Chol + DSF group was greater than in the Chol group at 45 d. Both were greater than in the groups that did not consume cholesterol. Liver TC and TG were significantly lower in rabbits fed the diet containing DSF plus 1% cholesterol than in those fed 1% cholesterol alone. Lipid peroxidation activity, measured as 2-thiobarbituric acid reactive substances (TBARS), was lower in the liver (P < 0.05) and serum (P = 0.06) of rabbits fed DSF plus cholesterol than in rabbits fed the cholesterol diet. Although we did not detect sesaminol glucosides in peripheral tissues, we observed abundant quantities of sesaminol in rabbits fed DSF, the principal metabolite. Our findings suggest that feeding DSF to rabbits does not protect cholesterol-induced hypercholesterolemia, but may decrease susceptibility to oxidative stress in rabbits fed cholesterol, perhaps due to the antioxidative activity of sesaminol.

Analysis of Variance↗
PubMed1998

Inhibition of 2,2'-azobis(2,4-dimethylvaleronitrile)-induced lipid peroxidation by sesaminols.

We found that sesaminols, a mixture of sesaminol and its stereoisomers, are potent inhibitors of the oxidation of low-density lipoprotein induced by 2,2'-azobis(2,4-dimethylvaleronitrile). Although sesaminols strongly inhibit lipid peroxidation related to their ability to scavenge free radicals, their antioxidant effects have not been investigated. To confirm the involvement of the phenolic moiety in the sesaminol structure in antioxidant activity, sesaminols were reacted with 2,2'-azobis(2,4-dimethylvaleronitrile). The reaction products were isolated by high-performance liquid chromatography and found to have a 1-cyano-1,3-dimethyl-butyl-peroxyl group in their structures. These chemical structures suggest that the sesaminols reacted with the alkylperoxyl radicals to form four major reaction products that are stereoisomers of each other, although the stereochemistry of each isomer has not yet been confirmed. Further instrumental analyses of the reaction products may increase our understanding of the antioxidant activity of sesaminols.

Antioxidants↗
PubMed1998

Sesamolin inhibits lipid peroxidation in rat liver and kidney.

Although the sesame lignans, sesaminol and sesamolinol, have been shown to possess antioxidative activity, less is known about the metabolism and antioxidative properties of sesamolin, a major constituent of sesame oil. To determine the ability of sesamolin to act as an antioxidant in vivo, we fed rats a diet containing 1% sesamolin for 2 wk and studied its metabolism and its effects on oxidative stress. About 75% of the ingested sesamolin was excreted unmetabolized in feces, but it was not detected in urine. Sesamolin and its metabolites, sesamol and sesamolinol, were excreted primarily as sulfates and glucuronides. The amount of sesamolin and its metabolites was lower in the plasma than in the liver or kidneys. When we compared rats fed a diet containing 1% sesamolin for 14 d with those fed a control diet, we found that liver weight was significantly greater in the former group. Lipid peroxidation activity, measured as 2-thiobarbituric acid reactive substances, was significantly lower in the kidneys and liver of the sesamolin-fed rats than in the controls. In addition, the amount of 8-hydroxy-2'-deoxyguanosine excreted in the urine was significantly lower in the sesamolin-fed rats. These results suggest that sesamolin and its metabolites may contribute to the antioxidative properties of sesame seeds and oil and support our hypothesis that sesame lignans reduce susceptibility to oxidative stress.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1998

Alteration in the sensitivity of GABA(A) receptors to allosteric modulatory drugs in rat hippocampus after chronic intermittent ethanol treatment.

Chronic intermittent ethanol (CIE)-treated rats exhibited a kindling-like persistent increase in withdrawal hyperexcitability. The alteration of GABA(A) receptor (GABA(A)R) function in the hippocampus was suggested as a possible mechanism underlying the hyperexcitability observed in CIE rats, because (1) GABA(A)R agonist (muscimol)-evoked 36Cl- efflux was decreased; (2) paired-pulse inhibition in the CA1 area, predominantly due to GABA(A)R-mediated recurrent inhibition, was persistently decreased; and (3) GABA(A)R subunit expression was altered in the hippocampus from CIE rats. To further characterize the functional alteration of GABA(A)R after CIE treatment, their sensitivity to acute ethanol, a steroid anesthetic (alphaxalone), and a benzodiazepine inverse agonist (DMCM; methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate) were studied using either synaptically evoked GABA(A)R responses or exogenously applied muscimol-evoked responses in hippocampal slices. Bath application of ethanol (60 mM) enhanced the area of GABA(A)R-mediated inhibitory postsynaptic potentials in the hippocampal CA1 region from control and CIE rats, and this potentiation was significantly (p = 0.027) greater in CIE rats (98%) than in control rats (53%). The positive modulatory effect of alphaxalone (1 microM) on GABA(A)R-inhibitory postsynaptic potentials was not significantly different between control and CIE rats (p = 0.375), whereas alphaxalone allosterically increased [3H]flunitrazepam binding in the CA1 area only in CIE rats (by 20 to 25%, p < 0.01), but not in controls. On the other hand, the negative modulatory effect of DMCM (1 microM) on muscimol-evoked responses was significantly larger in CIE rats (p = 0.002). These results suggest that the sensitization of GABA(A)R to acute ethanol and benzodiazepine inverse agonists, and possibly neurosteroids, may underlie ethanol dependence after multiple ethanol withdrawal episodes. These altered pharmacological properties are most consistent with changes in the subunit composition in the CA1 area of this rat model of alcohol dependence.

Alcoholism↗
PubMed1997

Increased sister chromatid exchanges in peripheral lymphocytes of patients with Crohn's disease.

A cytogenetic study was performed using Crohn's disease patients to determine whether the presence of chromosome instability is related to Crohn's disease, a chronic inflammatory bowel disease. Sister chromatid exchange (SCE) frequencies in peripheral blood lymphocyte cultures from 22 Crohn's disease patients and an equal number of healthy controls matched for sex and age were analyzed. The mean of SCE frequency in Crohn's disease patients was 11.64 +/- 0.42 (SEM) per cell, which was significantly higher than the value of 8.38 +/- 0.22 per cell in the matched controls (p < 0.0001). The Crohn's disease patients showed significantly increased high frequency cells (HFC) as compared to those among the matched controls. There was a significant correlation between HFC frequencies of the Crohn's disease patients and the severity of their disease as determined by the number of relapses per year and the degree of chronic activity after adjusting for the smoking status (r = 0.54, p = 0.011). In both smokers and non-smokers, the mean SCE and HFC frequencies of the patients were significantly higher than those of the controls. These results suggest that Crohn's disease is a condition with increased chromosome instability characterized by a high level of SCE frequencies which are associated with the inflammatory condition itself.

Adult↗
PubMed1997

Chronic intermittent ethanol treatment in rats increases GABA(A) receptor alpha4-subunit expression: possible relevance to alcohol dependence.

Chronic administration of ethanol to rats on an intermittent regimen, for 60 repeated intoxicating doses and repeated withdrawal episodes, results in a long-lasting kindling phenomenon. This involves an increasing severity of withdrawal, including a reduced threshold to seizures produced by the GABA(A) antagonist, pentylenetetrazol. We have shown previously that muscimol-evoked 36Cl- efflux and paired-pulse inhibition (involving GABA(A)-mediated recurrent inhibition) were decreased persistently in the CA1 region of hippocampal slices from chronic intermittent ethanol (CIE)-treated rats. We now report elevated levels of mRNA in forebrain for the alpha4 subunit of the GABA(A) receptor (GABAR), considered to be a constituent of pharmacologically and physiologically novel subtypes of GABARs. Using in situ hybridization with digoxigenin-labeled RNA probes, we show that at 2 days withdrawal, 60-dose CIE leads to a significant 30% increase in alpha4 subunit mRNA levels in the dentate gyrus, 46% increase in the CA3, and 26% increase in the CA1 regions. In contrast, there was no significant change in the mRNAs for the alpha5 subunit or glutamic acid decarboxylase 67 in the same regions. This study suggests that GABAR subunit-selective alterations occur after CIE treatment, possibly resulting in the alteration of the subunit composition of GABARs, with presumably altered physiological functions. This plasticity of GABARs may contribute to the increased withdrawal severity, reduced hippocampal inhibition, and increased seizure susceptibility of this animal model of human alcohol dependence.

Animals↗
PubMed1997

Chemopreventive effect of green tea (Camellia sinensis) against cigarette smoke-induced mutations (SCE) in humans.

Green tea (Camellia sinensis) is consumed daily between the meals or after meals in Japan and other Asian countries. In recent years, green tea and its major polyphenolics have been demonstrated to prevent chemically induced tumors in a variety of experimental animal models system. The exact mechanism(s) of its anticarcinogenic activity remains to be elucidated, but green tea polyphenolics have demonstrated antimutagenic, anticarcinogenic, antioxidant, and antipromotional effects, including inhibition of Phase I and inducing Phase II enzymes. Enzyme activities of glutathione peroxidase, catalase, and quinone reductase, and glutathione S-transferase are also induced. However, a paucity of green tea effects in humans prompted us to investigate antimutagenic effects of green tea against smoke-induced mutation in humans. Chemopreventive effects of green tea and coffee among cigarette smokers were examined in 52 clinically healthy male subjects between 20-51 years of age. Blood specimens were obtained from non-smokers (Group I), smokers (II), smokers consuming green tea (III), and smoker/coffee drinkers (IV). The mean years of cigarette smoking (> 10 cigarettes/day) of Groups II, III, and IV ranged from 13.4-14.7 years. Daily intake of green tea and coffee was 3 cups/day/6 months (III and IV). The frequencies of sister-chromatid exchange (SCE) in mitogen-stimulated peripheral lymphocytes from each experimental group were determined and statistically analyzed. SCE rates were significantly elevated in smokers (9.46 +/- 0.46) vs. non-smokers (7.03 +/- 0.33); however, the frequency of SCE in smokers who consumed green tea (7.94 +/- 0.31) was comparable to that of non-smokers, implying that green tea can block the cigarette-induced increase in SCE frequency. Coffee, by contrast, did not exhibit a significant inhibitory effect on smoking-induced SCE.

Adult↗