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Journal of the American College of Nutrition, Vol. 24, No. 5, 342-346 (2005)
Published by the American College of Nutrition

Green Tea Consumption and Serum Malondialdehyde-Modified LDL Concentrations in Healthy Subjects

Reiko Hirano-Ohmori, PhD, Rie Takahashi, MS, Yukihiko Momiyama, MD, PhD, Hiroaki Taniguchi, MD, Atsushi Yonemura, MD, Seiichi Tamai, MD, PhD, Keizo Umegaki, PhD, Haruo Nakamura, MD, PhD, Kazuo Kondo, MD, PhD and Fumitaka Ohsuzu, MD, PhD

National Defense Medical College, Saitama (R.O., Y.M., H.T., A.Y., S.T., H.N., F.O.)
Ochanomizu University, Tokyo (R.T., K.K.)
National Institute of Health and Nutrition, Tokyo (K.U.), JAPAN

Address reprint requests to: Reiko Hirano-Ohmori, PhD, First Department of Internal Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, JAPAN. E-mail : rhirano{at}yahoo.co.jp


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 REFERENCES
 
Objective: Green tea was shown to inhibit LDL oxidation, platelet aggregation, and matrix metalloproteinases (MMPs) activities in vitro. We tried to elucidate whether or not green tea consumption may have these effects in vivo, which may be protective against atherosclerotic disease.

Methods: We measured serum malondialdehyde-modified LDL (MDA-LDL) concentrations and urine 8-epi-prostaglandin (PG) F2{alpha} in 22 healthy male nonsmokers. They drank 7 cups/day of water for 2 weeks and drank 7 cups/day of green tea for the next 2 weeks. Regarding platelet aggregation, plasma thromboxane B2 (TXB2) and 6-keto-PGF1{alpha} concentrations and ex vivo platelet aggregation were evaluated. Plasma MMP-2 and -9 concentrations were also measured.

Results: Of the 22 subjects, 20 had been in the habit of drinking green tea before the study. Plasma catechins concentrations significantly decreased at the end of the water period and then increased at the end of the green tea period. Although no change in plasma LDL-cholesterol concentrations (110 ± 33 vs. 113 ± 28 mg/dL, p = NS) was found, MDA-LDL concentrations (84 ± 45 vs. 76 ± 40 IU/L, p < 0.05) and the ratio of MDA-LDL/LDL-cholesterol (0.74 ± 0.21 vs. 0.65 ± 0.20, p < 0.02) significantly decreased at the end of the green tea period. However, no significant changes were observed in urine 8-epi-PGF2{alpha} concentrations, in platelet aggregation, nor in plasma TXB2, 6-keto-PGF1{alpha} or MMP concentrations.

Conclusion: Daily consumption of green tea decreased serum MDA-LDL concentrations, but it had no significant effects on platelet aggregation, platelet TX production or plasma MMPs concentrations. Our results suggest that green tea consumption may inhibit LDL oxidation in vivo.

Key words: green tea, LDL oxidation, in vivo


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
SUBJECTS AND METHODS
 RESULTS
 REFERENCES
 
Flavonoids are polyphenols that are mainly contained in beverages, such as tea and wine, as well as in fruits and vegetables. Prospective studies have shown that the dietary intakes of flavonoids were associated with a reduced mortality from coronary artery disease (CAD) and a reduced risk of myocardial infarction (MI) [1–3]. In Western countries, black tea is a major source for the flavonoids intake [4,5]. One case-control study reported that the black tea intake was inversely associated with MI [4]. The population-based Rotterdam study demonstrated the black tea intake to be inversely associated with the degree of aortic atherosclerosis [5]. In Japan, green tea, which is very rich in catechins, is the most popular beverage and the major source for the flavonoids intake (>80% of the flavonoids intake) [1]. Two cross-sectional studies showed the green tea intake to be inversely associated with angiographically diagnosed CAD [6,7]. We also reported that the green tea intake was inversely associated with MI in Japanese patients [8].

In apo E-deficient mice, green tea ingestion inhibited aortic atherosclerosis [9]. Tijburg et al. [10] also showed green tea ingestion to reduce aortic atherosclerosis in hypercholesterolaemic rabbits, but the ingestion of black tea or vitamin E did not. In vitro, green tea has been reported to inhibit LDL oxidation by several studies [11,12]. Green tea was also shown to inhibit platelet aggregation [13,14] and matrix metalloproteinases (MMPs) activities [15,16] in vitro. However, these effects of green tea, which may be protective against atherosclerotic disease, such as CAD, have not yet been elucidated in vivo. Our study was done to elucidate whether or not green tea consumption may have some effects on LDL oxidation, platelet aggregation, and MMPs activities in vivo. To evaluate the inhibitory effect of green tea on LDL oxidation in vivo, we measured serum malondialdehyde-modified LDL (MDA-LDL) concentrations, one of oxidized LDLs, by a sensitive enzyme linked-immunosorbent assay (ELISA) [17], in addition to plasma thiobarbituric acid reactive substances (TBARS), vitamin C, and urine 8-epi-prostaglandin (PG) F2{alpha} concentrations (oxidative stress markers), in 22 healthy subjects. We also evaluated the effects of green tea consumption on platelet aggregation, platelet thromboxane (TX) production, and plasma MMPs concentrations.


   SUBJECTS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
RESULTS
 REFERENCES
 
Study Subjects and Design
Study subjects consisted of 22 healthy volunteers, whose mean age and body mass index were 32 ± 5 years and 23 ± 3 kg/m2, respectively. All of them were male nonsmokers. Our study was approved by our institutional ethics committee. All subjects gave their informed consent to participate in our study.

The green tea used in our study was a commercially available freeze-dried tea, [sarasara ryokucha] (Itoen Co., Tokyo, Japan), which is on sale for drinking in Japan. One stick (0.9 g) of the freeze-dried tea can be dissolved in 100 mL hot water and then be drunk as 1 cup of green tea. Our study consisted of a 1-week run-in period, a 2-week water intake period, and a next 2-week green tea intake period. Throughout the 3 periods, we asked all subjects to maintain their regular dietary habit but not to have any kinds of tea, wine, citrus liquor or vitamin supplements. After the run-in period, all the subjects drank 7 cups/day of water for 2 weeks (water period) and then drank 7 cups/day of green tea for the next 2 weeks (green tea period). During the water or green tea periods, they drank 2 cups (breakfast and lunch) and 3 cups (dinner) of water or green tea after each meal (a total of 7 cups/day comprising 700 mL). As shown in Table 1, 7 cups of green tea contain 542.5 mg of catechins, 108.5 mg of caffeine, and 56.7 mg of vitamin C. Overnight-fasting blood and spot urine samples were taken at 9:00 on the morning after water or green tea was consumed in the evening at the end of each period. The subjects kept a dietary record for the last 3-days of each period, and their daily energy and nutrient intakes were calculated using the Excel Eiyokun version 3.0 software package (Kenpakusha, Tokyo, Japan).


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  		Table 1. Composition of the Consumed Green Tea per Day (7 cups)

 
Biochemical Analyses and Platelet Aggregation Test
Plasma, serum and spot urine samples were stored at –80°C until analyzed. Serum MDA-LDL concentrations were measured by ELISA, as reported by Kotani et al. [17], and plasma TBARS concentrations were analyzed by a fluorometric method (Wako Pure Chemical Industries, Osaka, Japan). Plasma LDL-cholesterol concentrations were measured by direct enzymatic method with a commercially available kit (Cholestest LDL, Daiichi Pure Chemicals, Japan), and other lipids concentrations were measured by standard laboratory enzymatic methods. Plasma vitamin C and plasma epigallocatechin gallate (EGCg), gallocatechin gallate (GCg) and epicatechin gallate (ECg) concentrations were measured by high-performance liquid chromatography (HPLC) with electrochemical detection, as we previously reported [18]. The total catechins concentration was defined as the sum of EGCg, GCg and ECg values. We also evaluated spot urine 8-epi-PGF2{alpha} and plasma MMP-2 and MMP-9 concentrations by ELISA with commercially available kits: 8-epi-PGF2{alpha} (Cayman Chemical, Ann Arbor, MI) and MMPs (Daiichi Fine Chemical, Toyama, Japan). The results of urine 8-epi-PGF2{alpha} concentrations are expressed as pg/mg creatinine.

Regarding platelet TX production, we measured plasma TXB2 and 6-keto-PGF1{alpha} concentrations using radioimmunoassay kits (PerkinElmer Life Sciences, Boston, MA). In addition, we assessed the ability of platelet aggregation ex vivo. Platelet-rich plasma was prepared from citrated blood by centrifugation at 100 x g for 10 min at 22°C. Within 1 hr after blood sampling, platelet aggregation was evaluated as the 5-min and maximum changes in light transmission after the stimulations with epinephrine (1 and 2 µg/mL), adenosine 5`-diphosphates (ADP) (1 and 2 µmol/L), or collagen (1 and 2 µg/mL).

Statistical Analysis
To test whether or not the distributions of variables are deviating from a normal distribution, the F-test was applied to all measured variables. Since plasma catechin concentrations, urine 8-epi-PGF2{alpha} concentrations, and a 6-keto-PGF1{alpha}/TXB2 ratio were considered to be nonparametric variables, these results are expressed as the median value, and any differences in these variables among the 3 periods were evaluated by the Friedman’s test. For parametric variables, the results are expressed as the mean value ± S.D., and any differences among the 3 periods were evaluated by the repeated-measures ANOVA. A Bonferroni adjustment (0.05/3) was undertaken because the 3 periods were compared. A p value of <0.05 was considered to be statistically significant.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
REFERENCES
 
The dietary intakes of the subjects at each period are shown in Table 2. There were no differences in the intakes of energy and nutrients among the 3 periods. Of the 22 subjects, 20 had been in the habit of drinking green tea before the study. As shown in Table 3, plasma total catechins concentrations significantly decreased at the end of the water period and then increased at the end of the green tea period. Although no significant change in plasma LDL-cholesterol (LDL-C) concentrations (110 ± 33 vs. 113 ± 28 mg/dL, p = NS) were found, serum MDA-LDL concentrations (84 ± 45 vs. 76 ± 40 IU/L, p < 0.05) and the MDA-LDL/LDL-C ratio (0.74 ± 0.21 vs. 0.65 ± 0.20, p < 0.02) significantly decreased at the end of the green tea period. Regarding oxidative stress markers, no significant changes were observed in urine 8-epi-PGF2{alpha} or plasma TBARS concentrations. Plasma vitamin C concentrations decreased at the end of the water period and increased at the end of the green tea period, but these changes did not reach statistical significance. Regarding platelet aggregation, no changes were observed at the end of the green tea period (Table 4). Plasma 6-keto-PGF1{alpha} concentrations and the ratio of 6-keto-PGF1{alpha}/TXB2 tended to increase at the end of the green tea period, but these changes did not reach statistical significance. There were no changes in MMP-2 or MMP-9 concentrations.


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  		Table 2. Daily Energy and Nutrient Intakes during the Run-In, Water and Green Tea Periods

 

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  		Table 3. Plasma Catechins, Lipids, Serum MDA-LDL and Urine 8-epi-PGF2{alpha} Concentrations at the Ends of the 3 Periods

 

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  		Table 4. Platelet Aggregation in Response to Epinephrine, ADP and Collagen, and Plasma Concentrations of 6-keto-PGF1{alpha}, TXB2, and MMP-2, -9 at the Ends of the 3 Periods

 

   DISCUSSION
 
We investigated the effects of green tea consumption on LDL oxidation, platelet aggregation, and MMPs activities in vivo in 22 healthy subjects. Our study showed that the daily consumption of green tea (7 cups/day) significantly decreased serum MDA-LDL concentrations without any significant decrease in urine 8-epi-PGF2{alpha} concentrations. However, green tea consumption had no significant effects on platelet aggregation, platelet TX production, or MMPs concentrations.

Green tea was reported to inhibit LDL oxidation in vitro [11,12], but two studies [19,20] failed to show any effect of green tea consumption on LDL oxidation ex vivo. Miura et al. [21] reported that the 1-week intake of green tea extracts equivalent to 7–8 cups/day prolonged the lag time of LDL oxidation. However, they took blood samples 1 hr after a green tea intake, thus suggesting that their results may only reflect the acute effects of green tea intake. Freese et al. [22] reported that the 4-week intake of green tea extracts equivalent to 10 cups/day decreased plasma TBARS concentrations during a high-linoleic acid diet. However, their high-linoleic acid diet caused a significant decrease in total cholesterol concentrations, thereby making it difficult to elucidate the effect of green tea on LDL oxidation. Two other studies [19,21] and our study found no effect of green tea consumption on TBARS concentrations. In the present study, we measured serum concentrations of MDA-LDL, one of oxidized LDLs. Elevated MDA-LDL concentrations have been reported in patients with CAD, especially in those with MI [23,24]. We showed that daily consumption of green tea (7 cups/day) significantly decreased serum MDA-LDL concentrations, thus suggesting that green tea has an inhibitory effect against LDL oxidation in vivo. The green tea used in our study was a freeze-dried type that is on sale for drinking, and Japanese people ordinarily drink 7–8 cups/day of green tea [9]. Therefore, the ordinary consumption of green tea in Japanese may thus reduce oxidized LDL.

In our study, the daily dose of green tea also contained 56.7 mg of vitamin C. Plasma vitamin C concentrations increased after green tea consumption, but this change did not reach statistical significance. Moreover, there was no significant change in urine 8-epi-PGF2{alpha} concentrations. Two studies [22,25] also reported no changes in urine 8-epi-PGF2{alpha} after green tea consumption. Vitamin C, which is more hydrophilic than flavonoids, scavenges peroxyl radicals generated in the aqueous phase [26]. The consumption of vitamin C, but not of flavonoids, was shown to decrease 8-epi-PGF2{alpha} concentrations [27,28]. In contrast, catechins have both hydrophilic and lipophilic properties, and their antioxidant properties in lipid bilayers were shown to be related to a unique hydrophilic and lipophilic balance [29]. Moreover, Kajiya et al. [30] reported that catechins existed mainly in the lipid bilayers. Therefore, green tea, which is very rich in catechins, may characteristically protect LDL against oxidation without any significant reduction in oxidative stress.

Hodgson et al. [31] reported that black tea consumption did not affect platelet aggregation ex vivo. We also showed that green tea consumption did not affect platelet aggregation in response to epinephrine, ADP or collagen. Regarding platelet TX production, Freese et al. [22] measured urine 2,3-dinor-TXB2 concentrations and found no effect of green tea consumption on it. We also found no significant changes in plasma TXB2 or 6-keto-PGF1{alpha} concentrations. In vitro studies [13,14] showed catechins to inhibit platelet aggregation, but catechins concentrations in such studies were much higher than those detected in the plasma of our study subjects. The ordinary consumption of green tea may not be strong enough to affect platelet aggregation in vivo.

Blood MMP-2 and MMP-9 concentrations were reported to be elevated in patients with CAD, especially in those with MI [32]. Recently, Demeule et al. [15] reported catechins to inhibit both MMP-2 and -9 activities in rat tissues in vitro. Maeda et al. [16] also showed catechins to inhibit the MMP-2 activity in cultured bovine aortic smooth muscle cells. We measured plasma MMP-2 and MMP-9 concentrations using the ELISA kits, which measure the total concentrations of both active and inactive forms of MMPs. However, we found no significant changes in MMP-2 or -9 concentrations after green tea consumption.

Our study has some limitations. First, our study was in 22 healthy subjects. Our study was a sequential but not crossover design, thereby making it impossible to separate period effects from treatment effects. Moreover, green tea contained vitamin C. No significant change was found in plasma vitamin C concentrations, but vitamin C contained in green tea may explain the decrease in MDL-LDL concentrations. To clarify whether or not green tea has an inhibitory effect against LDL oxidation in vivo, a further study should be done using a crossover design in high-risk subjects, such as those with atherosclerotic risk factors. Second, any ELISA kit for detecting oxidized phosphatidylcholine-LDL is unavailable in Japan. Therefore, we measured MDA-LDL concentrations, one of oxidized LDLs, using a sensitive ELISA method with the combination of an anti-MDA-LDL antibody (ML25) and an apo B specific antibody (AB16) [17,21].

In conclusion, the daily consumption of green tea (7 cups/day) decreased serum MDA-LDL concentrations, but it had no significant effects on platelet aggregation, platelet TX production, or plasma MMPs concentrations. Our results suggest that the ordinary consumption of green tea in Japanese may inhibit LDL oxidation in vivo.

Received December 27, 2004. Accepted June 18, 2005.


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 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 REFERENCES
 

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