Catechins in green tea powder (matcha) are heat-stable scavengers of acrolein, a lipid peroxide-derived reactive carbonyl species.

Lipid peroxidation-derived reactive carbonyl species (RCS) such as acrolein and 4-hydroxynonenal pose health risks. We characterized the RCS-scavenging reactions of tea catechins in an aqueous solution and in baked cake. Acrolein's reaction with each of the major tea catechins (epicatechin, epigallocatechin, epicatechin gallate, and epigallocatechin gallate) resulted in the formation of mono-, di-, and tri-acrolein conjugates of each catechin as revealed by our LC-linear ion trap MS analysis. The formation of the acrolein-conjugates of the four catechins was confirmed in the reaction of acrolein with green tea powder (matcha) extract. The addition of matcha tea powder to cake dough significantly suppressed the accumulation of RCS during cake baking. The mono-acrolein conjugates of the four major catechins were detected in the baked cake. The RCS-scavenging capability of tea catechins offers a new functionality of matcha tea powder, and its heat stability demonstrates the usefulness of matcha as a food additive.

ST-T wave changes in a patient complicated with vasospastic angina and Brugada syndrome: differential responses to acetylcholine in right and left coronary artery.

A 49-year-old man with chest pain and syncope presented saddleback or occasionally coved type ST elevation in V1-V3. Coronary spasm in the left anterior descending artery was induced by acetylcholine injection and ST elevation changed from saddleback to coved type in V2-V3 together with ST depression in V4-V5, whereas acetylcholine injection into the right coronary artery did not provoke spasm, but induced augmented and coved type ST elevation in V2 without ST-T changes in V4-V5. These electrocardiographic changes in response to acetylcholine administration into each coronary artery are compatible with pathogenesis of vasospastic angina and Brugada syndrome, respectively.

Autonomic and pharmacological responses of idiopathic ventricular tachycardia arising from the left ventricular outflow tract.

BACKGROUND: It is well recognized that the mechanism of idiopathic ventricular tachycardia (VT) arising from the right ventricular outflow tract (RVOT) is mostly due to cyclic AMP-mediated triggered activity. The mechanism of VT arising from the left ventricular outflow tract (LVOT) has not been well clarified whether it is the same as VT of RVOT. METHODS: We studied autonomic modulations and pharmacological interventions on VT/premature ventricular contractions (PVCs) from LVOT to explore its possible mechanism in six patients (age: 49 +/- 14, three males). None of them had structural heart diseases. RESULTS: Isoproterenol application easily induced VT and/or PVCs from LVOT. Valsalva maneuvers suppressed isoproterenol-induced VT in two and PVCs in two, and carotid sinus massage (CSM) suppressed PVCs in one patient. Adenosine triphosphate inhibited both VT and PVCs in all six patients. Propranolol, lidocaine, and procainamide eliminated VT/PVCs in four, three, and four patients, respectively. Verapamil terminated VT in one and PVCs in another one patient, but aggravated PVCs to VT in one patient. CONCLUSION: The results suggest that the mechanism of VT from LVOT is mostly due to cAMP-mediated triggered activity as similar to that in VT from RVOT.

Prevention of aortic calcification by etidronate in the renal failure rat model.

Our recent clinical study indicated that etidronate may inhibit the progression of aortic calcification in hemodialysis patients. To determine whether etidronate inhibits aortic calcification in renal failure rats, renal failure was induced by subtotal nephrectomy, in which 5/6 of the kidneys were removed. Significant increases in serum creatinine levels were observed 2 weeks after the operation, at which point treatment with etidronate and calcitriol was initiated. Etidronate at 5 or 10 mg/kg significantly reduced the thoracic and abdominal aortic calcification induced by calcitriol. It also reduced the dysfunction in aortic contraction. The elevation of bone metabolism and reduction of bone mineral density observed in the nephrectomized rats were not affected by treatment with 5 mg/kg etidronate. No changes in serum Ca and the product of Ca and P levels were observed between the non etidronate-treated group and the 5 mg/kg etidronate-treated group. Moreover, the reduction in the aortic expression of matrix Gla protein mRNA observed in nephrectomized rats was reversed by 5 mg/kg etidronate. These results show that etidronate at concentrations that do not affect the bone mineral density inhibits aortic calcification and recovers vascular dysfunction in renal failure rats.

Characterization of endothelium-dependent relaxation and modulation by treatment with pioglitazone in the hypercholesterolemic rabbit renal artery.

The present study was undertaken to investigate vascular function in hypercholesterolemic rabbits and also to characterize the effects of pioglitazone on it. Rabbits were fed normal, 0.5% cholesterol chow, or 0.5% cholesterol chow plus 300 ppm pioglitazone for 5 or 10 weeks. The tension of isolated renal artery rings was measured isometrically, and morphometric analysis was performed. The cholesterol chow diet administered for 5 weeks did not affect acetylcholine-induced relaxation in the renal artery but that for 10 weeks decreased it. The N(G)-nitro-L-arginine (L-NOARG)- and indomethacin-resistant endothelium-dependent relaxation induced by acetylcholine in the renal artery was enhanced in rabbits receiving the cholesterol chow for 5 or 10 weeks, as compared to rabbits receiving the control diet, and the percentage of plaque area formation was increased in the renal artery by the cholesterol chow for 10 weeks. Pioglitazone normalized them without lowering serum lipid levels. The resistant parts of acetylcholine-induced relaxation was significantly inhibited when the renal artery was treated with charybdotoxin, an inhibitor of large and intermediate conductance Ca(2+)-activated K(+) channels, or N,N-diethylaminoethyl-2,2-diphenylvalerate hydrochloride (SKF 525a), a cytochrome P-450 monooxygenase inhibitor. Results indicate that hypercholesterolemia enhances endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation in the rabbit renal artery and pioglitazon normalizes it without lowering serum lipid levels, and suggest that the maintenance of endothelial function by pioglitazon is related to the mechanisms for its anti-atheromatous activity.

A sulforaphane analogue that potently activates the Nrf2-dependent detoxification pathway.

Exposure of cells to a wide variety of chemoprotective compounds confers resistance to a broad set of carcinogens. For a subset of the chemoprotective compounds, protection is generated by an increase in the abundance of the protective phase II detoxification enzymes, such as glutathione S-transferase (GST). We have recently developed a cell culture system, using rat liver epithelial RL 34 cells, that potently responds to the phenolic antioxidants resulting in the induction of GST activity (Kawamoto, Y., Nakamura, Y., Naito, Y., Torii, Y., Kumagai, T., Osawa, T., Ohigashi, H., Satoh, K., Imagawa, M., and Uchida, K. (2000) J. Biol. Chem. 275, 11291-11299.) In the present study, we investigated the phase II-inducing potency of an isothiocyanate compound in vitro and in vivo and examined a possible induction mechanism. Based on an extensive screening of vegetable extracts for GST inducer activity in RL34 cells, we found Japanese horseradish, wasabi (Wasabia japonica, syn. Eutrema wasabi), as the richest source and identified 6-methylsulfinylhexyl isothiocyanate (6-HITC), an analogue of sulforaphane (4-methylsulfinylbutyl isothiocyanate) isolated from broccoli, as the major GST inducer in wasabi. 6-HITC potently induced both class alpha GSTA1 and class pi GSTP1 isozymes in RL34 cells. In animal experiments, we found that 6-MSHI was rapidly absorbed into the body and induced hepatic phase II detoxification enzymes more potently than sulforaphane. The observations that (i) 6-HITC activated the antioxidant response element (ARE), (ii) 6-HITC induced nuclear localization of the transcription factor Nrf2 that binds to ARE, and (iii) the induction of phase II enzyme genes by 6-HITC was completely abrogated in the nrf2-deficient mice, suggest that 6-HITC is a potential activator of the Nrf2/ARE-dependent detoxification pathway.