TRANSFER OF CESIUM AND IODINE FROM THE SURFACE TO THE INTERIOR OF APPLE FRUIT.

We investigated the transfer of stable Cs + and I- applied as droplets directly on the fruit surface of 3-y-old plumleaf crab apple trees to the fruit interior at different developmental stages. The proportions of Cs and I transferred to the fruit flesh by harvest time were 21-66% and 41-53%, respectively, with decreasing trends as the developmental stage progressed. Most of the Cs+ was gradually transferred from the surface to the skin and flesh, while I- rapidly penetrated the fruit in the days after the application, followed by slow transfer of small proportions. For both elements, prompt penetration of the flesh occurred 1-2 d after application. A compartment model for simulating each element's behavior was constructed using all the data obtained. The Cs transfer model to the flesh can simulate the measured values well. For the model of I, prompt distribution to the skin is also necessary.

IODINE ABSORPTION BY APPLE LEAF SURFACES.

Apple is an important agricultural product in Aomori Prefecture, Japan, where the first commercial nuclear fuel reprocessing plant is currently under construction. As the behavior of radioiodine deposited on the surface of apple leaves is not well known, we studied the absorption and transfer to fruit of stable iodine applied onto the leaf surface. Droplets of NaI solution were applied to the leaf surface $\sim$86-89 days after flowering. The leaves were collected periodically and washed with detergent solution, followed by determination of iodine amounts absorbed or remaining on the leaf surface. Subsequently, iodine levels were determined separately for each part of the apple tree. Our results indicated that iodine applied on the surface of the leaf was absorbed and accumulated inside the leaf, but the transfer of absorbed iodine to the fruit was negligible; hence, iodine was less likely to accumulate in the fruit.

Effect of the counter anion of cesium on foliar uptake and translocation.

Direct deposition of radioactive material onto crops is one important pathway for safety assessment of radionuclides released from nuclear facilities. Foliar uptake of Cs by radish (Raphanus sativus L. cv. Redchim) was studied by applying droplets of Cs solution (CsCl or CsNO3) on an upper leaf surface. The uptake of Cs was strongly affected by counter anions of Cs in the applied solution. Approximately 80% of Cs was absorbed for CsCl solution, while only 20% was absorbed for CsNO3. The partition of absorbed Cs between leaf and root tuber was quite similar for both Cs compounds, which indicated that behavior of the absorbed Cs in radish was the same for both.

Deposition of 137Cs in Rokkasho, Japan and its relation to Asian dust.

Biweekly atmospheric depositions of (137)Cs were measured in Rokkasho, Aomori, Japan from March 2000 to March 2006 to study recent (137)Cs deposition. Although the deposition level was generally lower than the detectable limit, deposition samples collected in spring occasionally had measurable levels of (137)Cs. The annual (137)Cs deposition from 2001 to 2005 was 0.04-0.69 Bq m(-2) with a mean value of 0.27 Bq m(-2). Depositions of insoluble Al, Fe and Ti were strongly correlated with the (137)Cs deposition, suggesting that suspension of soil particles was the main source of the recent (137)Cs deposition. Asian dust events were coincident with some of the significant (137)Cs depositions in spring. It was found that the ratios of (137)Cs/Al and Fe/Al could be used as indices for discriminating Asian dust from suspension of the local surface soil. Backward trajectory analysis suggested southern Mongolian and northeastern China regions as sources of the significant (137)Cs depositions.

Cardioprotection by metformin is abolished by a nitric oxide synthase inhibitor in ischemic rabbit hearts.

We investigated the effects of metformin on myocardial metabolism during ischemia by 31P-nuclear magnetic resonance (NMR) in isolated rabbit hearts. Metformin was administered 60 min prior to induction of global ischemia, or in combination with a nitric oxide synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), at 5 min or 60 min prior to the ischemia. Normothermic global ischemia was then carried out for 45 min. Twenty-eight hearts were divided into 4 experimental groups consisting of 7 hearts each: a control (C) group; an M group receiving metformin treatment alone; an M+L (5) group receiving metformin treatment with L-NAME at 5 min before ischemia; and an M+L (60) group receiving metformin treatment with L-NAME at 60 min before ischemia. During ischemia, the decrease in adenosine triphosphate (ATP) was significantly inhibited in the M group in comparison with the C group (p < 0.01). However, this preservation of ATP in the M group was inhibited in the M+L (5) group during ischemia. In contrast, in the M+L (60) group, this preservation of ATP in the M group was not inhibited during, but not at the end of, ischemia. These results suggest that metformin has a significant beneficial effect for improving the myocardial energy metabolism during myocardial ischemia. This cardioprotection may be more dependent on nitric oxide synthase during ischemia than during pre-ischemia.

Effects of an HMG-CoA reductase inhibitor in combination with an ACE inhibitor or angiotensin II type 1 receptor antagonist on myocardial metabolism in ischemic rabbit hearts.

We investigated the effects of a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, pravastatin, an angiotensin converting enzyme (ACE) inhibitor, temocaprilat, and an angiotensin II type 1 (AT1) receptor antagonist, CV-11974, on myocardial metabolism during ischemia in isolated rabbit hearts using phosphorus 31-nuclear magnetic resonance (31P-NMR) imaging. Forty-five minutes of continuous normothermic global ischemia was carried out. Pravastatin, temocaprilat, CV-11974 or a nitric oxide synthase inhibitor, L-NAME was administered from 60 min prior to the global ischemia. Japanese white rabbits were divided into the following experimental groups, a control group (n=7), a group treated with pravastatin (P group; n=7), a group treated with pravastatin and temocaprilat (P+T group; n=7), a group treated with pravastatin and CV-11974 (P+CV group; n=7), and a group treated with pravastatin and L-NAME (P+L-NAME group; n=7). During ischemia, P group, as well as either P+T group or P+CV group, showed a significant inhibition of the decreases in adenosine triphosphate (ATP) and intracellular pH (pHi) (p<0.01, respectively, at the end of ischemia compared to the control group as well as P+L-NAME group), and a significant inhibition of the increase in inorganic phosphate (Pi) (p<0.01, respectively, compared with the control group as well as P+L-NAME group). These results suggest that pravastatin significantly improved myocardial energy metabolism during myocardial ischemia. This beneficial effect was dependent on NO synthase. However, this beneficial effect was not enhanced by either temocaprilat or CV-11974.

A novel cardioprotective agent, JTV-519, is abolished by nitric oxide synthase inhibitor on myocardial metabolism in ischemia-reperfused rabbit hearts.

We investigated the effect of a novel cardioprotective agent, JTV-519, with or without a nitric oxide synthase inhibitor, L-NAME, on the myocardial metabolism and contraction during ischemia and reperfusion by means of phosphorus 31-nuclear magnetic resonance (31P-NMR) in Langendorff rabbit hearts. After 20 min normothermic global ischemia, postischemic reperfusion was carried out for 30 min. JTV-519 was administered from 40 min prior to the global ischemia. Twenty-one hearts were divided into three experimental groups consisting of 7 hearts each: a control group, a JTV-519 group perfused with JTV-519, and a JTV-519+L-NAME group perfused with a combination of JTV-519 and L-NAME. During ischemia, the JTV-519 group showed a significant inhibition of the decrease in adenosine triphosphate (ATP) compared with both the control and JTV-519+L-NAME groups (p<0.01); the levels of ATP were 20+/-6, 56+/-9, and 40+/-4% in the control group, JTV-519 group, and JTV-519+L-NAME group, respectively. Both the JTV-519 group and JTV-519+L-NAME group showed a significant inhibition of the increase in left ventricular end-diastolic pressure (LVEDP) compared with the control group (p<0.01). After postischemic reperfusion, the JTV-519 group again showed a significant improvement of ATP as compared with both the control and JTV-519+L-NAME groups (p<0.01); the ATP levels were 52+/-4, 82+/-3, and 64+/-3% in the control group, JTV-519 group, and JTV-519+L-NAME group. In conclusion, JTV-519 has a significant beneficial effect on myocardial energy metabolism during both ischemia and reperfusion. This beneficial effect was dependent on NO synthase. Furthermore, JTV-519 showed significant potential for improving myocardial relaxation during ischemia. This effect was not dependent on NO synthase.

Cardioprotection with pioglitazone is abolished by nitric oxide synthase inhibitor in ischemic rabbit hearts--comparison of the effects of pioglitazone and metformin.

BACKGROUND: The effects of two drugs representing different classes of antidiabetic pharmacology (pioglitazone, a thiazolidinedione; and metformin, a biguanide) on the myocardial metabolism in the ischemia are poorly understood. METHODS: To test the hypothesis that cardioprotection of pioglitazone and metformin is associated with nitric oxide (NO), we studied the high energy phosphate metabolism by 31P-nuclear magnetic resonance (NMR) in isolated rabbit hearts. Forty-five minutes of continuous normothermic global ischemia was carried out. Pioglitazone or metformin was administered at the beginning, 60 min prior to the global ischemia, with or without the nitric oxide synthase inhibitor, L-NAME, administered 5 min or 60 min prior to the ischemia. In the first experiment, whether NO was produced or not by administration of pioglitazone, for the prevention of myocardial ischemic injury, was investigated. Hearts of male Japanese white rabbits were divided into 4 experimental groups: the control (C) group, the P group consisting of pioglitazone treatment, the P + L5 group consisting of pioglitazone treatment with L-NAME (5 min before ischemia), and the P + L60 group consisting of pioglitazone treatment with L-NAME (60 min before ischemia). In the next experiment, a comparison between the effects of pioglitazone and metformin in preventing ischemic injury were studied. The hearts were divided into 4 experimental groups: the control (C) group, the P group consisting of pioglitazone treatment, the P + L5 group consisting of pioglitazone treatment with L-NAME (5 min before ischemia), the M group consisting of metformin treatment, and the M + L5 group consisting of metformin treatment with L-NAME (5 min before ischemia). RESULTS: In the first experiment, the decrease in adenosine triphosphate (ATP) during ischemia was significantly inhibited in the P group in comparison with the C group (P < 0.01). However, the decrease in ATP was not inhibited in the P + L5 group during ischemia. In contrast, in the P + L60 group, the decrease in ATP was not inhibited during a part of ischemia. In the next experiment, a comparison between the effects of pioglitazone and metformin in preventing ischemic injury was studied. As a result of administration of either pioglitazone or metformin, there was no difference between groups with and without L-NAME. CONCLUSION: These results suggest that pioglitazone has a significant beneficial effect on improving the myocardial energy metabolism during ischemia. This cardioprotection may be dependent on nitric oxide (NO) synthase during ischemia more than preischemia. Furthermore, the present findings suggest that both pioglitazone and metformin have equal cardioprotective effects mediated by NO on myocardial ischemic injury in rabbits.