The correlation between markers of oxidative stress and risk factors of coronary artery disease in Thai patients.

An imbalance between oxidative damage and antioxidative protection in association with the pathophysiology of atherosclerosis has been suggested. The aim of our study was to investigate the relationship between plasma lipids, the antioxidant system and oxidative damage in Thai patients with stable coronary artery disease (CAD). Sixty-one patients (40 males, 21 females), who were angiographically defined as having CAD and were clinically stable, participated in this study. Thirty-two healthy subjects (20 males, 12 females) served as normal controls. The investigation included the measurements of plasma lipid profiles and plasma total antioxidative status (TAS) such as plasma vitamin E erythrocyte glutathione (GSH) and glutathione peroxidase (GPx), as well as malondialdehyde (MDA) and total plasma total protein thiols (P-SH). In patients with CAD, erythrocyte GSH and GPx were significantly lower than those found in controls. However plasma TAS and vitamin E were not significantly different between groups. Patients with CAD also had higher MDA and lower P-SH levels than the controls, which represents the oxidative damage products of lipid and proteins. Multiple regression analysis revealed negative correlations between GSH and cholesterol, GSH and low density lipoprotein (LDL), vitamin E and MDA, as well as P-SH and MDA. This study demonstrated the status of oxidative stress in patients with stable CAD. Since oxidative stress is the imbalance between the total oxidants and antioxidants in the body, any single oxidant/antioxidant parameter may not reflect the overall oxidative stress system. Thus, in patients with CAD, diets with various types of antioxidants may be more beneficial in increasing antioxidant activity than any particular antioxidant supplementation.

Magnesium status of patients with renal stones and its effect on urinary citrate excretion.

OBJECTIVES: To assess the magnesium status and its effect on urinary citrate excretion in patients with renal stones, as they have a low muscular magnesium content. PATIENTS, SUBJECTS AND METHODS: Using a magnesium-tolerance test (0.1 mmol/L MgSO4/kg body weight, delivered intravenously), the magnesium status was assessed in 17 patients with renal stones from rural North-east Thailand, and in three groups of normal subjects from different environments (i.e. 17 from rural Central Thailand, 16 from urban and 14 from rural North-east Thailand). Participants with magnesium deficiency (magnesium retention > 50%) were supplemented with 300 mg chelated magnesium daily for 1 month and reassessed. Their urinary citrate excretion was also measured before and after supplementation. RESULTS: Nine of the patients with renal stones were magnesium deficient, as were six normal subjects from the same area, whereas only one and two of the rural Central and urban North-east Thais had magnesium deficiency. The magnesium status of the 13 deficient subjects significantly improved (P = 0.003) after supplementation with chelated magnesium. The supplement also caused a significant increase in mean (sd) urinary citrate excretion, from 237.7 (173.1) to 361.3 (284.1) mg/day (P= 0.012). CONCLUSIONS: These results indicate that magnesium deficiency is common among patients with renal stones in rural North-east Thailand, and that the probable cause is environmental. The increase in urinary citrate excretion after magnesium supplementation suggests that magnesium is important in renal stone formation, through its effect on citrate metabolism.

Potassium needed for maintaining its balance in healthy male subjects residing in an area of low potassium intake and with a high environmental temperature.

Low potassium (K) intake and high prevalence of hypokalemia and hypokaliuria among rural dewellers in the northeast region of Thailand have been repeatedly reported and they were speculated to be in a state of low K status. In this communication we studied K balance of 10 rural (R) and 5 urban (U) male subjects in this region during a 10-day period of semi-free-living and eating group-selected diets. While K in intake, 24-h urine and feces were measured daily in all subjects, the direct measurement of K lost in sweat was made only in one subject coded R3. These parameters were then used to calculate the K balance. The results showed that mean K intakes were 1731 +/- 138 and 1839 +/- 145 mg/day for R and U subjects, respectively. Their mean K balances, calculated by subtracting the K excretions in 24-h urine (721 +/- 129 mg/day for R and 919 +/- 186 mg/day for U) and in feces (148 +/- 25 mg/day for R and 164 +/- 21 mg/day for U) from intakes, were +860 +/- 140 and +756 +/- 222 mg/day for R and U, respectively. In the subject R3, his mean K balances without and with subtracting the sweat K excretion (451 +/- 57 mg/day), were +847 +/- 373 and +396 +/- 344 mg/day, respectively. Regression of K balance versus intake indicated that R and U subjects needed K of 832 and 884 mg/day to stay in balance. Since the study was performed during the hot season (average temperature = 35.2 +/- 2.0 degrees C at 3 pm) and sweating was clearly observed (estimated sweat volume per day was 1927 +/- 420 ml for R and 1759 +/- 408 ml for U), therefore, K balance calculated without sweat K was overestimated. This was apparently seen in the subject R3 where he actually needed K of 1203 mg/day, instead of 814 mg/day calculated without sweat K, to stay in balance. The similarities in K balance data among the two groups suggested they both had the same food habit and K status. Our results indicate that any calculation for the levels of dietary K, or probably also for other minerals, to achieve the balance could be underestimated if loss via sweat is not taken into consideration.

Blood and urinary aggregator and inhibitor composition in controls and renal-stone patients from northeastern Thailand.

Renal-stone disease (RSD) is common in the rural communities of northeastern Thailand. We report the biochemical composition of blood and urine in 25 healthy city dwellers (G1), 12 healthy village dwellers (G2) and 25 village dwellers who had RSD (G3). They were male with a range of ages between 20 and 50 years and were free of renal failure, urinary infection, urinary obstruction and systemic illness. The results showed that hypocitraturia, hypokalemia and hypokaliuria were more common in the latter 2 groups. The 24-h urinary citrate excretion correlated significantly with urinary potassium in G3 cases (r = 0.704, p = 0.0002). After potassium chloride supplementation, serum and urinary potassium increased remarkably (p less than 0.003 and p = 0.002, respectively), whereas urinary citrate remained unchanged. Our results suggest that the predominant abnormality in our RSD patients were hypocitraturia and potassium deficiency and that these may be related.

Chemical interactions between thiamin and tannic acid. II. Separation of products.

Bio Rex 70 column chromatography and high voltage paper electrophoresis were used to fractionate and define the reaction products of thiamin-tannic acid and thiamin-tea mixtures. Fractions separated indicated the presence of (a) thiamin-tannic acid adduct(s) and several modified forms of thiamin among the products. Using radioactive thiamin and determining the intact form by scintillation counting, the extent of thiamin modification under various conditions was compared with previous results as determined by the thiochrome method. The elution profile of the thiamin-tea mixture and the electrophoretogram showed features similar to those of the thiamin-tannic acid mixture. The effectiveness of the tea extract and tannic acid in modifying thiamin was compared. Ascorbic acid was found to protect the modification of thiamin by tannic acid, not only at acidic pH as previously found, but also at neutral pH, thus making vitamin C a strong candidate for the protection of thiamin in the alimentary system.