Influences of low intensity exercise on body composition, food intake and aerobic power of sedentary young females.

The present study was designed to investigate the influences of aerobic training on the body composition, aerobic power and food intake of sedentary young females in relation to the initial levels of these variables. Thirty one untrained college females (age = 19.8 +/- 0.2 yr, stature = 154.4 +/- 0.8 cm, body mass = 53.3 +/- 1.2 kg, mean +/- SEM) participated in an exercise regimen consisting of 40% of maximum oxygen uptake (VO2max) for 30 minutes per day on a bicycle ergometer 5 times a week in a training period of 12 weeks. Food consumption was ad libitum but the content of daily food intake was recorded accurately throughout the whole training period and analyzed weekly. The average body mass index (BMI) and fat mass relative to body mass (% FM), estimated from the data of skinfold thickness, decreased significantly after the 12 wk training. There were significant negative correlations between the relative changes (% delta s) and initial levels of both body mass (r = -0.447, p < 0.05) and fat mass (r = -0.638, p < 0.05), but the corresponding correlation for lean body mass (LBM) was not significant (r = 0.186, p > 0.05). While the energy intake during the training period did not differ significantly from that during the control period on the average, the % delta value in energy intake between the two periods was negatively correlated to the energy intake during the control period (r = -0.604, p < 0.05). In addition, there were low but significant negative correlations between both the initial levels of BMI and %FM and % delta in energy intake; r = -0.413 (p < 0.05) for BMI and r = -0.393 (p < 0.05) for %FM. However, no significant correlations were found between % delta in energy intake and those in body composition variables (r = 0.116 to 0.237, p > 0.05). On the average VO2max relative to body mass (VO2max/BM) increased significantly, but VO2max relative to LBM (VO2max/LBM) did not. However, not only VO2max/BM but also VO2max/LBM was negatively correlated to the initial level; r = -0.671 (p < 0.05) for VO2max/BM and r = -0.625 for VO2max/LBM. Thus, the present results indicate that whether the body composition, food intake and aerobic power of sedentary young females can be modified by the exercise regimen eliciting 40% of VO2max depends on their initial levels.

Time-lag effect of dietary fiber and fat intake ratio on Japanese colon cancer mortality.

The daily intake of total dietary fiber (TDF) was evaluated from data of the National Nutrition Survey (NNS) in Japan for 41 years since 1947. An interrelationship between the nutrient intake, including TDF, and the mortality from colon cancer in Japanese people was calculated by a simple correlation coefficient and time-series correlation coefficient. TDF intake per capita decreased rapidly from 27.4 g in 1947 to 15.8 g in 1963, and subsequently decreased by a lesser rate to 15.3 g in 1987. Fat intake increased rapidly from 18.0 g in 1950 to 56.6 g in 1987. The age-adjusted mortality from colon cancer shows a significant positive correlation with both the intakes of animal protein and of total fat, and the fat energy ratio. A time-series analysis indicates that the mortality from colon cancer was negatively correlated with TDF with a 15-27 year delay, the maximum correlation existing with a 23-year lag (r = -0.947). The TDF intake was less than 17.9 g in 1965. At the same time, the mortality from colon cancer increased rapidly. A fat/TDF ratio above 3.0 resulted in a rapid increase in colon cancer mortality. The non-adjusted mortality from colon cancer has much the same interrelationship with TDF and fat intake as the adjusted figures. It is suggested that the cause of the increased mortality from colon cancer in Japan is positively related to the increased intake of fat and protein. In addition, the decrease in TDF intake has accelerated the mortality of colon cancer after a delay of 23-24 years. The importance of fat/TDF as a nutritional criterion for the incidence of colon cancer needs to be better recognized.

[The chemistry of porphyrins and their precursors on the heme biosynthetic chain].

There are two ways for numbering the positions of C and N atoms in the porphyrin ring. The Fisher numeration is relatively old styled, but at present, is most widely employed among chemists because of its simpler and easier technique than that of the IUPAC numeration which is more effective in numbering the complicated structures of recent synthetic chemical including recent porphyrin derivatives. Uroporphyrinogen III, Coproporphyrinogen III and Protoporphynogen IX have been described as the porphyrin intermediates in heme biosynthesis. Uroporphyrins, Coproporphyrins and Protoporphyrin IX which are found in blood, urine, feces of either normal or porphyric subjects are their auto-oxidized products and can not be true intermediates for heme biosynthesis except for Protoporphyrin. Delta aminolevulinic acid (ALA), Porphobilinogen (PBG) and Hydroxymethylbilane have been described as the precursors to porphyrin biosynthesis. Besides the recent advance of porphyrin research within the limit of medical fields the pure organic chemistry of porphyrins symbolized by its large electron conjugated system have been unexpectedly developed for the last 20 years, suggesting that its application will quickly be extended to the new fields of macromolecular engineering and polymer electronics.

Direct injection method for quantitation of delta-aminolevulinic acid in urine by high-performance liquid chromatography.

A highly sensitive and simple method for determining delta-aminolevulinic acid (ALA) in urine was established, using direct injection of urine into a high-performance liquid chromatographic column, with fluorometric detection after post-column derivatization with o-phthalaldehyde (OPA). The recovery of ALA was about 100% and ALA was completely separated on an ion exchange column (retention time, 38 min). The detection limit for ALA was 10 pmol (S/N = 2). The mean levels of urinary ALA of 10 healthy volunteers, 4 patients with acute intermittent porphyria, and 2 workers occupationally exposed to lead were 0.76, 5.25, and 23.54 mg/l, respectively. Because of its simplicity, the method is considered to be suitable for routine analysis of urinary ALA in the clinical laboratory.

Effect of fish oil and safflower oil in common Japanese diet on human plasma fatty acid composition.

The influence of fish oil and safflower oil contained in the common Japanese diet as the main dietary polyunsaturated fatty acid source on plasma fatty acids in ten female student volunteers (21-22 years old) was investigated. The subjects were divided into two groups and fed the experimental diets for five days. The total daily fat intake in the fish diet and safflower oil diet was 54.4 g and 56.2 g, respectively, and the fat derived from fish and safflower oil was 16 g and 23 g, respectively. The proportion of linoleic acid was reduced in the plasma of subjects fed the fish diet and increased in the plasma of subjects fed the safflower oil diet. The plasma levels of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were significantly elevated in the fish diet group. The ratio of EPA/arachidonic acid (AA) was higher, and those of n-6/n-3 and n-9/n-3 were lower in the plasma of subjects fed the fish diet when compared to the results obtained from plasma of subjects fed the safflower oil diet. From these results, it seems likely that fish oil in the common Japanese diet is a favorable source of plasma EPA and DHA even in such short term supplementation and with such a small amount of daily consumption.

Radiochemical microassay of delta-aminolevulinic acid dehydratase activity in whole blood and bone marrow.

We describe an assay for delta-aminolevulinic acid dehydratase (EC 4.2.1.24) activity. Radioactive [14C]porphobilinogen, formed by action of this enzyme on [14C]delta-aminolevulinic acid, is purified by passage through an ion-exchange chromatographic column before measurement with a liquid scintillation counter. The radioactive substance in the final solution was identified as solely [14C]porphobilinogen by paper-chromatographic analysis. The present assay procedure requires only a 0.1-microL sample of blood and is about 100-fold more sensitive than the conventional colorimetric methods involving Ehrlich's reagent. Using this method, we found that activity of this enzyme in the bone marrow of rats decreases abruptly and sharply two weeks after birth.

Decreased liver delta-aminolaevulinate dehydratase activity in porphyria cutanea tarda and in alcoholism.

delta-Aminolaevulinate dehydratase activity was measured in liver biopsy specimens from 13 patients with porphyria cutanea tarda, 13 alcoholics and 10 control subjects. The mean enzyme activities in liver of porphyria cutanea tarda and alcoholics were 34% (P less than 0.001) and 49% (P less than 0.001) respectively of the control level. Heat treatment of liver supernatant caused slight inhibition of the enzyme activity in porphyria cutanea tarda and in controls. Addition of Zn2+ to liver supernatants slightly increased the enzyme activity in both porphyria cutanea tarda and controls. The addition of liver supernatant from the porphyria cutanea tarda to purified bovine delta-aminolaevulinate dehydratase did not result in suppression of the enzyme activity. The apparent Km value of delta-aminolaevulinate dehydratase was 4.3 X 10(-4) mol/l for porphyria cutanea tarda livers and 3.3 X 10(-4) mol/l for control livers. The difference between the two was not significant.

Alteration of activities of delta-aminolevulinic acid synthase, delta-aminolevulinic acid dehydratase and delta-aminolevulinic acid dehydratase inhibitor in the bone marrow cells of lead poisoned rats.

A new modified method for the determination of delta-aminolevulinic acid (ALA) dehydratase activity has been developed. This modified method involves addition of 0.1 mM Zn2+ and then preheating the enzyme solution at 60 degrees C for 5 min before following commonly used procedures. The ALA dehydratase activity in the peripheral blood of lead poisoned rats, determined by this procedure, was approximately 7.5-fold higher than control values. The activity of ALA dehydratase in the bone marrow cells of lead poisoned rats increased approximately 2-fold. These increases were accompanied by a simultaneous decrease in an inhibitor specific for ALA dehydratase. Consequently, these results suggest that ALA dehydratase is induced after the reduction of ALA dehydratase activity, and that ALA dehydratase activity is controlled by a new specific ALA dehydratase inhibitor.

Changes in aminolevulinate synthase and aminolevulinate dehydratase activity in cirrhotic liver.

Delta-Aminolevulinate synthase and delta-aminolevulinate dehydratase activities were determined in liver biopsy specimens obtained from 12 patients with hepatic cirrhosis. Delta-Aminolevulinate synthase activity was determined by the incorporation of [1,4-14C]succinyl coenzyme A into delta-aminolevulinate. The mean activity of delta-aminolevulinate synthase was significantly higher in cirrhotic liver specimens (mean +/- SE, 193.7 +/- 34.5 picomoles delta-aminolevulinate per milligram protein per 30 minutes) than in controls with minimal histologic changes (32.7 +/- 13.6, p less than 0.01). Furthermore, the mean activity of delta-aminolevulinate synthase was higher in micronodular cirrhosis (281.6 +/- 58.8) than in the other types of cirrhosis (131.0 +/- 23.1, p less than 0.05). Levels of indocyanine green retention at 15 min correlated with the activity of hepatic delta-aminolevulinate synthase (p less than 0.05). The mean activity of delta-aminolevulinate dehydratase, in contrast, was significantly lower in cirrhotic liver specimens (9.4 +/- 1.3 nanomoles porphobilinogen per milligram protein per hour) than in controls (22.0 +/- 2.6, p less than 0.05). These results suggest that the extent of liver injury or the degree of portosystemic shunting, or both, influence the rate of hepatic heme biosynthesis.

Increase of delta-aminolevulinic acid dehydratase (ALAD) in rat erythrocytes in lead poisoning.

The well known fact that the activity of delta-aminolevulinic acid dehydratase (ALAD: EC 4.2.1.24) is reduced in red cells of animals with lead poisoning was found to be upset, by using a modified method of Gibson's original procedure, for determination of activated ALAD activity. The modified method involves addition of 0.2 mM Zn2+ and then preheating the enzyme solution at 60 degrees C for 5 min before following Gibson's original procedure. With this methodological modification, the ALAD activity of erythrocytes of rats poisoned with lead was found increased. Furthermore, the enzyme was purified from the peripheral blood of lead-poisoned rats. ALAD protein in peripheral blood was also determined by single radial immuno diffusion using rabbit anti-serum raised against rat liver ALAD. As the result, the ALAD activity obtained from the modified method was found to be directly proportional to the absolute amount of enzyme proteins determined both by chemically and immunochemically. The modified method for measuring true ALAD content in blood cells in lead poisoning is more reliable than previous ones.

Induction of delta-aminolevulinic acid synthase and delta-aminolevulinic acid dehydratase in normal human bone marrow cultures.

Activities of delta-aminolevulinic acid (ALA) synthase and ALA dehydratase, the first and the second enzymes of the heme biosynthetic pathway, were determined in erythroid colonies derived from normal human bone marrow in culture. ALA synthase and ALA dehydratase were induced when normal human bone marrow cells were incubated in the presence of erythropoietin (Ep) in culture, and the extent of induction of ALA synthase as well as ALA dehydratase was dependent on Ep concentrations and culture periods. Both ALA synthase and ALA dehydratase were increased in cultured erythroid cells before the appearance of morphologically recognizable hemoglobinized colonies, corroborating the sequential induction of heme biosynthetic pathway enzymes in human bone marrow erythroid cells.

A case of lead intoxication: clinical and biochemical studies.

A 23-year-old Japanese male with severe lead intoxication accompanied by hemolytic anemia was studied. The patient had taken 12 g to lead in about a month. He had moderate hemolytic anemia (Hb 8.9 g/100 ml) with reticulocytosis ranging from 2.5 to 11.7%. Peripheral blood smear showed nucleated red cells (42/200 white blood cells) and marked basophilic stippling in the red cells. Activities of erythrocyte enzymes were either normal or increased except for pyrimidine 5'-nucleotidase (P5N) and delta-aminolevulinic acid dehydratase (ALA-D) both of which were found to be decreased, being 48.8% and 4.1% of the normal controls respectively. Erythrocyte reduced glutathione (GSH) was high (145.6 mg/100 ml RBC). Erythrocyte pyrimidine nucleotides were accumulated up to 10.2% of total nucleotides. The level of lead in peripheral blood was 112 microgram per 100 ml blood. Ca2+-Na2-EDTA was given to the patient as treatment. The level of lead in the blood decreased gradually and hemolytic anemia improved. Basophilic stippling in the red cells disappeared. These results confirmed the findings of Valentine et al [1] that lead-induced deficiency of P5N resulted in basophilic stippling and hemolytic anemia just like hereditary hemolytic anemia due to P5N deficiency.

Excretion of porphyrins in urine and bile after the administration of delta-aminolevulinic acid.

Excretion of porphyrins into bile and urine after intravenous injection of delta-ALA was studied in three patients with catheters inserted into the bile duct because of biliary obstruction and in two healthy volunteers. Excretion of porphyrins into bile increased in response to increasing doses of delta-ALA--up to 18 mumol/kg. On the other hand, excretion into urine reached a constant rate at 2 to 4 mumol/kg delta-ALA and did not increase further with larger doses. These findings suggest that transport of porphyrins across the liver cell membrane to the blood must be an important factor in determining the rate of excretion into the urine. After administration of delta-ALA,excretion of coproporphyrin III into urine increased more than that of coproporphyrin I. As a result, the former was the predominant form of urinary coproporphyrin. When radioactive delta-ALA was administered intravenously, far greater radioactivity was recovered in urine as coproporphyrin III than as coproporphyrin I. These results indicate that only a small portion of urinary coproporphyrin I is derived from the liver. A possible source of coproporphyrin I may be erythropoietic tissues, since the amount of urinary coproporphyrin I was considerably decreased in patients with severely suppressed erythropoiesis.

Uroporphyrinogen III cosynthetase in liver and blood in the Dubin-Johnson syndrome.

The activities of uroporphyrinogen III cosynthetase in blood lysates from five patients with the Dubin-Johnson syndrome (DJS) and four control subjects and in liver homogenates from four patients and four control subjects were determined. No significant difference was found in enzyme activity between the two groups in either blood lysate or liver homogenate. These results indicate that low urinary coproporphyrin III output in the DJS is not due to deficiency of uroporphyrinogen III cosynthetase in the liver and the erythropoietic system.