Castrated male rats were injected intramuscularly with testosterone (5mg/day) and dehydroepiandrosterone (5mg/day) continuously for two weeks. Animals were sacrificed and the various metabolites of ascorbic acid in liver and urine were determined. Total ascorbic acid and the activities of hepatic ascorbic acid synthesizing enzymes were also determined. The activities of both liver and kidney ascorbic acid degrading enzymes were studied. In contrast to testosterone, dehydroepiandrosterone failed to modify the ascorbic acid metabolism in castrated rats. Testosterone administration to castrated rats was found to restore the hepatic contents of as-corbic acid metabolites to the sham control levels. It was suggested that the functional OH group at C-17 in androgens might have some role in as-corbic acid metabolism. Castration was found to cause decrease in the activities of two out of the three biosynthetic enzymes of ascorbic acid, namely D-glucurono-δ-lactone hydrolase and L-gulono-γ-lactone oxidase in rat liver. The activity of L-gulono-γ-lactone hydrolase was found to be unchanged in castration. This result which is in slight disagreement with the earlier work of STUBBS et al. has been discussed. Testosterone was observed to restore the decrease in the activities of both D-glucurono-δ-lactone hydrolase and L-gulono-γ-lactone oxidase in castrated rats. Testosterone was also found to restore the increased activity of both renal and hepatic dehydroascorbatase observed in castration to the level of sham control rats. However, exogeneous administration of testosterone intramuscularly (5mg/day) for two weeks to normal rats did not show any significant alteration in the ascorbic acid metabolism.
A study of the parameters has been made of the assay of the specific activities of the succinate dehydrogenase-coenzyme Q10 reductase in mitochondrial preparations from leucocytes to reveal saturation or a deficiency of coenzyme Q10 at its site. These parameters include the key steps from the drawing of blood through the differential determinations for this enzyme system. The variations in the specific activities of the CoQ10-enzyme, both in the absence and in the presence of coenzyme Q3, was about 10% (mean value). The variations in the final and important criterion, i.e., the deficiency of CoQ10-enzyme activity was about 7%. The variations were not significantly greater, when compared as groups, for duplicate blood samples drawn immediately and sequentially from the same patient. The data from blood samples collected from the same patient over weeks and months of time showed variations in the specific activities of this CoQ10-enzyme which are believed to be primarily due to changes in the metabolism and/or nutrition of the patient. Initial data point to at least some correlation of the deficiencies of CoQ10-enzyme activities in leucocytes and skeletal muscle of the same patient. In the future, primary assays for human deficiencies of coenzyme Q10 might be based on leucocytes with subsequent assays of other tissues as specifically justified.
Distributions of thermostable thiamine-inactivating factors in about 10 kinds of ferns and brackens and 42 kinds of other plants were investigated. It was observed that besides ferns and brackens, some plants (most of them greenish or yellowish in color) had thermostable thiamine-inactivating activities, and that shiitake, okra, fukinoto (butterbur flower stalk), diluted water extract of green tea, and diluted coffee had activities which oxidized thiamine into thiamine disulfide. The present study showed that one of the factors isolated from fern 3, 4-dihydroxycinnamic acid (caffeic acid) and catechol distributed in plants accelerated decomposition of thiamine at pH 7-7.5 into 2-methyl-4-amino-5-aminomethyl-pyrimidine, decomposing the thiazole moiety, probably into γ-aceto-γ-mercapto-propylalcohol and formic acid. However, some flavonoids, especially 6, 7, 4'-trihydroxyisoflavone (Factor 2) were proved to have the ability to accelerate oxidation of thiamine into thiamine disulfide at pH 7.5. Estimation was made of the decomposition products of thiamine with caffeic acid, catechol and Factor 2 under certain conditions.
An attempt was made to elucidate the interaction between PCB toxicity and vitamin A. The effects of vitamin A addition or vitamin A deficiency in altering the toxicity of dietary PCB were examined. Rats fed a 0.1% PCB diet supplemented with 3, 400 IU of vitamin A for 6 weeks showed better growth than those fed a 0.1% PCB diet only. However, rats given a vitamin A deficient diet with 0.1% PCB showed a significant growth retardation than those given a 0.1% PCB diet only. All rats which were fed a vitamin A deficient diet with PCB closed their eyes 50% or entirely in the last period of the experiment, but such symptom was not seen in the rats given a 0.1% PCB diet only or a vitamin A deficient diet. Vitamin A content in the liver decreased significantly with 0.1% PCB administration. It was found that a larger supply of dietary vitamin A than the level contained in the basal diet is required to prevent, to some extent, the growth retardation by PCB administration and to sustain the same level of vitamin A content in the liver of rats fed the same 0.1% PCB diet as that of basal diet group. It was concluded that animals fed PCB require more vitamin A than usual. This suggests the possibility that vitamin A may play a role in the detoxication of PCB.
Simultaneous determinations of erythrocyte transketolase activity in maternal umbilical cord and newborn baby's blood of 60 full term healthy women from a low socioeconomic group of Bangkok were conducted. Forty-two percent of the women were found to be deficient as judged from thiamine pyrophosphate (TPP) effect. The erythrocyte transketolase activities in umbilical cord and newborn baby's blood were significantly higher than those in maternal blood. During the neonatal period, the thiamine status was normal even though the mother was considered to have a deficiency. The importance of thiamine supplementation to lactating women is discussed.
Studies were made on the effects of splenectomy on the red cells of rats receiving various dietary levels of protein. Anemia was pronounced and the survival time of red cells (T/2 Rbc) was reduced in rats on a protein-free diet as compared with rats on standard and low protein diets. The spleen appeared to be relatively hypofunctional in rats on low protein diets since (a) splenectomy had the least effect on increasing T/2 Rbc in rats on low protein diet and largest effect on survival of Rbc's in rats on a normal diet; (b) splenectomy had the least effect on osmotic fragility of red cells in rats on low protein diet and the most effect was shown on osmotic fragility of rats on normal diet; (c) the weight of the spleen was least in rats on a low protein diet in comparison with the other two groups. The red cells of normal rats on a protein-free diet were most sensitive to lytic effect with lysolecithin, and Rbc's from splenectomized rats were more resistant to osmotic lysis than Rbc's from intact rats. The decrease in the T/2 Rbc and the sensitivity to a hemolytic agent (lysolecithin) of cells of rats on low protein or protein-free diet observed in this study may be related to the mechanism of anemia during inadequate protein nutrition.
Serum proteins of 44 persons from a Bangkok university and 53 persons from a rural area in northeast Thailand were examined by electrophoresis in polyacrylamide gel. Serum proteins in the prealbumin and pretransferrin range, including transferrin, were determined quantitatively. The transferrin level and the levels of some alpha-l-globulin proteins were found to be significantly higher in the rural group. The role of nutritional factors in causing these differences is discussed.
In order to observe the influence of intestinal microbes, nitrogen (N) of the carcasses and of the gut contents of 80-day-old germfree (GF), Escherichia coil (E. coil) or Staphylococcus epidermidis (Staph.) monocontaminated (at 56 days of age) gnotobiotic (GB) and conventional (CV) mice was estimated. The body weight of CV mice was greater than that of GF and both GB mice. The same tendencies were also shown in the weights of liver and kidney. However, there were no remarkable differences between GF and GB mice. Total N of the whole carcass per 100g of body weight (except for intestinal contents) of CV mice was higher than that of other mice. The rank was CV, Staph., E. coli and GF mice. There was no major difference in 15N accumulation in the whole carcass, liver and leg muscles of three mice in each group two days after they were given a 0.2% 15N-labelled secondary ammonium phosphate-supplemented diet in any group, but accumulation in CV mice tended to be higher than in GF and GB mice. Total N of the whole intestinal contents per 100g of body weight was high in GF, E. coil, Staph. and CV mice in that, order. N in cecal contents in GF and both GB mice was remarkably higher than that in CV mice. The ratio of protein N to total N of gut contents showed almost the same tendencies in all groups until the lower part of the small intestine, however from the cecum the tendencies were different. CV mice showed an especially high protein N ratio and high total N per unit chromic oxide of intestinal contents until the cecum, but they decreased in the colon and rectum, which might suggest more reabsorption of non-protein N in the cecum, colon and rectum than in GF and both GB mice.
The nutritional effect of a diet containing amino acid mixture simulating casein was compared with that of casein diet using the rat repletion method. The repletion of rats fed amino acid diet ad libitum was lower than that with a casein diet whether rats were depleted by the 7-day fasting or by the 20-day feeding of nonprotein diet. The use of spacepair-feeding in the repletion tests resulted in approximately similar re-pletion responses to both the diets. These results confirm that the in-ferior repletion response to amino acid diet under ad libitum feeding conditions may be due to the lower food intake when compared to the response to the casein diet.