The calcium balance of 12 presumed healthy human young adult subjects was assessed. Subjects consumed a constant laboratorycontrolled diet supplemented with one of four calcium-fortified food products: orange juice (OJ), milk (M), experimental pasteurized processed cheese (T), soda (S), or a calcium carbonate plus vitamin D tablet (CC). Study length was 6 weeks with seven-day experimental periods (2days allowed for adjustment with 5-days combined for purposes of analysis). All urine and fecal samples were collected by the subjects for the duration of the study. Blood samples were drawn at the end of each experimental period. Urine and fecal calcium contents were determined. Blood samples were analyzed for alkaline phosphatase. Results of this study indicate a higher fecal calcium content (mg/day) when subjects consumed CC and T, and when subjects consumed self-selected diets, than when given S, M, or OJ. Urinary calcium excretion was significantly lower when subjects consumed OJ than when they consumed M, T, or their self-selected diets. A significantly larger positive calcium balance was demonstrated when subjects consumed OJ as compared to T. Fecal transmit time did not vary significantly. Serum alkaline phosphatase was significantly lower when subjects consumed T than when they consumed self-selected diets.
Genotoxic effect of agriculture-used concentration of organophosphorous pesticide, Malathion, is decreased by the dietary concentration of sodium salt of L-ascorbic acid for parameters like mitoticindex and clastogeny in onion root-tip cells, clastogeny and meiotic-index in mice, and lethal mutation rate in Drosophila melanogaster. The vitamin itself is not genotoxic, and its concurrent administration is more effective than pretreatment with it. Possible mechanism of such vitamin Cmediated minimization of pesticide-genotoxicity is discussed
[3H] Pyridoxamine was orally administered to mice in physiological amounts, and the distribution of isotope between the six recognized forms of vitamin B6 and pyridoxac acid was determined at different times in the intestine, liver, blood, and brain. After 7 min about 50% of the radioactivity in pyridoxamine had been absorbed by the intestine and transported to the blood and other organs. Labeled pyridoxal phosphate was found in the intestine and liver. Labeled pyridoxamine could not be detected in the peripheral blood, but substantial amounts of labeled pyridoxal and pyridoxal phosphate were found in the blood. However, when a large amount (40-140 nmol) was given, a significant amount of labeled pyridoxamine was found in the blood, together with labeled pyridoxal and pyridoxal phosphate. These results suggest that the intestine and/or liver play a major role in completely converting physiological amounts of pyridoxamine to circulating pyridoxal, which is then taken up and phosphorylated by other organs.
The effect of vitamin B6 deficiency was studied on glycogen metabolism in the gastrocnemius muscle, heart, and liver of rats. The glycogen phosphorylase activities in the gastrocnemius muscle and heart but not in the liver of vitamin B6-deficient rats were significantly decreased. The decrease in the enzyme activity in the gastrocnemius muscle was due to decrease in the amount of enzyme. The glycogen content of the muscle of vitamin B6-deficient rats was higher than that of the controls, but the glycogen content of the liver was similar in the two groups. These data suggest that glycogen degradation was impaired in the muscle but not the liver of vitamin B6-deficient rats.
It is well known that vitamins E and C exhibit synergistic action in in vitro systems, but with regard to in vivo systems, much of the available data are confusing. To elucidate this problem we used a new nutant of Wistar-strain rats that cannot synthesize vitamin C, namely, DDS rats. Two experiments were planned: (1) during development of vitamin E deficiency, whether vitamin C could spare the consumption of vitamin E; and (2) under conditions of a regular level of vitamin E intake, whether different dose levels of vitamin C can affect vitamin E concentration in tissues. The results obtained show that with vitamin C intake, higher levels of vitamin E were deposited in tissues in both experiments. With the development of vitamin E deficiency, rats in the group with a higher dose of vitamin C deposited higher concentrations of α-tocopherol. With simultaneous administration of vitamin E and vitamin C to the same mutant rats, the rats in the group with a higher dose of vitamin C deposited higher levels of vitamin E in all tissues tested. Thus, we concluded that vitamin C can spare the consumption of vitamin E in vivo as well as in vitro.
The effect of ascorbate (AsA) on the synthesis of carnitine from γ-butyrobetaine (BB) in primary cultured guinea pig hepatocytes was investigated. The hepatocyte monolayers preloaded with AsA were incubated for 4 h in medium with various concentrations of BB as the precursor of carnitine. The accumulation of carnitine reached a maximum when the cells were incubated with 0.05-1.0mM BB and significantly decreased with excess BB (5mM). In contrast, increasing concentrations of AsA supplemented to medium led to an increase in carnitine content, but AsA and total AsA contents in cells decreased by BB supplementation. Regarding the enhancement of hydroxylation of BB in the hepatocytes, AsA was the most effective among such other reducing agents as glutathione and dithiothreitol. Although erythorbate (ErA) also stimulated the hydroxylation of BB, carnitine content in cells preloaded with ErA was only 60% of that with AsA. These results suggest that AsA is specifically required for the hydroxylation of BB. Furthermore, AsA can regulate carnitine synthesis in the primary cultured guinea pig hepatocytes.
We monitored the absorption and movement of dietary soluble components along the gastrointestinal tract of rats by using p-aminobenzoic acid (PABA) as a marker after feeding 8 and 16% casein or soybean protein isolate (SPI) diets containing 1 % PABA. The portal concentration of PABA, as an index of absorption, increased rapidly and reached the same high level 10min after the feeding of all four diets, and the increased level of portal PABA was maintained for 30-80 min in each group. The increased levels of the SPI-fed groups continued longer than those of the casein-fed groups. In contrast, the gastric emptying rate slowed after 20min in all the groups, and the gastric emptying of PABA for the initial 60min in the 8% casein group was significantly faster than that in the 8% SPI group. The PABA content of the first small intestinal segment, which may be influenced by small intestinal transit, was higher in the casein group. These results indicate that the absorptive rate of PABA is determined not only by gastric emptying but also by small intestinal transit. The gastric emptying and the content of PABA in the first segment of the small intestine was not correlated in 8% protein groups. This suggests that the effect of SPI on gastrointestinal movement is different from that of casein.
Young male Sprague-Dawley rats were fed diets containing 10% fat with P/S and n-6/n-3 ratios of 1.2 and 5.0, respectively, and differing levels of dietary cholesterol (0.05 to 1.0% by weight) for 3 weeks, following which the tissue lipid concentration, fatty acid composition, desaturation of linoleic acid, and eicosanoid production were examined. The composition of dietary fat was that recommended for the prevention of atherosclerosis. Dietary cholesterol did not largely influence the concentration of serum cholesterol, but it markedly increased liver cholesterol in a dose-depended manner. The Δ6-desaturase activity in liver microsomes, linoleate desaturation index in liver phosphatidylcholine, and the production of prostaglandin by the aorta and thromboxane A2 by platelets all decreased to a similar extent in relation to dietary cholesterol above 0.2%. Thus, dietary cholesterol influenced various lipid parameters characteristically even when dietary fat with a fatty acid composition desirable for the prevention of atherosclerosis was consumed simultaneously. The dietary cholesterol level of 0.2% was the point of maximum influence in rats upon the indices examined.
The fatty acid composition of serum phospholipids of 277 persons, aged 63-97y (average 78y), was measured. Subjects had been living independently in a facility with full food service for 1y or more. Eleven saturated and unsaturated fatty acids were detected in all the subjects. Stearic acid (18:0) was positively (p=0.028) and dihomo-gamma-linolenic acid (20:3 n-6) was negatively (p=0.012) related to age. Arachidonic acid (20:4 n-6) tended to decline with age (p=0.063). In addition, the oleic acid (18:1 n-9)/18:0 ratio decreased significantly with age (p=0.024). 18:0 and total saturated fatty acids were lower, and linoleic acid (18:2 n-6) and 20:4 n-6 and n-6 fatty acids were higher in males than in females. These results suggest deficits in n-6 essential fatty acids as age advances, particularly in females.
The object of this experiment was to examine whether the administration of clenbuterol exerts clenbuterol's repartitioning effects in rats with hypothyroidism induced by the oral administration of propylthiouracil (PTU). Male Wistar rats aged 5 weeks were divided into 4 groups: control, PTU administrated (PTU), Clenbuterol administrated (CL), and PTU plus clenbuterol administrated (PTU/CL) groups. Rats were raised for 7 weeks at 26°C and given 13g of diet every day. The PTU and PTU/CL groups were fed a basal diet containing PTU at the level of 30mg/kg diet throughout the experimental period. Clenbuterol was added to the diet of the CL and PTU/CL groups at the dose of 0.1ppm from the 3rd week. Serum thyroxine concentrations of rats were significantly lower in rats in the PTU and PTU/CL groups than those in the control and CL groups. Thus, the administration of PTU succeeded to induce hypothyroidism. The clenbuterol administration seemed to exert its repartitioning effects in euthyroid rats, while the administration neither increased body protein nor decreased body fat in hypothyroid rats. This result therefore suggests that the effects of clenbuterol on the alteration of body composition may vary with the level of thyroid activity in rats.
Highly purified lysosomes were isolated from the livers of control and pyridoxine-deficient rats. The calculation of the lysosomal protein contents indicated that the livers of both groups of rats contain virtually the same amounts of the lysosomal proteins (12.0 and 13.0mg lysosomal proteins/g liver proteins for the control and pyridoxine-deficient rats, respectively). The immunoblotting of the lysosomal proteins with anti-cytosolic aspartate aminotransferase (cAspAT) showed 46 kDa band, corresponding to the subunit molecular weight of cAspAT, as well as the bands representing degradative intermediates of cAspAT. The relative amounts of the immuno-reactive substances were estimated by scanning the immuno-stained bands and measuring the densitometric tracings. It was found that the lysosomes in the pyridoxine-deficient rat liver contain almost twice as much cAspAT and its degradative intermediates as those in the control rat liver. On the basis of these observations, it was concluded that the increased rate of degradation of cAspAT in the liver of the pyridoxine-deficient rats is brought about by the increased rate of sequestration of cAspAT into lysosomes.
The effects of selenium (Se) deficiency on urinary ketone body excretion in starved rats were examined. Rats were fed a basal diet which was Se-deficient (Se content: 0.011μg/g) or a Se-adequate diet (the basal diet supplemented with 0.1μg Se/g as sodium selenite). On the 11th and 22nd week of the feeding period, Se-deficient status in rats fed the basal diet was verified by the observation that the Se content and glutathione peroxidase activity in their plasma, erythrocytes, and livers were markedly lowered. On the 4th, 6th, 11th, 15th, and 22nd week, the rats were starved for 48h and the urinary excretion of ketone bodies (acetoacetate (AcAc) and 3-hydroxybutyrate (3-OHBA)), urea, and creatinine were examined. The urinary excretion of AcAc and 3-OHBA during the second 24h of the 48-h starvation period were markedly higher in the Se-deficient rats than in the Se-adequate rats for all weeks examined, while the urine volume and the excretion of urea and creatinine were similar in the Se-deficient and Se-adequate rats, irrespective of the feeding period and the number of hours of starvation. On the 22nd week, the plasma ketone body levels were also determined and significantly higher plasma 3-OHBA levels were observed in the Se-deficient rats than in the Seadequate rats 72h after starvation began. These results indicate that Se deficiency causes an increase of urinary ketone body excretion in starved rats and that the increase is ketone-specific with no changes in major urinary profiles.
The fatty acid composition of samples of breast milk obtained from well-nourished Nigerian and Japanese women was determined by gas chromatography. The cultural differences in dietary intake was reflected in the fatty acid composition of breast milk samples. The milk of Nigerian women contained a significantly higher percentage of saturated fatty acids (48.75%) than that of Japanese women (46.65%). Nigerian milks were also richer in arachidonic (20:4 n-6), eicosatrienoic (20:3 n-6), and docosatetraenoic (22:4 n-6) acids. Conversely, the milk of Japanese woman contained significantly higher percentages of monounsaturates as palmitoleic, heptadecenoic, oleic, and polyunsaturates of n-3 series as α-linolenic, eicosapentaenoic, and docosahexaenoic acid.