Consecutive zinc balance trials in growing rats

Rats were fed a purified egg white-based diet containing 5 ppm Cu and 2, 14, or 57 ppm Zn. Zinc and copper balances were determined for eight consecutive weekly trial periods. The zinc-deficient group almost ceased to gain weight and was in slightly negative zinc balance. Groups of rats fed 14 and 57 ppm Zn gained weight at equal rates. These groups were in strongly positive zinc balance for four weeks; thereafter, they fed 57 ppm Zn retained about two times as much zinc as did the group fed the diet containing 14 ppm Zn. All groups were in null or slightly negative copper balance throughout the trial. These results suggest that zinc accumulation may be homeostatically controlled to a level in excess of that needed for maximum growth.     

Cadmium accumulation, zinc status, and mineral bioavailability of growing rats fed diets high in zinc with increasing amounts of phytic acid

Five groups of individually housed albino rats (n=7, initial average weight=48 g) were fed diets based on egg albumen and cornstarch (basal diet 8.2 g Ca, 6.0 g P, 0.7 g Mg, 225 mg Zn, 150 mg Fe, 60 mg Mn, 8 mg Cu, and 5 mg Cd) over a 4-wk period. Group I (control) was fed the basal diet free of phytic acid (PA). In groups II, III, IV, and V, cornstarch was replaced by 3.5, 7.0, 10.5, and 14.0 g sodium phytate/kg diet, respectively. Daily gain, feed efficiency, Zn status (Zn in plasma, femur, testes, liver and kidneys, activity of the plasma alkaline phosphatase) and apparent absorption of Zn, Fe, Cu, and Mn remained unchanged by the different dietary treatments. PA decreased apparent Mg absorption significantly and apparent absorption of Ca in tendency. Increasing the amount of phytate caused a corresponding enhancement of amount of the digestible P. Cd accumulation in the liver was not significantly altered, and kidney Cd accumulation slightly increased owing to PA. In conclusion, it was shown that under conditions of high dietary Zn, PA had only little effect on the carryover of Cd in growing rats.     

Effect of aluminium on metabolism of starch and sugars in growing rice seedlings

The effect of increasing concentrations of Al₂(SO₄)₃ in situ on the content of starch, sugars and activity behaviour of enzymes related to their metabolism were studied in growing seedlings of two rice cvs. Malviya-36 and Pant-12 in sand cultures. Al₂(SO₄)₃ levels of 80 and 160 μM in the growth medium caused an increase in the contents of starch, total sugars as well as reducing sugars in roots as well as shoots of the rice seedlings during a 5–20 days growth period. The activities of the enzymes of starch hydrolysis α-amylase, β-amylase and starch phosphorylase declined in Al-exposed seedlings, whereas the activities of sucrose hydrolyzing enzymes sucrose synthase and acid invertase increased in the seedlings due to Al³⁺ treatment. The enzyme of sucrose synthesis, sucrose phosphate synthase showed decreased activity in Al³⁺ treated seedlings compared to controls. Results suggest that Al³⁺ toxicity in rice seedlings impairs the metabolism of starch and sugars and favours the accumulation of hexoses by enhancing the activities of sucrose hydrolyzing enzymes.     

Dietary zinc effects on zinc, calcium, and magnesium content in bones of growing rats

The aim of the present study was to assess dietary zinc effects on femur weight and mineral content in growing rats. For this purpose, 70 weanling Sprague-Dawley rats were divided into four groups. Each group was subject to a diet containing 2 (BZ), 5 (DZ), 10 (MZ), and 30 (CZ) ppm zinc. The calcium and magnesium content in all diets was 5 g/kg and 507 mg/kg, respectively. The animals were kept on this regime for 28 d and then sacrificed and their femurs were removed for analysis using atomic absorption spectrophotometry. The weights of the BZ and DZ groups were significantly different from the MZ and CZ groups (38.5±10.5, 89.9±13.7, 118.6±13.6 and 134±19.9 g, p<0.01) respectively. There were no differences between the MZ and CZ groups. Femur weight also varied with dietary zinc, as it was significantly different among all groups (BZ, 265±49 mg; DZ, 380±40 mg; MZ, 452±54 mg; CZ, 735±66 mg; p<0.01). The femur zinc content varied with diets, following a different pattern than the above parameters. Femur zinc from the BZ group (51.5±5.4 ppm) was significantly different from the MZ and CZ groups (115.9±14.2 and 175.0±13.5 ppm, respectively), whereas the DZ group (62.5±11.3 ppm) did not differ from the other three groups. The femur content of calcium (BZ, 83.2±9.8 mg/g; DZ, 88.0±9.2 mg/g; MZ, 90.2±13.6 mg/g; CZ, 83.1±14.7 mg/g) and magnesium (BZ, 1.82±0.13 mg/g; DZ, 1.98±0.09 mg/g; MZ, 1.93±14 mg/g; CZ, 1.83±0.19 mg/g) were not significantly different among the groups, nor was the calcium-magnesium ratio. These results suggest that although dietary zinc deficiency retards growth and causes bone fragility, bone deposition of calcium and magnesium and its ratio are not affected.     

Effects of cadmium administration on the endogenous metal balance in rats

The concentrations of cadmium and other metal ions in selected organs, urine, and blood of female rats were measured after exposure to cadmium chloride through their diet or by oral or intravenous administration. The hematological and urinary variations were followed for 4 wk. Body weight gain and the weights of livers and kidneys from all treated groups were not significantly different from the controls. No gross morphological changes were observed in any of the tissues studied at necropsy. The accumulation of cadmium occurred in the liver and kidney. The zinc levels in these organs were elevated relative to controls, in all treated groups regardless of dose and exposure route. Copper was elevated in the liver, kidney, bone, and blood of animals subject to intravenous administration of cadmium. Hepatic iron was decreased in the dietary and orally treated groups, but was not affected in the intravenous study group. The level of magnesium in kidney was increased for all exposure routes, but that of liver was increased only in the intravenously injected groups. The changes in the concentrations of sodium, potassium, calcium, and phosphorus did not follow a specific pattern and varied from organ to organ, depending on the exposure route. The discussion includes a relationship between tissue injury and the alteration of tissue essential element concentrations.     

Skeletal effects of zinc deficiency in growing rats.

There is ample evidence that zinc plays an important role in bone metabolism and zinc deficiency has been implicated as a risk factor in the development of osteoporosis. It was the aim of the present study to investigate the skeletal effects of alimentary zinc deficiency in growing rats using quantitative bone histomorphometry. Twenty-four male Sprague Dawley rats with a mean initial body weight of 101 +/- 2 g were allocated in two groups of 12 rats each and had free access to a semi-synthetic, casein-based, zinc-deficient diet (0.76 mg zinc/kg) or to the same diet supplemented with 60 mg zinc per kg. All rats were sacrificed 42 days after the start of the experiment and the right distal femur was removed for bone histomorphometry. Relative to controls (+Zn), the zinc-deficient rats (-Zn) had a significantly lower body weight and about an 80% reduction in plasma and femur zinc concentration. The histomorphometric evaluation of the distal femoral metaphysis showed that zinc deficiency led to a 45% reduction (p < 0.01) in cancellous bone mass and to a deterioration of trabecular bone architecture, with fewer and thinner trabeculae. The osteopenia in -Zn rats was accompanied by significant reductions in osteoid perimeter (-31%, p < 0.05), osteoblast perimeter (-30%, p < 0.05), and osteoclast number (-38%, p < 0.01) relative to +Zn controls. We conclude that zinc deficiency induced low turnover osteopenia in femoral cancellous bone of growing rats. These results support the hypothesis that zinc deficiency during growth may impair the accumulation of maximal bone mass in humans; additionally, they suggest that zinc deficiency may play a role as a risk factor in the pathogenesis of osteoporosis.     

The effect of various dietary zinc concentrations on the biological interactions of zinc,copper, and iron in rats

Three groups (14 rats each) were fed one of the following diets for 8 wks: a control purified basal diet containing 12 ppm zinc, 5 ppm copper, and 35 ppm iron; the basal diet with less than 2 ppm zinc; or the basal diet supplemented with 1000 ppm zinc. Rats fed the zinc-deficient diet had decreased weight gain, moderate polydipsia, and intermittent mild diarrhea. The zinc-supplemented rats had a cyclical pattern of food intake and weight loss from weeks 5 to 8. Tissue concentrations suggest that zinc and copper were not mutually antagonistic with chronic dietary imbalances. If tissue element concentrations reflected intestinal uptake, then competition and/or inhibition of intestinal uptake occurred between zinc and iron. The fluctuations in tissue element concentrations that occurred with increased duration of the study were at variance with previous studies of shorter time periods. The dietary proportions of zinc, copper, and iron appear to influence zinc, copper, and iron metabolism at the intestinal and cellular transport levels over a given period of time.     

Role of endogenous zinc in bones of newborn rats

Concentration of abundant elements e.g. calcium as well as of elements present in trace amount e.g. zinc in mandibles of 7, 14 an 28 day old newborn rats were determined by X-ray fluorescence analysis. The measurements were carried out by using a measurement system containing X-ray tube ECLIPSE-III and X-ray and gamma ray detector XR-100T-CdTe (Amptek Inc.). Concentration of calcium and zinc depended on the region of interest on the rat's mandible due to mineralization degree conditioned by its function. Increasing age produced a remarkable increase in Ca content in contrast to Zn content in the bone tissue obtained from 7, 14 and 28 day old newborn rats. The calculated Zn/Ca concentration ratio was the biggest for 7 day old newborns and successively decreased with age indicating the important role of zinc at the beginning of bone ontogenesis.     

Structural changes in liver parenchyma of rats kept on diets with various protein contents

The influence of diets with different protein content on the liver structural organization has been studied. Adaptation processes such as hepatocyte proliferation and an increase in the number of secondary lysosomes with the following atrophy of hepatocytes were observed in rats on low protein diet. High protein diet caused hypertrophy of hepatocytes and hyperplasia of subcellular structures.     

Oxalate balance in fat sand rats feeding on high and low calcium diets

Oxalate reduces calcium availability of food because it chelates calcium, forming the sparingly soluble salt calcium-oxalate. Nevertheless, fat sand rats (Psammomys obesus; Gerbillinae) feed exclusively on plants containing much oxalate. We measured the effects of calcium intake on oxalate balance by comparing oxalate intake and excretion in wild fat sand rats feeding on their natural, oxalate-rich, calcium-poor diet with commercially-bred fat sand rats feeding on an artificial, calcium-rich, oxalate-poor diet of rodent pellets. We also tested for the presence of the oxalate degrading bacterium Oxalobacter sp. in the faeces of both groups. Fat sand rats feeding on saltbush ingested significantly more oxalate than fat sand rats feeding on pellets (P < 0.001) and excreted significantly more oxalate in urine and faeces (P < 0.01 for both). However the fraction of oxalate recovered in excreta [(oxalate excreted in urine + oxalate excreted in faeces)/oxalate ingested] was significantly higher in pellet-fed fat sand rats (61%) than saltbush-fed fat sand rats (27%). We found O. sp. in the faeces of both groups indicating that fat sand rats harbor oxalate degrading bacteria, and these are able, to some extent, to degrade oxalate in its insoluble form.     

Absorption and excretion of tablet disintegrating β-cyclodextrin polymer in rats

Absorption and excretion of a new tablet disintegrating agent, a crosslinked β-cyclodextrin polymer was investigated following per os administration in the rat. The polymer, which is insoluble but swells in water, was prepared from β-cyclodextrin by reacting with [2-¹⁴C]epichlorohydrin in an alkaline medium. Radioactivity of blood, urine, faeces, exhaled carbon dioxide and the gastrointestinal tract was determined by a liquid scintillation method. No radioactivity could be detected in the blood up to 24 h after the administration of the polymer. Radioactivity of urine and exhaled carbon dioxide together did not exceed 0·11% of the total administered radioactivity, 98% of which was found in the large intestine and the faeces. Therefore, it is assumed that β-cyclodextrin polymer could not be absorbed from the gastrointestinal tract.     

Turnover of the amino sugars of erythrocyte and thrombocyte glycoproteins in rats maintained on different carbohydrate diets

The turnover of erythrocyte and platelet glycoprotein amino sugars in rats fed carbohydrates has been studied. Partial replacement of starch by sucrose results in an almost 3-fold increase in the half-life of erythrocyte glycoprotein amino sugars and in a 2-fold increase in that of platelets as early as 14 days after keeping the animals on carbohydrates. It is concluded that study of dynamic parameters of cell amino sugars can be used for evaluation of the role played by food in metabolic and adaptive reactions both in experimental animals and man.     

Effect of dietary taurine on endogenous hypercholesterolemia in rats fed on phenobarbital-containing diets.

The effect of dietary taurine on endogenous hypercholesterolemia induced by a phenobarbital-containing diet was investigated. Supplemented taurine did not affect the concentrations of serum cholesterol, but further potentiated the accumulation of hepatic cholesterol in the hypercholesterolemic state induced by phenobarbital. It is suggested that taurine might amplify the hepatic cholesterogenesis in phenobarbital-induced hypercholesterolemia.