Preventive action of vitamin E-containing liposomes on cataractogenesis in young adult rats fed a 25% galactose diet

The preventive action of vitamin E (Vit. E)-containing liposomes on cataractogenesis was examined in male Wistar rats (five weeks old) fed a 25% galactose diet. Vit. E-containing liposomes prepared with dipalmitoylphosphatidylcholine were instilled into both eyes three times a day over a 45-day period. Cataract appeared at 18-day galactose feeding and developed gradually thereafter. Simultaneous Vit. E-containing liposome instillation delayed this cataractogenesis. Lenses of 18-day galactose-fed rats showed decreases in Vit. E and reduced glutathione (GSH) contents and Na+, K(+)-ATPase activity and increases in lipid peroxide (LPO), galactitol, and water contents. Lenses of 45-day galactose fed rats showed decreases in GSH content and Na+,K(+)-ATPase activity and increases in Vit. E, LPO, galactitol, and water contents. Serum Vit. E and cholesterol levels decreased in 18-day galactose-fed rats, while both levels increased in 45-day galactose-fed rats. Simultaneous Vit. E-containing liposome instillation prevented these changes except for the changes of lenticular galactitol and water contents and serum Vit. E and cholesterol levels. These results indicate that simultaneously instilled Vit. E-containing liposomes can delay cataractogenesis in young adult rats fed a 25% galactose diet mainly by the antioxidative action of Vit. E contained in the instilled liposomes.     

Effect of ascorbic acid administration on B and E apoproteins in rats fed a cholesterol enriched diet

The current study was designed to investigate the role of two potent vasoactive substances, endothelin (ET) and platelet-activating factor (PAF), in the pathogenesis of indomethacin-induced gastric lesions in rats. Treatment with anti-ET antibody before indomethacin administration resulted in a significant decline in the total length of the lesions as determined by gross evaluation. In contrast, CV-6209, a specific PAF antagonist, had no effect on the total length of the lesions. The results strongly suggest the incorporation of endogenous ET in the mechanism of gastric damage after indomethacin administration.     

Diminished kidney function and nephrocalcinosis in rats fed a magnesium-deficient diet

Microcapsules have been used as drug delivery systems in the pharmaceutical field for sustained or controlled release of drug, and for artificial cells and organs. Biodegradable polymers, especially polylactic acid, have been widely used in this field. In this study, an attempt was made to develop a new method to prepare polylactic acid microcapsules for drug delivery. The biodegradable polylactic acid microcapsules were made by the phase separation process: two types of polylactic acid, poly[(D,L)lactic acid] and poly[(L)lactic acid] were combined as the membrane material. Because of the difference of the crystal properties of the two polymers, the aggregation which happens frequently in the phase separation process was prevented. As a model drug, Ciprofloxacin was encapsulated in the polylactic acid microcapsules.     

Vitamin B12 improves cognitive disturbance in rodents fed a choline-deficient diet

The effect of vitamin B12 on learning disturbance was tested in rats. Rats were fed a choline-enriched, choline-deficient, and choline-deficient diet with vitamin B12. Concentrations of acetylcholine in the brain were significantly lower in rats fed a choline-deficient diet than rats fed a choline-enriched diet. Passive avoidance learning shows that rats on a choline-deficient diet showed significantly impaired learning compared to rats on a choline-enriched diet. However, there was no significant difference of acetylcholine in the brain or in the passive avoidance learning between rats fed a choline-enriched and a choline-deficient with vitamin B12 diet. We, therefore, suggest that vitamin B12 potentiates learning in an acetylcholine-deprived brain.     

Molecular species of phosphoglycerides in liver microsomes of rats fed a fat-free diet

The influence of a fat-free diet on the molecular species composition of phosphatidylcholine (PC), phosphatidylethanolamine (PE), and phosphatidylinositol (PI) of rat liver microsomes was studied by using reversed-phase high-pressure liquid chromatography. In the three phosphoglyceride classes analyzed, the fat-free diet produced a large decrease in the 18:0/20:4n-6 species but less important changes were found in the 16:0/20:4n-6 species. In PC, the most abundant phosphoglyceride class of rat liver microsomes, the fall in the 18:0/20:4n-6 species was counterbalanced mainly by an enhancement in the 16:0/18:1n-9 species although it was not evident in PE. In PI, the decrease in the 18:0/20:4n-6 species was counterbalanced by an increase in the 18:0/20:3n-9 species. Fluorescence polarization measurements of 1,7-diphenyl-1,3,5-hexatriene in liposomes of 16:0/18:1n-9, 18:0/18:1n-9-, 16:0/20:4n-6-, and 18:0/20:4n-6-PC indicated that the change in the saturated fatty acid in the sn-1 position accompanying the replacement of 20:4n-6 by 18:1n-9 could be very important for a homeoviscous compensation, maintaining the membrane physical properties without large alterations in spite of the essential fatty acid deficiency due to the fat-free diet.     

Different cholesterol deposition in aorta of Dahl salt-sensitive rats and spontaneously hypertensive rats fed a high-cholesterol diet

1. We compared the serum and aortic lipid levels in spontaneously hypertensive rats (SHR) and Dahl salt-sensitive rats (DSR) fed a high-cholesterol (HC) diet. 2. In SHR fed the HC diet, the serum cholesterol level significantly increased, but no aortic cholesterol deposition was observed. 3. The serum cholesterol level in DSR fed the HC diet markedly increased compared to that in DSR fed the basal diet, and this change was greater with the diet containing 8% NaCl than 0.4% NaCl. A significant increase in the content of aortic cholesterol, notably cholesteryl ester, was observed in only DSR fed the HC diet containing 8% NaCl. 4. These results suggest that the combination of hypercholesterolaemia with salt-induced hypertension acts as a greater risk factor for atherosclerosis than that with genetic hypertension.     

A vitamin E-deficient diet affects nerve regeneration in rats

BLAST searches of 61 equine microsatellite sequences revealed two related families of retroposons. The first family included seven markers, all of which showed significant homology to the Equine Repetitive Element-1 (ERE-1) Short Interspersed Nucleotide Element (SINE) sequence. Length of homology ranged from 76 to 171 bases with identities to the ERE-1 consensus sequence ranging from 71% to 83%. The second family referred to as Equine Repetitive Element-2 (ERE-2) has a consensus sequence that showed homology to ERE-1 over approximately 60 bases. These 60 bases comprised subunit I. Sequence comparisons for the two retroposons led to the identification of a subunit II, subunit III, as well as the tRNAser subunit. The subunit structure of ERE-1 was tRNAser-I-II. By contrast, the subunit structure of ERE-2 was I-III-III. The nine markers related to ERE-2 showed homology lengths ranging from 84 to 163 bases with identities ranging from 75% to 99%. In addition to being present in microsatellites, ERE-2 appeared in three separate equine genes. It occurred in an intron of DNA-PK, in an untranslated region as well as in the promoter of PGHS, and in the coding region of PAM. The amino acids corresponding to the ERE-2 sequence in PAM were not present in the human or mouse PAM homologs. These amino acids associated with the ERE-2 sequence were present on the cytosolic side of the transmembrane domain of the PAM enzyme. Microsatellite markers in the ERE-1 and ERE-2 families were found throughout the genus equus and also for rhinoceros, indicating that the appearance of both retroposons predates the divergence of equids from the other perissodactyls. The markers did not amplify in human or bovine DNA. This indicated that ERE-1 and ERE-2 are, at least, perissodactyl specific.     

Decreased expression of transforming growth factor beta 1 in blood plasma of guinea pigs fed vitamin C deficient diet

Liposarcoma is a malignant neoplasm of soft tissue. Its occurrence in the head and neck region is extremely rare. The case of a 26-year-old woman with neck liposarcoma is presented. The clinical manifestation, histopathology, possibility and results of the tumor treatment are described according to the literature.     

Effect of methionine on the metabolism of formate and histidine by rats fed folate/vitamin B-12-methionine-deficient diet

The metabolism of formate and histidine were compared in rats and in perfused livers of rats on diets deficient in vitamin B-12, methionine, and folic acid. Excretion of formate and formiminoglutamic acid, and the oxidation of [2-14C]histidine and [14C]formate to 14CO2 were measured. Liver folate levels decreased to 40% of normal on the vitamin B-12- and methionine-deficient diets but the rate of oxidation of histidine to CO2 in the whole animal decreased to 15% of normal. This indicated a reduction in the metabolic activity of the liver folates in vitamin B-12deficiency. Comparison of formate and histidine catabolism in folic acid deficiency showed that the oxidation of histine was decreased to 5% of normal but formate oxidation was decreased to only 30% of normal. This indicates that 25% of formate oxidation normally proceeds by a non-folate-dependent pathway.     

Vitamin A and lysosomal stability in rats fed an atherogenic diet

The relation between vitamin A status and lysosomal stability was studied in rats fed a high fat-cholesterol diet. Increase in the total activity of lysosomal enzymes as well as that in the nuclear fraction, intact lysosomal fraction and free activity (activity present in the 15,000 X g supernatant) in the liver was observed in rats fed an atherogenic diet with adequate vit. A. Vitamin A deficiency and hypervitaminosis (10,000 IU) augmented this increase in the total enzyme activity as well as the activity in the subcellular fractions except in the case of intact lysosomes where the activity was not significantly altered. At 2,000 IU, there was no significant alteration in either the total activity or the activity of the subcellular fractions. An analysis of the ratio of soluble activity (released from the lysosomes) to the activity present in the intact lysosomes, showed that hepatic lysosomal stability was decreased in the rats fed an atherogenic diet with normal dose of vit. A. Vitamin A deficiency as well as hypervitaminosis decreased the lysosomal stability still further. At a dose of 2,000 IU, lysosomal stability increased as compared to the rats fed an adequate dose of vit. A, while total lysosomal activity remained not significantly altered. Studies on the rate of release of enzymes from the lysosomes revealed that there was significantly more release of the enzyme between 30 and 45 min in the liver and aorta in the rats fed a high fat-cholesterol diet with adequate vit. A This release was still more in the rats fed a low dose of vit. A. At 2,000 IU, there was no significant difference in the enzyme release. But the pattern of change in the liver and aorta in the hypervitaminotic group was different. In the case of hepatic lysosomes, there was an increase in the enzymes released while in the aorta there was significant decrease. This has been attributed to the fact that lytic concentration of the vitamin A is not attained in the aorta.     

Toxicity in rats fed diet containing iron lactate for 26 weeks

In order to characterize the toxicity of iron lactate, a 26-week feeding study was performed in male and female F344 rats. Animals were divided into 2 groups, and given diet containing iron lactate at concentration of 0 or 2%. No animals died during the administration period. Body weight gain was suppressed in both sexes of the 2% group compared with the 0% group. Hematologically, anemia was observed in male of the 2% group. Serum alkaline phosphatase decreased in both sexes of the 2% group. The spleen weight of both sexes and kidney weight of females were higher in the 2% group than in the 0% group. Lipid peroxide increased not only in the liver and the kidney homogenates of treated males and females, but also in the serum of treated females. Histopathologically, iron deposition was observed in the liver, the kidney and the spleen of treated males and females, and in the intestine of treated females. The present results indicate that the iron lactate administration caused iron deposition in the liver and the other several organs, resulting in lipid peroxidation in these organs.     

Biotin deficiency in chicks fed a wheat-based diet

A wheat-based diet produced severe biotin deficiency symptoms appearing at the age of ten to fourteen days and becoming very severe in the third and fourth week (group 1). Biotin supplementation with 50 mug/kg (group 2) reduced the symptoms almost completely, but did not restore completely growth compared to chicks receiving the diet supplemented with 300 mug biotin/kg compared to chicks receiving the diet supplemented with 300 mug biotin/kg (group 3). The plasma level of biotin was about, or lower than, 100 ng/100 ml plasma in groups 1 and 2, indicating biotin deficiency. In group 3, plasma biotin was above 200 ng/100 ml. Liver biotin, after two weeks, was low in group 1 (less than 600 ng/g), medium in group 2 (1000 to 1500 ng/g) and in group 3 above 2000 ng/g. Plasma and liver biotin levels are found to be suitable parameters for diagnosis of subclinical biotin deficiency in chicks.     

Flavor preferences conditioned by intragastric nutrient infusions in rats fed chow or a cafeteria diet

Numerous studies demonstrate that chow-fed rats learn to prefer flavors that are associated with the postingestive effects of nutrients. The rats> limited dietary experience (i.e. only lab chow) may have facilitated preference learning because of the novelty of the training stimuli. This possibility was investigated by comparing nutrient conditioning in rats fed chow or a varied "cafeteria" diet. Rats in Experiment 1 were trained during alternate sessions (30 min/day) to drink two different flavors paired with concurrent intragastric infusions of 16% Polycose or water. Both diet groups displayed similarly strong preferences (89%) for and increased acceptance of the Polycose-paired flavor. A more demanding learning task was used in Experiment 2: new flavors were paired with delayed (15 min) infusions of Polycose or water. The chow and cafeteria groups both showed reduced, but comparable (78%, 77%) preferences for the Polycose-paired flavor. In Experiment 3, new flavors were paired with concurrent infusions of 7.1% corn oil or water. Again, the cafeteria and chow groups developed similar preferences for the nutrient-paired flavor (85%, 78%). Also, both groups preferred the Polycose-paired flavor of Experiment 1 to the oil-paired flavor of Experiment 3 (76%, 78%). These results indicate that dietary variety does not interfere with nutrient-conditioned flavor preference learning in rats.     

Nutritional and toxicological study of rats fed a diet containing tin (author's transl)

A toxicological, nutritional and histological study of rats on a diet containing 0.5 g of tin (Sn Cl2) per 100 g of dry food for one month has been made. By gamma radioactivity measurements (with 113Sn used as a tracer) it is shown that this metal does not practically clear the digestive barrier. Otherwise the classical coefficients of nitrogen nutrition and the urinary parameters (volume, glucose, pH) are not influenced; but the growth of treated animals is obviously slower than control animals because of their reduced ingestion of food. Moreover after one month of treatment a marked anaemia results since the hematocrit and hemoglobin levels are perceptibly reduced. Lastly the histological investigations give evidence of notable irritation of the total gastrointestinal tract. This study, as that of many authors, raises the question of present permissible levels of tin (up to 250 ppm) in foods.     

Extraction, quantification, and biological availability of fumonisin B1 incorporated into the Oregon test diet and fed to rainbow trout

The purpose of this study was (i) to determine whether pure fumonisin B1 could be incorporated into, recovered, and detected by high-pressure liquid chromatographic analysis from the semipurified Oregon test diet (OTD) used in rainbow trout feeding studies, and (ii) to determine if the incorporated fumonisin B1 was biologically available using the change in free sphingoid bases in liver, kidney, and serum as a mechanism-based biomarker. The results indicate that fumonisin is not easily quantified in the OTD. Recoveries ranged from 12 to 81% of the calculated concentrations based on the fumonisin B1 added to the OTD. However, the fumonisin B1 in the OTD was readily absorbed and biologically active as evidenced by marked increases in free sphinganine in liver, kidney, and serum. The magnitude of the increase in free sphinganine at 100 ppm in the OTD was comparable to that known to be associated with liver toxicity in rats, pigs, and ponies.     

Effect of the slimming agent oleoyl-estrone in liposomes on the body weight of rats fed a cafeteria diet

In previous studies we observed that inhibition of cyclic 3',5'-nucleotide phosphodiesterase (PDE) isozymes, namely isozyme PDE3, suppresses proliferation of rat renal glomerular mesangial cells in vitro and in vivo. To determine whether activation of the cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling pathway coupled to specific PDE isozymes modulates accelerated proliferation of renal epithelial cells, we investigated the effect of selective PDE isozyme inhibition on renal epithelial cell proliferation induced in rats by injection of folic acid (FA). In extracts from suspensions of renal cortical tubules, cAMP was metabolized predominantly by isozyme PDE4; activity of PDE3 was about three times lower. The increase in proliferative activity of renal cortical tissue from FA-injected rats, evaluated by immunostaining with Mib-1 antibody, was limited to tubular epithelial cells. Administration of the PDE3 inhibitors cilostazol or cilostamide together with the PDE4 inhibitor rolipram blocked mitogenic synthesis of DNA, as determined by (3H)-thymidine incorporation into renal cortical DNA, in FA-treated rats. FA injection caused an increase of more than 10-fold in proliferating cell nuclear antigen (PCNA) in renal cortical tissue; administration of the potent PDE3 inhibitor lixazinone or, to a lesser degree, cilostazol suppressed these high PCNA levels, whereas rolipram alone had no effect. The results indicate that FA-stimulated in vivo proliferation of renal tubular epithelial cells is down-regulated by activation of a cAMP-PKA signaling pathway linked to PDE3 isozymes. These observations are consistent with the notion that negative crosstalk between cAMP signaling and mitogen-stimulated signaling pathways regulates mitogenesis of renal cells of different terminal differentiation, including tubular epithelial cells.     

Early destruction of tryptophan residues of apolipoprotein B is a vitamin E-independent process during copper-mediated oxidation of LDL

The decrease of the tryptophan fluorescence (Ex/Em = 282/331 nm) was used to monitor the kinetics of copper-mediated LDL oxidation. Cu2+ causes a concentration-dependent quenching of the LDL Trp-fluorescence, the maximum of about 22% suggests that 8-9 Trp residues (out of a total of 37) are accessible for Cu2+ ions. Decomposition of LDL tryptophan commences immediately after addition of Cu2+ and proceeds in two stages with quite different rates. At a molar ratio of Cu2+/LDL = 33:1 the LDL particle looses 1 Trp every 13.5 min in the initial slow phase and every 4.1 min in the subsequent rapid The second, stage temporarily coincides with the propagating lipid peroxidation. In the initial phase loss of Trp proceeds with a constant rate for up to 200 min depending on the copper concentration. Whereas lipid peroxidation accelerates after consumption of vitamin E, rate of Trp loss does not increase. Loading of LDL with vitamin E has also no effect on the initial rate of Trp loss. During the initial phase a loss of one Trp residue/LDL is accompanied by the loss of two alpha-tocopherols and the generation of two conjugated lipid hydroperoxides. The results suggest Trp residues play a role in initiating the lipid peroxidation process in the LDL particle. In such kinetic studies, precautions must be taken to avoid photodecomposition of LDL-Trp. The LDL vitamin E fluorescence (Ex/Em = 290/323 nm) does not interfere with the Trp fluorescence even at high concentrations.     

Craniofacial bone remodeling in growing rats fed a low-calcium and vitamin-D-deficient diet and the influence of masticatory muscle function

Fifty-two male growing rats were randomly divided into three groups. The first group (n = 18) received a hard deficient diet, and the second (n = 18) a soft deficient diet. The control group (n = 16) was fed the normal hard diet. At the beginning and in the middle of the 28-day experimental period oxytetracycline was injected. Two representative coronal sections of the snout and the corresponding contact microradiographs were analyzed. The bone mass of the premaxillary and nasal bones seemed to be less in the two deficient diet groups than in the normal one, due to an increased endosteal bone resorption and decreased bone formation. No difference in the bone apposition rate and pattern could be seen between the deficient hard and soft diet groups, except in the dorsal part of the premaxilla, where the bone formed in the first half of the experiment was markedly more resorbed in the deficient soft diet group during the remaining period than in the deficient hard diet group. The morphology of the sutures was influenced by the altered function, since the sutural space became narrower, and premature obliterations of the internasal suture were observed in the deficient soft diet group. In conclusion, poor bone quality was observed in the skull of rats fed a low-calcium and vitamin-D-deficient diet, with less bone mass than in normal conditions. Masticatory function was a significant factor influencing bone remodeling and sutural growth even in situations in which a metabolic bone disturbance exists.