phosphorus-radioisotopes and Body-Weight

Glucocorticoid treatments are associated with increased whole-body oxygen consumption. We hypothesised that an impairment of muscle energy metabolism can participate in this increased energy expenditure.. To investigate this possibility, we have studied muscle energetics of dexamethasone-treated rats (1.5 mg kg(-1) day(-1) for 6 days), in vivo by (31)P NMR spectroscopy. Results were compared with control and pair-fed (PF) rats before and after overnight fasting.. Dexamethasone treatment resulted in decreased phosphocreatine (PCr) concentration and PCr:ATP ratio, increased ADP concentration and higher PCr to gamma-ATP flux but no change in beta-ATP to beta-ADP flux in gastrocnemius muscle. Neither 4 days of food restriction (PF rats) nor 24 h fasting affected high-energy phosphate metabolism. In dexamethasone-treated rats, there was an increase in plasma insulin and non-esterified fatty acid concentration.. We conclude that dexamethasone treatment altered resting in vivo skeletal muscle energy metabolism, by decreasing oxidative phosphorylation, producing ATP at the expense of PCr.

Topics: 3-Hydroxybutyric Acid; Adenine Nucleotides; Animals; Body Weight; Dexamethasone; Energy Metabolism; Fatty Acids, Nonesterified; Hydrogen-Ion Concentration; Insulin; Leptin; Magnetic Resonance Spectroscopy; Male; Muscle, Skeletal; Oxygen Consumption; Phosphates; Phosphocreatine; Phosphorus Radioisotopes; Rats; Rats, Sprague-Dawley

Topics: Animals; Body Weight; Humans; Metabolic Clearance Rate; Nitrogen Radioisotopes; Phosphorus Radioisotopes; Radioactive Tracers; Radioisotopes; Rats; Scintillation Counting; Tissue Distribution

Chinese-herb nephropathy (CHN) is a progressive renal interstitial fibrosis initially reported after concomitant intake of an anorexigen, (dex)fenfluramine, and a Chinese herb ( Aristolochia fangchi) containing nephrotoxic and carcinogenic aristolochic acid (AA). We thus tested the possible enhancing effect of the active enantiomer dexfenfluramine (DXF) on AA nephrotoxicity in a rat model for CHN. Groups of 12 salt-depleted male Wistar rats received daily subcutaneous injections of 7 mg/kg body weight DXF (DXF group), 7 mg/kg body weight AA (AA group), a combination of the same doses of AA and DXF (AA+DXF group), or vehicle (control group) for up to 35 days. Six animals per group were killed on day 10 and the remaining six on day 35. Renal function was evaluated by determining serum creatinine and urinary leucine aminopeptidase activity. Histological evaluation of kidney samples was performed and tubulointerstitial injuries were semiquantified. The DXF group did not differ from controls for any parameter. Similarly elevated serum creatinine levels, decreased leucine aminopeptidase enzymuria, and renal lesions were observed in the AA and the AA+DXF groups after both 10 and 35 days. The formation of specific AA-DNA adducts in liver and renal tissue samples was assessed by the (32)P-postlabelling method. Specific AA-DNA adduct levels were significantly increased in kidney tissues from AA+DXF rats compared with AA rats. These functional and histological data suggest that DXF does not enhance AA nephrotoxicity in a rat model for CHN. Further investigations are needed to clarify the mechanism by which DXF may enhance AA-DNA adduct formation.

Topics: Animals; Aristolochic Acids; Autoradiography; Body Weight; Creatinine; Dexfenfluramine; Disease Models, Animal; DNA Adducts; Drug Synergism; Drugs, Chinese Herbal; Fibrosis; Injections, Subcutaneous; Kidney; Liver; Longevity; Male; Mutagens; Nephritis, Interstitial; Phosphorus Radioisotopes; Rats; Rats, Wistar; Serotonin Receptor Agonists

Intestinal inorganic phosphate transport and its regulation have not been studied in fish. In this study, we initially characterized the mechanisms of intestinal inorganic phosphate transport in rainbow trout (Oncorhynchus mykiss) then determined the effects of dietary phosphorus concentrations on intestinal inorganic phosphate uptake, plasma inorganic phosphate, and intestinal luminal inorganic phosphate concentrations. In 11-g trout, the saturable mechanism of brushborder inorganic phosphate uptake had a Kt= 1.2 mmol l(-1) and a Vmax = 0.22 nmol mg(-1) min(-1), while the diffusive component had a Kd = 0.012 min(-1). Similar kinetic constants were obtained from 51-g trout, suggesting that development or size had little effect on transport. Tracer inorganic phosphate (1.18 mmol l(-1)) uptake was almost completely inhibited (>95%) by 20 mmol l(-1) unlabeled inorganic phosphate. Inorganic phosphate uptake (0.2 mmol l(-1)) was strongly inhibited (approximately 75% inhibition) by phosphonoformic acid, a competitive inhibitor of mammalian inorganic phosphate transport, as well as by the absence of Na+ (approximately 90% inhibition). Northern blot and reverse transcription-polymerase chain reaction indicated that the intestinal inorganic phosphate transporter in trout is not related to the cloned Na+ inorganic phosphate-II transporter of winter flounder. Intestinal luminal and plasma inorganic phosphate concentrations each increased with dietary P concentrations. Intestinal inorganic phosphate, but not proline, absorption rates decreased with dietary phosphorus concentrations. As in mammals and birds, a Na-dependent inorganic phosphate carrier that is tightly regulated by diet is present in trout small intestine.

Topics: Animal Nutritional Physiological Phenomena; Animals; Binding, Competitive; Body Weight; Eating; Intestinal Absorption; Intestine, Small; Oncorhynchus mykiss; Phosphorus Radioisotopes; Phosphorus, Dietary; Proline

The effect of chemical aging on the bioavailability and subsequent genotoxicity of coal tar (CT)-contaminated soils was evaluated in a 17-day feeding study using Fischer 344 male rats. Rats consumed a control diet or diets amended with soil, 0.35% CT, or soil freshly prepared or aged for 9 months with 0.35% CT. Mild treatment-related microscopic lesions in liver tissue and elevated enzyme levels in serum were detected in all CT treatment groups. The (32)P-postlabeling assay was employed to determine DNA adduct formation in treated animals. All CT treatment groups induced DNA adducts in both the liver and lung. Adduct levels were 3-fold higher in lung DNA compared to hepatic DNA. After correcting adduct levels for total ingested polycyclic aromatic hydrocarbons (PAHs), a significant decrease (p < 0.05) in adduct levels was observed in both CT/soil treatment groups compared to CT control in liver and lung DNA. Adduct profiles of (32)P-postlabeled hepatic and lung DNA displayed several nonpolar DNA adducts that comigrated with PAH-adducted calf thymus DNA standards as determined through both thin-layer chromatography (TLC) and high-pressure liquid chromatography (HPLC). These results suggest that soil, but not aging of contaminants in soil, decreases the bioavailability of genotoxic components in CT, as evidenced by DNA adduct analysis.

Topics: Animals; Biological Availability; Body Weight; Chromatography, High Pressure Liquid; Chromatography, Thin Layer; Coal Tar; DNA Adducts; DNA Damage; Eating; Liver; Male; Mutagens; Phosphorus Radioisotopes; Polycyclic Aromatic Hydrocarbons; Rats; Rats, Inbred F344; Soil Pollutants; Tissue Distribution

It is known that lower-chlorinated biphenyls are metabolically activated to electrophilic quinoid species capable of binding to DNA. Also, certain metabolites are capable of redox cycling, thereby increasing oxidative stress in biological systems. In the present study, we tested mono-, di-, tri-, tetra-, penta-, hexa-, and heptachlorinated biphenyls for their ability to bind with DNA and to induce oxidative DNA damage. We present additional evidence that several PCB congeners form DNA adducts after metabolic activation, which can be detected by the nuclease P1- or butanol-enrichment procedures of the (32)P-postlabeling technique. Butanol and nuclease P1 enrichments showed different adduct recoveries, depending on the level of chlorination of the biphenyls. Application of the nuclease P1 enrichment showed that the incubation of 2-chloro-; 3, 4-dichloro-; 2,4,4'-trichloro-; 3,4,5-trichloro-; and 2,2',5, 5'-tetrachlorobiphenyl with calf thymus DNA and liver microsomes from rats treated with phenobarbital, followed by oxidation with a peroxidase, produced five to eight different DNA adducts. For these lower-chlorinated biphenyls, butanol enrichment generally showed a lower recovery. For some higher substituted congeners (3,3',4,4', 5-pentachloro-, 2,2',3,4,4',5'-hexachloro-, 2,2',4,4',5, 5'-hexachloro-, and 2,2',3,4,4',5,5'-heptachlorobiphenyl), after butanol enrichment a single dominant spot was observed, which was absent in the nuclease P1 procedure. After incubation of calf thymus DNA with either higher- or lower-chlorinated PCB congeners, we were not able to detect significantly increased levels of oxidative DNA damage above background levels, measured as 8-oxo-7, 8-dihydro-2'deoxyguanosine. In view of the carcinogenicity of PCB mixtures in animals and the ability of PCB metabolites to bind covalently to DNA, rats were orally treated with a mixture of PCBs (Aroclor 1242). PCB-DNA adduct levels were analyzed in PCB target organs: liver, thymus, glandular stomach, spleen, testes, seminal vesicles and prostate DNA. In vivo PCB-DNA adducts could not be detected by either the butanol- or by the NP1-enrichment procedure in rat target tissue DNA. Also, no differences in oxidative DNA damage could be observed between PCB-treated rats and controls. These results indicate a lack of DNA reactivity of PCB mixtures in vivo.

Topics: Administration, Oral; Animals; Body Weight; DNA Adducts; DNA Damage; Isotope Labeling; Male; Microsomes, Liver; Phosphorus Radioisotopes; Polychlorinated Biphenyls; Prostate; Rats; Rats, Inbred Lew; Single-Strand Specific DNA and RNA Endonucleases; Spleen; Testis; Thymus Gland; Tissue Distribution; Toxicity Tests

To study the possible reduction by eugenol of the mutagenicity and genotoxicity of benzo[a]pyrene (B[a]P) in vivo, the lambda-lacZ-transgenic mouse strain 40.6 (Muta Mouse) was used. Male mice were fed a diet containing 0.4% (w/w) eugenol or a control diet for 58 days. On day 10, half of the mice received an i.p. dose of 100 mg/kg b.w. B[a]P. The lacZ mutants were recovered by packaging of DNA isolated from liver into lambda phage, and expressed in E. coli C lacZ-recA-galE- bacteria. In both control mice and mice fed the eugenol diet, B[a]P treatment resulted in a similar, significant increase in lacZ mutant frequency. Eugenol was not mutagenic by itself. By 32P-postlabelling analysis of the liver DNA using an analysis method with chromatographic conditions for B[a]P-DNA adducts, no effect of eugenol on the formation of B[a]P-DNA adducts in the lambda-lacZ-transgenic mouse was found. By 32P-postlabelling analysis using an alkenylbenzene solvent system the amount of B[a]P-DNA adducts was lower in mice fed the eugenol diet than in mice fed the control diet but the decrease was not statistically significant. However, one spot indicative of an eugenol-associated DNA adduct was detected. The present data provide no evidence for antimutagenic or antigenotoxic potential of eugenol in vivo. Furthermore, they suggest genotoxicity in vivo of eugenol per se.

Topics: Animals; Antimutagenic Agents; Benzo(a)pyrene; Biotransformation; Body Weight; Diet; DNA Adducts; Eugenol; Glutathione Transferase; Lac Operon; Liver; Male; Mice; Mice, Transgenic; Mutagens; Phosphorus Radioisotopes

Hepatic microsomal xenobiotic metabolizing enzyme activities of laboratory animals can be modulated by Dietary restriction (DR). The modulation of xenobiotic metabolizing enzyme activities can affect the metabolic activation of chemical carcinogens. Acute DR (60% of the food consumption of ad libitum (AL)-fed mice for 7 weeks) reduced the body weights of the male B6C3F1 mice, and increased mouse pulmonary cytochrome P4501A1-dependent BaP metabolizing enzyme activity. The effects of DR on the formation of the specific BaP-DNA adduct, 10-(N2-deoxyguanosinyl)-7,8,9-trihydroxy-7,8,9,10-tetrahydro-BaP (BaP-N2-dG) in mouse lung can be detected by using 32P-postlabeling technique. In both AL- and DR-mice total BaP-DNA adduct formation in lung reached a peak at 48 hours after treatment with [3H]BaP and the in vivo formation of BaP-N2-dG was greater in DR mouse lung than in that of AL-animals by 22%. DR increased in vitro BaP-N2-dG formation by 39% when calf-thymus DNA was incubated with BaP using liver microsomes obtained from DR- or AL-mice as the enzyme source. The formation of the specific BaP-N2-dG adducts, measured by 32P-postlabeling, was only 20% of the total [3H]BaP-DNA adducts as determined by liquid scintillation counting. The increase of BaP-DNA adduct formation in mouse lung was correlated to the enhancement of the mouse pulmonary BaP metabolizing enzyme activity. Our results indicated that the effect of DR on the metabolic activation of BaP in mouse lung was dependent upon the mouse lung cytochrome P4501A1-dependent BaP metabolizing enzymes activities which was significantly increased by DR.

Topics: Animals; Aryl Hydrocarbon Hydroxylases; Benzo(a)pyrene; Benzopyrene Hydroxylase; Biotransformation; Body Weight; Carcinogens; Chromatography, Thin Layer; DNA Adducts; Dose-Response Relationship, Drug; Food Deprivation; Lung; Male; Mice; Microsomes; Organ Size; Phosphorus Radioisotopes; Time Factors; Weight Gain

N-Hydroxy-N-2-fluorenylacetamide (N-OH-2-FAA) and its benzamide analogue N-OH-2-FBA are mammary gland carcinogens in the female Sprague-Dawley rat. Ovariectomy inhibits tumorigenicity of topically applied N-OH-2-FAA suggesting modulation of carcinogen-activating enzymes in the gland. This study concerned the activation of N-OH-2-FAA and N-OH-2-FBA by the mammary gland and liver, a chief site of metabolism, from 50-day-old female rats and effects on the activation of ovariectomy performed at 22 days of age. The levels of N-debenzolyation of N-OH-2-FBA to N-hydroxy-N-2-fluorenamine (N-OH-2-FA), catalyzed by microsomal carboxylesterases in mammary gland and liver were similar and increased 1.5- and 1.7-fold, respectively, by ovariectomy. N-Debenzoylating activity in cytosols of both tissues appeared to be partially of microsomal origin. Mammary gland cytosol contained N-, O- and N,O-acyltransferase activities at levels 40-50% those of liver. N-Acyltransferase activity was determined via acetyl coenzyme A (AcCoA)-dependent acetylation of 2-FA and a new assay, N-OH-2-FAA-dependent acetylation of 9-oxo-2-FA. The latter activity was decreased in mammary gland by ovariectomy. Microsomal N-acyltransferase activities were <36% those of cytosols. AcCoA-dependent binding of N-OH-2-[ring-[3H]FBA to DNA, catalyzed by cytosol, was consistent with a two-step activation of N-OH-2-FBA involving esterase-catalyzed N-debenzoylation to N-OH-2-FA and its O-acyltransferase-catalyzed acetylation to the electrophilic N-acetoxy-2-FA. O-Acetyltransfer by mammary gland appeared to be rate-limiting since ovariectomy-dependent increases in N-debenzoylation did not increase binding with S9 fraction. Little or no sulfotransferase-catalyzed binding of N-OH-2-[ring-3H]FBA-derived N-OH-2-[ring-3H]FA was detected in the liver or mammary gland cytosol, respectively. The level of binding of N-OH-2-[ring-3H]FAA to DNA catalyzed by cytosolic N,O-acyltransferase was decreased approximately 23% in mammary gland and increased 1.2-fold in liver by ovariectomy. 32P-Postlabeling analyses indicated a single adduct N-(deoxyguanosin-8-yl)-2-fluorenamine in DNA of both tissues 24 h after one intraperitoneal injection of N-OH-2-FBA or N-OH-2-FAA. Respective levels were 3.6- and 5.5-fold greater in liver than mammary gland. After ovariectomy, the adduct levels from N-OH-2-FBA increased 1.8-fold in mammary gland and from N-OH-2-FAA decreased approximately 50% in both tissues. Thus, the ovariectomy-dependent

Topics: Acetylation; Animals; Biotransformation; Body Weight; Carcinogens; DNA; DNA Adducts; Female; Fluorenes; Liver; Mammary Glands, Animal; Ovariectomy; Ovary; Phosphorus Radioisotopes; Proteins; Rats; Rats, Sprague-Dawley; Tritium

In this investigation we studied developmentally regulated endogenous protein kinase activity in cytoskeletal proteins in the cerebral cortex of rats and the effect of early malnutrition imposed on dams on the pattern of 32P incorporation into the cytoskeleton of pups. Our results indicated that in vitro incorporation was maximum in 7-day-old pups for both normal and malnourished groups, decreasing with development, and reaching minimum values in adult animals. However, 32P incorporation into NF-M and tubulin was significantly lower in 7-day-old malnourished pups than in normal pups.

Topics: Aging; Animals; Autoradiography; Body Weight; Cerebral Cortex; Cytoskeletal Proteins; Electrophoresis, Polyacrylamide Gel; Nutrition Disorders; Organ Size; Phosphoproteins; Phosphorus Radioisotopes; Phosphorylation; Protein Kinases; Rats; Reference Values

In order to study the effect of nutrition on the onset of disturbances in Wistar rat pancreatic beta cells, we compared the effects of a low protein diet (8% protein) and a normal protein diet (25% protein) supplied to the dams (6 in each group) during the first 12 days of lactation. The parameter evaluated was the beta cells phosphate flush in response to stimulatory concentration of glucose (16.7 mM) of isolated islets of Langerhans from 60-day old pups. Using a collagenase digestion technique, islets were isolated from the pups and the 32P fractional outflow rate (FOR) of the beta cells was used as a metabolic index in both experimental groups (N = 36). We observed that although the weights of the pups of the two groups were not significantly different at 60 days of age (control = 186 +/- 18 g; undernourished during lactation = 179 +/- 19 g), the typical phosphate flush response (FOR = 2.4 +/- 0.4%/min) to a stimulatory glucose concentration (16.7 mM) was abolished in the rats from undernourished mothers. Our data are consistent with the hypothesis that undernutrition may be an important cause of diabetes mellitus type II.

Topics: Animals; Animals, Newborn; Animals, Suckling; Body Weight; Dietary Proteins; Female; Glucose; Islets of Langerhans; Lactation; Phosphates; Phosphorus Radioisotopes; Pregnancy; Rats; Rats, Wistar; Time Factors

The chemical constituents of cigarette smoke are greatly diluted in environmental tobacco smoke (ETS). In the typical indoor environment where cigarettes are smoked, the mean value of respirable suspended particles is approximately 0.1 mg/m3. In this study, we used aged and diluted sidestream smoke (ADSS) of 1R4F University of Kentucky research cigarettes as a surrogate for ETS and exposed Sprague-Dawley rats nose-only to 0, 0.1, 1.0, and 10 mg wet total particulate matter (WTPM)/m3 for 6 hr per day for 14 consecutive days. DNA from lung, heart, larynx, and liver was tested for adduct formation after 7 and 14 days of exposure and after 14 days of recovery. In addition, alveolar macrophages from animals exposed for 7 days were examined for chromosomal aberrations. Exposure-related DNA adducts were not observed in any of the animals at 0.1 or 1.0 mg WTPM/m3, which represent ambient and 10-fold exaggerated ETS concentrations, respectively. Slight diagonal radioactive zones, characteristic of adducts observed in human smokers and in animals exposed to mainstream smoke, were observed, but only in lung and heart DNA of animals exposed to the highest concentration of ADSS (10 mg WTPM/m3), a 100-fold exaggeration of typical field measurements of ETS. The mean relative adduct labeling values (+/- SE) were 8.7 (+/- 0.2) adducts per 10(9) nucleotides for lung DNA and 5.7 (+/- 0.7) adducts per 10(9) nucleotides for heart DNA after 14 days of exposure. No elevation in chromosomal aberrations was observed in alveolar macrophages.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Administration, Inhalation; Animals; Body Weight; Chromosome Aberrations; DNA; Dose-Response Relationship, Drug; Female; Heart; Lung; Macrophages, Alveolar; Male; Myocardium; Phosphorus Radioisotopes; Rats; Rats, Sprague-Dawley; Time Factors; Tobacco Smoke Pollution

In 30-day-old offspring of mice treated with 5-HT and/or Na2H32PO4, there was a decrease in the fresh weight of the organs, being more noticeable in males than in females. In relation to a group injected with Na2H32PO4 and that to which both 5-HT and Na2H32PO4 were administered, a greater fresh weight of the organs in mice treated with 5-HT only was found. No differences in the radioactivity of 32P in the organs of 30-day-old offspring between the group of mice treated with Na2H32PO4 only and that injected with both 5-HT and Na2H32PO4, were observed.

Topics: Animals; Animals, Newborn; Body Weight; Female; Heart; Kidney; Liver; Lung; Maternal-Fetal Exchange; Mice; Mice, Inbred C57BL; Myocardium; Organ Size; Phosphorus Radioisotopes; Pregnancy; Pregnancy, Animal; Serotonin; Spleen; Tissue Distribution

Radioactive phosphorus (P-32) was administered intraperitoneally to Wistar female rats at 2-week intervals. P-32 was administered at a total dose of 3 mCi (a single dose of 200 microCi, 15 times) to Group 1, 2.4 mCi (1 microCi/g body weight, 15 times) to Group 2, and 1.4 mCi (1 microCi/g, 10 times) to Group 3. Osteosarcoma was induced in 29 out of 80 rats (36%) in Group 1, 28 out of 40 (70%) in Group 2, and 31 out of 40 (78%) in Group 3. Bone tumor was predominant in the trunk (spine, ilium etc.) in Group 1 (86%), and in the extremities (femur, tibia etc.) in Group 2 (64%) and Group 3 (71%). Histological findings revealed neoplastic osteoid formation in all lesions. Osteoblastic type developed more in Group 1 than in Group 3, and fibroblastic type developed more in Group 3 than in Group 1. The rate of lung metastasis was significantly higher in Group 3 (94%) than in Group 1 (21%, p less than 0.01) or Group 2 (72%, p less than 0.05). This experimental method, especially that used for Group 3, appears to be useful for studying the basis of human osteosarcoma.

Topics: Animals; Body Weight; Female; Lung Neoplasms; Neoplasms, Radiation-Induced; Osteosarcoma; Phosphorus Radioisotopes; Rats; Rats, Inbred Strains; Sarcoma, Experimental

I-Compounds have been recently identified as adduct-like nonpolar covalent DNA modifications that are detectable by 32P-postlabeling assay in tissues of untreated experimental animals and increase with age. Additional I-compounds have now been observed in liver DNA of male Sprague-Dawley rats when the chromatographic conditions were modified to allow for the detection of more polar adducts exhibiting low affinity to polyethyleneimine (PEI)--cellulose anion-exchange thin-layer material. The total I-compound level in 10-month-old animals was as high as one modification in approximately 10(7) nucleotides. This represented a minimum estimate since 100% recovery of all rat liver I-compounds in 32P-labeled form presumably was not achieved by the procedures used. The I-compound pattern was reproducible and variation of I-compound levels among individual animals of the same age was small. We have used regenerating rat liver herein as a model to compare the properties of I-compounds with those of persistent 2-acetylaminofluorene (AAF)-induced DNA adducts and of 5-methylcytosine (m5C), a normal enzymatic DNA modification. Eight- to 10-month-old male Sprague-Dawley rats were given 2-AAF (50 mg/kg in DMSO) or vehicle (DMSO) by i.p. injection. Partial hepatectomy was performed 6 weeks later (i.e. after AAF adduct levels had stabilized) and regenerating liver samples were taken 1 week after the operation for DNA analysis. Consistent with the restoration of cell and tissue loss, the overall levels of I-compounds and 2-AAF adducts were reduced to approximately 47% and approximately 45% respectively of control in regenerating liver by dilution with newly synthesized DNA, while the m5C level was not affected. Thus, in regenerating liver, I-compounds resembled carcinogen--DNA adducts and not m5C. This supports our hypothesis that the formation of these DNA modifications may be due to the binding to DNA of small amounts of reactive electrophilic by-products of normal metabolic activities, leading to the slow accumulation of I-compounds in tissue DNA with ageing.

Topics: 2-Acetylaminofluorene; 5-Methylcytosine; Adenosine Triphosphate; Animals; Body Weight; Cytosine; DNA; Liver; Liver Regeneration; Male; Organ Size; Phosphorus Radioisotopes; Rats; Rats, Inbred Strains; Reference Values

An experiment was conducted using isotope-dilution and comparative balance techniques to estimate urinary and fecal P excretion of laying hens fed different levels of dietary Ca. Two levels of dietary Ca (3.46 and 4.2%) were fed to eight hens for 30 days. After 30 days, 50 microCi of the radioisotope 33P was injected intramuscularly to label endogenous P. On the 2nd day after 33P dosing and at 1 h postoviposition, plasma, liver, kidney, femur bone, whole egg, ileum, ileal digesta, and excreta samples were collected from each hen. Results showed a favorable effect of increasing dietary Ca consumption (2.91 vs 3.57 g/hen per day): femur ash increased (P less than .08), excreta P decreased (P less than .03), and urinary P decreased (P less than .06). The P content of ileal digesta was not affected by dietary Ca intake, but excreta P was greater for hens consuming less Ca, indicating that, during the collection period, excretion of P in urine was increased by the low Ca diet. Endogenous P secretions constituted less than 1% of the P in ileal digesta and excreta samples and this proportion was not changed by dietary Ca consumed.

Topics: Animals; Body Weight; Calcium, Dietary; Chickens; Feces; Female; Intestinal Absorption; Oviposition; Phosphorus; Phosphorus Radioisotopes; Tissue Distribution

Continuous irradiation in utero is reported to produce mental retardation and gross abnormalities of the brain in the human. A few experimental studies conducted so far also report gross brain defects in animals exposed to continuous irradiation in utero. Despite the increasing use of nuclear energy for power and radioisotopes in medicine, there is hardly any literature available on the effect of continuous irradiation on the structural details of the developing brain. After intraperitoneal injections of different doses of 131I (8, 18 and 32 microCi) and 32P (10 microCi) in new-born rats on the 6th postnatal day, cerebella stained by Golgi techniques were cut sagittally and the sections were examined on the 10th, 15th and 21st postnatal days. In the animals injected with 18 and 32 microCi of 131I and 10 microCi of 32P a large number of Purkinje cells showed morphological alterations not seen in the control groups or in the groups injected with 8 microCi of 131I. The changes observed included persistence of the perisomatic processes beyond the 10th postnatal day, multiple primary dendrites, angulation of the primary dendrites, long segments of primary dendrites without branches and significantly reduced dendritic volume. The number of affected cells was less on the 21st postnatal day. The effective radiation dose estimated in these groups ranged from 15 to 26 rad. Since the rats irradiated with 6 rad had not shown such changes it is believed that there is a threshold dose of radiation beyond which only changes are perceptible at neuronal level.

Topics: Age Factors; Animals; Body Weight; Brain; Injections, Intraperitoneal; Iodine Radioisotopes; Organ Size; Phosphorus Radioisotopes; Purkinje Cells; Radiation Dosage; Rats; Rats, Inbred Strains; Staining and Labeling

Androgenic deprivation resulted in marked impairment of prostate weight and significant alterations in cytosolic and particulate protein kinase activities and cyclic AMP-binding capacity of this tissue. Whereas rats orchidectomized for 7 days exhibited significant enhancement in the specific activity of cytosolic cyclic AMP-dependent (73%) and -independent (45%) protein kinases as well as cyclic AMP-binding protein (196%), administration of testosterone (5.0 mg/100 g, i.m., 5 days) exerted little or no effect in reversing these responses. In contrast, when expressed as total enzyme activity per prostate, castration led to marked decreases in protein kinase activity assayed in the presence (87%) and absence of the cyclic nucleotide (91%). Likewise, the cyclic AMP-binding capacity of the soluble enzyme was depressed (77%) following androgenic deprivation. Although testosterone treatment for 3 days significantly reversed these effects, complete restoration was not achieved even after 5 days of androgen replacement therapy. Moreover, while exogenous cyclic AMP had no effect on protein kinase activity from crude nuclear preparations, the phosphorylation of endogenous nuclear substrates was dependent on androgenic status of the animals. Whereas castration produced decreases in the specific and total activity of prostatic particulate protein kinase as well as the cyclic AMP-binding protein, testosterone replenishment was effective in abolishing these alterations seen in orchidectomized rats. Data from the present study provide additional support to the concept that changes in cyclic AMP-adenylate cyclase-protein kinase system play an important role in the overall mechanism(s) by which male sex steroids exert their diverse anabolic effects on male accessory sex tissues.

Topics: Androgens; Animals; Body Weight; Cyclic AMP; Male; Phosphorus Radioisotopes; Prostate; Protein Binding; Protein Kinases; Proteins; Rats; Testis; Testosterone

Topics: Animals; Ascorbic Acid; Body Weight; Columbidae; Leukocytes; Male; Mice; Mice, Inbred C57BL; Phosphates; Phosphorus Radioisotopes; Radiation Injuries; Radiation, Ionizing

Topics: Aminopropionitrile; Animals; Body Weight; Bone and Bones; Calcium; Calcium Radioisotopes; Chickens; Duodenum; Intestinal Absorption; Lathyrism; Male; Phosphates; Phosphorus Radioisotopes; Protein Binding; Proteins; Semicarbazides

Topics: Adenosine Triphosphate; Animals; Animals, Newborn; Body Weight; Brain; Cyclic AMP; Enzyme Activation; Hyperthyroidism; Kinetics; Microsomes; Organ Size; Phosphorus Radioisotopes; Protein Kinases; Rats; Thyroxine; Triiodothyronine

Rat skeletal-muscle elongation factor 2 was assayed by causing it to react with NAD(+) by using fragment A of diphtheria toxin as the catalyst. Dietary protein restriction decreased the concentration of elongation factor 2 in homogenates of whole muscle. These decreases paralleled a decline in muscle RNA so that the number of molecules of elongation factor 2 per ribosome appeared to be independent of the diet. We conclude that elongation factor 2 is probably not the factor limiting the rate of muscle protein synthesis and is not responsible for the fall in the protein-synthetic rate in vivo observed in the muscles of animals whose dietary protein intake is inadequate.

Topics: Animals; Body Weight; Diet; Male; Muscle Proteins; Muscles; NAD; Phosphorus Radioisotopes; Protein Deficiency; Rats; RNA

Topics: Animals; Autopsy; Body Weight; Gold Colloid, Radioactive; Injections, Intraperitoneal; Intestinal Diseases; Intestinal Mucosa; Intestine, Large; Intestine, Small; Intestines; Mice; Mice, Inbred BALB C; Muscle, Smooth; Peritoneum; Phosphorus Radioisotopes; Radiation Injuries, Experimental

Topics: Age Factors; Anemia, Hypochromic; Animals; Body Weight; Circadian Rhythm; DNA; Feeding Behavior; Growth; Iron Deficiencies; Iron-Dextran Complex; Liver; Organ Size; Phosphorus Radioisotopes; Rats; Thymidine; Thymidine Kinase; Tritium

Topics: Animals; Body Weight; Diet; Lung; Ozone; Phosphorus Radioisotopes; Rats; Respiratory Tract Infections; Staphylococcal Infections; Time Factors; Vitamin E; Vitamin E Deficiency

Topics: Administration, Oral; Animals; Body Weight; Bone and Bones; Brain Chemistry; Digestive System; Female; Half-Life; Intestinal Absorption; Kidney; Liver; Lung; Male; Molecular Weight; Myocardium; Organ Size; Organophosphonates; Phosphorus Radioisotopes; Polyethylenes; Rats; Tibia

Topics: Adrenalectomy; Animals; Body Weight; Diabetes Mellitus; Dogs; Glucose; Hypophysectomy; Injections, Intravenous; Insulin; Phosphorus; Phosphorus Radioisotopes; Stimulation, Chemical; Thyroidectomy

Topics: Blood Volume; Blood Volume Determination; Body Weight; Erythrocytes; Humans; Phosphorus; Phosphorus Radioisotopes