ascorbic-acid and Hypertrophy

Topics: Adrenal Glands; Animals; Antioxidants; Ascorbic Acid; Biotransformation; Chemical and Drug Induced Liver Injury; Female; Food Additives; Growth; Hypertrophy; Lipid Metabolism; Liver; Mice; Phenols; Rats; Reproduction; Vitamin E

The aim of this study was to examine whether antioxidant vitamin supplementation with vitamin C (VitC) and vitamin E (VitE) affects the hypertrophic and functional adaptations to resistance training in trained men.. This was a double-blind, randomized controlled trial in which participants were supplemented daily with VitC and VitE ( n = 12) or placebo ( n = 11) while completing a 10-wk resistance training program accompanied by a dietary intervention (300 kcal surplus and adequate protein intake) designed to optimize hypertrophy. Body composition (dual-energy x-ray absorptiometry), handgrip strength, and one-repetition maximum (1-RM), maximal force (F0), velocity (V0), and power (Pmax) were measured in bench press (BP) and squat (SQ) tests conducted before and after the intervention. To detect between-group differences, multiple-mixed analysis of variance, standardized differences, and qualitative differences were estimated. Relative changes within each group were assessed using a paired Student's t test.. In both groups, similar improvements were produced in BP 1-RM , SQ 1-RM SQ, and BP F0 (P < 0.05) after the resistance training program. A small effect size was observed for BP 1-RM (d = 0.53), BP F0 (d = 0.48), and SQ 1-RM (d = -0.39), but not for SQ F0 (d = 0.03). Dominant handgrip strength was significantly increased only in the placebo group (P < 0.05). According to body composition data, a significant increase was produced in upper body fat-free mass soft tissue (FFMST; P < 0.05) in the placebo group, whereas neither total nor segmental FFMST was increased in the vitamin group. Small intervention effect sizes were observed for upper body FFSMT (d = 0.32), non-dominant and dominant leg FFMST (d = -0.39; d = -0.42). Although a significant increase in total body fat was observed in both groups (P < 0.05) only the placebo group showed an increase in visceral adipose tissue (P < 0.05), showing a substantial intervention effect (d = 0.85).. The data indicated that, although VitC/VitE supplementation seemed to blunt upper body strength and hypertrophy adaptations to resistance training, it could also mitigate gains in visceral adipose tissue elicited by an energy surplus.

Topics: Antioxidants; Ascorbic Acid; Body Composition; Dietary Supplements; Double-Blind Method; Hand Strength; Humans; Hypertrophy; Male; Muscle Strength; Muscle, Skeletal; Resistance Training; Vitamin E; Vitamins

This was a placebo-controlled randomized study that aimed to investigate the effects of strength training (ST) combined with antioxidant supplementation on muscle performance and thickness. Forty-two women (age, 23.8 ± 2.7 years; body mass, 58.7 ± 11.0 kg; height, 1.63 ± 0.1 m) were allocated into 3 groups: vitamins (n = 15), placebo (n = 12), or control (n = 15). The vitamins and placebo groups underwent an ST program, twice a week, for 10 weeks. The vitamins group was supplemented with vitamins C (1 g/day) and E (400 IU/day) during the ST period. Before and after training, peak torque (PT) and total work (TW) were measured on an isokinetic dynamometer, and quadriceps muscle thickness (MT) was assessed by ultrasound. Mixed-factor ANOVA was used to analyze data and showed a significant group × time interaction for PT and TW. Both the vitamins (37.2 ± 5.4 to 40.3 ± 5.6 mm) and placebo (39.7 ± 5.2 to 42.5 ± 5.6 mm) groups increased MT after the intervention (P < 0.05) with no difference between them. The vitamins (146.0 ± 29.1 to 170.1 ± 30.3 N·m) and placebo (158.9 ± 22.4 to 182.7 ± 23.2 N·m) groups increased PT after training (P < 0.05) and PT was higher in the placebo compared with the control group (P = 0.01). The vitamins (2068.3 ± 401.2 to 2295.5 ± 426.8 J) and placebo (2165.1 ± 369.5 to 2480.8 ± 241.3 J) groups increased TW after training (P < 0.05) and TW was higher in the placebo compared with the control group (P = 0.01). Thus, chronic antioxidant supplementation may attenuate peak torque and total work improvement in young women after 10 weeks of ST.

Topics: Adult; Antioxidants; Ascorbic Acid; Biomechanical Phenomena; Brazil; Dietary Supplements; Double-Blind Method; Female; Humans; Hypertrophy; Muscle Contraction; Muscle Strength; Muscle, Skeletal; Resistance Training; Time Factors; Torque; Treatment Outcome; Ultrasonography; Vitamin A; Young Adult

Ascorbic acid has been suggested to regulate obesity in obese male rodents. Moreover, increased adipocyte size has been associated with metabolic disease. Thus, we investigated the effects of ascorbic acid on adipocyte hypertrophy and insulin resistance in high-fat diet (HFD)-induced obese ovariectomized (OVX) C57BL/6J mice, an animal model of obese postmenopausal women. Administration of ascorbic acid (5% w/w in diet for 18 weeks) reduced the size of visceral adipocytes without changes in body weight and adipose tissue mass in HFD-fed obese OVX mice compared with obese OVX mice that did not receive ascorbic acid. Ascorbic acid inhibited adipose tissue inflammation, as shown by the decreased number of crown-like structures and CD68-positive macrophages in visceral adipose tissues. Ascorbic acid-treated mice exhibited improved hyperglycemia, hyperinsulinemia, and glucose and insulin tolerance compared with nontreated obese mice. Pancreatic islet size and insulin-positive β-cell area in ascorbic acid-treated obese OVX mice decreased to the levels observed in low-fat diet-fed lean mice. Ascorbic acid also suppressed pancreatic triglyceride accumulation in obese mice. These results suggest that ascorbic acid may reduce insulin resistance and pancreatic steatosis partly by suppressing visceral adipocyte hypertrophy and adipose tissue inflammation in obese OVX mice.

Topics: Adipocytes; Animals; Ascorbic Acid; Diet, High-Fat; Female; Hypertrophy; Inflammation; Insulin; Insulin Resistance; Male; Mice; Mice, Inbred C57BL; Mice, Obese; Obesity; Pancreatic Diseases

This study aimed to investigate the effects of vitamin C administration on skeletal muscle hypertrophy induced by mechanical overload in rats.. Male Wistar rats were randomly assigned to three groups: (i) sham-operated group (n = 8), (ii) placebo-administered group (n = 8) and (iii) vitamin C-administered group (n = 8). In the placebo-administered and vitamin C-administered groups, the gastrocnemius and soleus muscles of the right hindlimb were surgically removed to overload the plantaris muscle. Vitamin C (500 mg kg(-1)) was orally administered to the vitamin C-administered group once a day for 14 days.. Synergist muscle ablation caused significant increases in wet weight and protein concentration of the plantaris muscle in both the placebo-administered (P < 0.01) and vitamin C-administered groups (P < 0.01) compared with the sham-operated group (SHA). However, the magnitude of plantaris muscle hypertrophy (expressed as a percentage of the contralateral plantaris muscle) was significantly smaller (P < 0.01) in the vitamin C-administered group (141%) than in the placebo-administered group (PLA) (152%). Compared with the SHA, only the PLA showed higher expressions of phosphorylated p70s6k and Erk1/2 (positive regulators of muscle protein synthesis) and a lower expression of atrogin-1 (a muscle atrophy marker). Concentrations of vitamin C and oxidative stress markers in the overloaded muscle were similar between the placebo-administered and vitamin C-administered groups.. Oral vitamin C administration can attenuate overload-induced skeletal muscle hypertrophy, which may have implications for antioxidant supplementation during exercise training.

Topics: Administration, Oral; Animals; Antioxidants; Ascorbic Acid; Hindlimb; Hypertrophy; Male; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; Muscle Contraction; Muscle Proteins; Muscle, Skeletal; Organ Size; Oxidative Stress; Phosphorylation; Physical Exertion; Rats; Rats, Wistar; Ribosomal Protein S6 Kinases, 70-kDa; Signal Transduction; SKP Cullin F-Box Protein Ligases; Time Factors

The ATDC5 cell line exhibits the multistep chondrogenic differentiation observed during endochondral bone formation. However, it takes up to two months to complete the process of cell expansion, insulin addition to promote differentiation and further changes in culture conditions effectively to induce hypertrophy. We sought to produce consistent chondrogenesis with significant hypertrophic differentiation with simpler conditions in a more practical time period. By adding ascorbate, the prechondrogenic proliferation phase was shortened from 21 to 7 days, with production of cartilaginous nodules during the chondrogenic phase, after insulin addition, that were greater in number and larger in size. Immunohistochemistry indicated much greater matrix elaboration and the mRNA expression of sox9, aggrecan and collagen type II were all significantly increased earlier and to a much higher degree when compared with controls. Moreover, there was a robust induction of hypertrophy: Col10a1, Runx2 and Mmp13 were all induced within 7-10 days. In conclusion, addition of ascorbate to ATDC5 cultures shortened the prechondrogenic proliferation phase, produced earlier chondrogenic differentiation, heightened gene expression and robust hypertrophic differentiation, abrogating the need for extended culture times and the changes in culture conditions. This simple modification considerably enhances the practicality of this cell line for studies of chondrogenesis.

Topics: Aggrecans; Animals; Ascorbic Acid; Biomarkers; Cell Differentiation; Cells, Cultured; Chondrocytes; Chondrogenesis; Collagen Type II; High Mobility Group Proteins; Hypertrophy; Mice; RNA, Messenger; SOX9 Transcription Factor; Transcription Factors; Up-Regulation

Peroral administration of 70 mg/kg ascovertin and 150 mg/kg Leuzea extract to rats with cerebral ischemia for 5 days prevented destructive changes and decrease in the density of synapses in the cerebral cortex. These preparations activated compensatory and reparative mechanisms underlying plasticity of the synaptic pool, which was realized through hypertrophy and destruction of synaptic contacts. Ascovertin possessed more pronounced cerebroprotective activity than Leuzea extract.

Topics: Animals; Ascorbic Acid; Brain; Cerebral Cortex; Drug Combinations; Female; Hypertrophy; Ischemia; Male; Plant Extracts; Quercetin; Rats; Rats, Wistar; Synapses

Chondrocytes show an unusual ability to thrive under serum-free conditions as long as insulin, thyroxine, and cysteine are present. Studies with sternal chondrocytes from chick embryos indicate that thymidine incorporation in chondrocytes cultured under serum-free conditions is 30-50% of that seen with fetal bovine serum (FBS). In contrast, skin fibroblast proliferation in serum-free culture is <5% of that seen with serum. Addition of 30-50 microM ascorbic acid to serum-free medium stimulates chondrocyte proliferation 4-5x, resulting in levels of thymidine incorporation higher than that seen with 10% serum. Three to five hours of ascorbate exposure is sufficient to stimulate proliferation, with maximal stimulation seen after 12-15 h. Bromo-deoxyuridine (BrdU) labelling indicated that approximately 25% of chondrocytes transit S phase during a 4-h period (16-20 h after ascorbate). Once maximal stimulation is reached, the proliferation rate remains fairly constant over at least 40 h. Ascorbate therefore increases the steady-state level of chondrocytes in the cycle. Because the stimulation of chondrocyte proliferation was greater than the net increase in cell numbers, we examined the level of apoptosis. Nuclear morphology, terminal uridine nucleotide end-labelling (TUNEL) assay, and 7-AAD/Hoechst dye FACS analyses all indicated that approximately 15% of the ascorbate-treated chondrocytes were undergoing apoptosis, while only 5% of the control chondrocytes were apoptotic. When prehypertrophic chondrocytes from the cephalic region of embryonic sternae were stimulated to undergo hypertrophy with rhBMP-2 + ascorbate, levels of apoptosis were similar to that seen with ascorbate alone. In contrast, treatment of caudal chondrocytes with BMP plus ascorbate does not induce hypertrophy, and the proportion of apoptotic cells was less than that seen with ascorbate alone. These results imply that in chondrocytes the transition to hypertrophy is associated with a decreased number of proliferating cells and a relatively high level of apoptosis.

Topics: Animals; Apoptosis; Ascorbic Acid; Bone Morphogenetic Protein 2; Bone Morphogenetic Proteins; Cell Count; Cell Division; Cells, Cultured; Chick Embryo; Chondrocytes; Hypertrophy; Thymidine; Transforming Growth Factor beta; Tritium

In serum-containing medium, ascorbic acid induces maturation of prehypertrophic chick embryo sternal chondrocytes. Recently, cultured chondrocytes have also been reported to undergo maturation in the presence of bone morphogenetic proteins or in serum-free medium supplemented with thyroxine. In the present study, we have examined the combined effect of ascorbic acid, BMP-2, and serum-free conditions on the induction of alkaline phosphatase and type X collagen in chick sternal chondrocytes. Addition of either ascorbate or rhBMP-2 to nonconfluent cephalic sternal chondrocytes produced elevated alkaline phosphatase levels within 24-72 h, and simultaneous exposure to both ascorbate and BMP yielded enzyme levels at least threefold those of either inducer alone. The effects of ascorbate and BMP were markedly potentiated by culture in serum-free medium, and alkaline phosphatase levels of preconfluent serum-free cultures treated for 48 h with BMP+ascorbate were equivalent to those reached in serum-containing medium only after confluence. While ascorbate addition was required for maximal alkaline phosphatase activity, it did not induce a rapid increase in type X collagen mRNA. In contrast, BMP added to serum-free medium induced a three- to fourfold increase in type X collagen mRNA within 24 h even in the presence of cyclohexamide, indicating that new protein synthesis was not required. Addition of thyroid hormone to serum-free medium was required for maximal ascorbate effects but not for BMP stimulation. Neither ascorbate nor BMP induced alkaline phosphatase activity in caudal sternal chondrocytes, which do not undergo hypertrophy during embryonic development. These results indicate that ascorbate+BMP in serum-free culture induces rapid chondrocyte maturation of prehypertrophic chondrocytes. The mechanisms for ascorbate and BMP action appear to be distinct, while BMP and thyroid hormone may share a similar mechanism for induction.

Topics: Alkaline Phosphatase; Animals; Ascorbic Acid; Bone Morphogenetic Protein 2; Bone Morphogenetic Proteins; Cartilage; Cell Size; Cells, Cultured; Chick Embryo; Collagen; Culture Media, Serum-Free; Dexamethasone; Dose-Response Relationship, Drug; Hypertrophy; Insulin; Phenotype; Sternum; Transforming Growth Factor beta

Meckel's cartilage in the avian mandible is a neural crest-derived permanent cartilage. To investigate whether chondrocytes that form Meckel's cartilage can be induced to undergo maturation and mineralization by manipulating the environment, we used in vitro micromass culture in which young embryonic mandibular ectomesenchymal cells were maintained at a high cell density (2 x 10(7) cells/ml) and treated with ascorbic acid (AA) or with dexamethasone and ascorbic acid (DEX + AA). Chondrogenesis and chondrocyte maturation were analyzed by histological, immunohistochemical and SDS/PAGE techniques. Chick mandibular ectomesenchymal cells from Hamburger and Hamilton (J. Morphol. 88:49-92, 1951) stage 21 (HH stage 21) chick embryos undergo chondrogenesis forming cartilage nodules when maintained under micromass culture conditions. These chondrocytes undergo maturation in response to AA but not DEX. Addition of AA to culture medium induced type X collagen expression by these chondrocytes. With prolonged culture, chondrocytes began to mineralize turning cartilage nodules into completely mineralized structures. There was no correlation between chondrocyte size and type X collagen expression. Small chondrocytes as well as large (hypertrophic) chondrocytes expressed type X collagen and then underwent mineralization. Co-treatment of cultures with DEX + AA caused reduction of chondrogenesis and inhibited chondrocyte maturation and mineralization seen with AA alone.

Topics: Animals; Ascorbic Acid; Calcification, Physiologic; Cartilage; Cell Count; Cells, Cultured; Chick Embryo; Collagen; Dexamethasone; Electrophoresis, Polyacrylamide Gel; Fluorescent Antibody Technique; Hypertrophy; Immunohistochemistry; Mandible; Mesoderm

Numerous studies of experimental hypo- and hypervitaminosis A have long suggested that retinoic acid (RA) is involved in chondrocyte maturation during endochondral ossification and skeletogenesis. However, the specific and direct roles of RA in these complex processes remain unclear. Based on recent studies from our laboratories, we tested the hypothesis that RA induces the expression of genes associated with the terminal mineralization phase of chondrocyte maturation and promotes apatite deposition in the extracellular matrix. Cell populations containing chondrocytes at advanced stages of maturation were isolated from the upper portion of Day 18 chick embryo sterna and grown for 2 weeks in monolayer until confluent. The cells were then treated with low doses (10-100 nM) of RA for up to 6 days in the presence of a phosphate donor (beta-glycerophosphate) but in the absence of ascorbic acid. Within 4 days of treatment, RA dramatically induced expression of the alkaline phosphatase (APase), osteonectin, and osteopontin genes, caused a several-fold increase in APase activity, and provoked massive mineral formation while it left type X collagen gene expression largely unchanged. The mineral had a mean Ca/Pi molar ratio of 1.5; Fourier transform infrared spectra confirmed that it represented hydroxyapatite. Mineralization was completely abolished by treatment with parathyroid hormone; this profound effect confirmed that RA induced cell-mediated mineralization and not nonspecific precipitation. When cultures were treated with both RA and ascorbic acid, there was a slight further increase in APase activity and increased calcium accumulation. The effects of RA were also studied in cultures of immature chondrocytes isolated from the caudal portion of sternum; however, RA only had minimal effects on mineralization and gene expression in these cells. Thus, RA appears to be a rapid, potent, maturation-dependent, ascorbate-independent promoter of terminal maturation and matrix calcification in chondrocytes.

Topics: Alkaline Phosphatase; Animals; Apatites; Ascorbic Acid; Calcification, Physiologic; Calcium; Cartilage; Cells, Cultured; Chick Embryo; Collagen; Dose-Response Relationship, Drug; Extracellular Matrix; Fluorescent Antibody Technique; Gene Expression; Hypertrophy; Minerals; Osteonectin; Osteopontin; Parathyroid Hormone; Sialoglycoproteins; Time Factors; Tretinoin

Dedifferentiated chick embryo chondrocytes (Castagnola, P., G. Moro, F. Descalzi-Cancedda, and R. Cancedda, 1986, J. Cell Biol., 102:2310-2317), when transferred to suspension culture on agarose-coated dishes in the presence of ascorbic acid, aggregate and remain clustered. With time in culture, clusters grow in size and adhere to each other, forming structures that may be several millimeters in dimension. These structures after 7 d of culture have the histologic appearance of mature hypertrophic cartilage partially surrounded by a layer of elongated cells resembling the perichondrium. Cells inside the aggregates have ultrastructural features of stage I (proliferating) or stage II (hypertrophic) chondrocytes depending on their location. Occurrence and distribution of type I, II, and X collagens in the in vitro-formed cartilage at different times of culture, show a temporal and spatial distribution of these antigens reminiscent of the maturation events occurring in the cartilage in vivo. A comparable histologic appearance is shown also by cell aggregates obtained starting with a population of cells derived from a single, cloned, dedifferentiated chondrocyte.

Topics: Animals; Ascorbic Acid; Cartilage; Cell Aggregation; Cell Differentiation; Cells, Cultured; Chick Embryo; Fluorescent Antibody Technique; Hypertrophy; Microscopy, Electron; Morphogenesis

During compensatory growth of kidney, microsomal lipid peroxidation is unchanged in the hypertrophy phase and is doubled in a period of hyperplasia. The maximum lipid peroxidation is preceded by a 2-fold increase in the content of cytochrome P-450. Both in microsomes and cytosol, intense peroxidation of lipids is accompanied by a decrease in glutathione content.

Topics: Animals; Ascorbic Acid; Cytochrome P-450 Enzyme System; Glutathione; Hypertrophy; Kidney; Lipid Peroxides; Male; Microsomes; Rats; Rats, Inbred Strains

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Animals; Ascorbic Acid; Hypertrophy; Organ Size; Pituitary Gland; Rats; Rats, Inbred Strains; Stress, Physiological

The influence of extraneous supplementation of L-ascorbic acid in chronic chlordane toxicity has been studied in rats. Oral administration of chlordane brings about a marked growth retardative effect, stimulates vitamin C synthesis in the system, elevates the vitamin C status of the liver and kidney tissues and also the urinary excretion. It inhibits the activities of acid and alkaline phosphatases, SDH and Mg2+-ATPase of both hepatic and renal tissues. The activities of serum and mitochondrial GOT, serum alkaline phosphatase, and glucose-6-phosphatase of both hepatic and renal tissues are markedly stimulated. The normal histological patterns of both liver and kidney tissues are grossly altered under chlordane toxicity condition. There occurs marked increase in the hepatic lipid composition. Supplementation of L-ascorbic acid in high doses to the chlordane treated rats can effectively counteract some of these alterations in respect of enzyme activities, morphological characteristics and of hepatic lipid composition.

Topics: Animals; Ascorbic Acid; Chlordan; Diet; Growth Disorders; Hypertrophy; Kidney; Liver; Male; Rats; Stereoisomerism

We determined the respiration, respiratory control, and Pi:O ratios with different substrates in mitochondria isolated from five cases of human neuromuscular disorders (two cases of central core disease, two cases of neuropathy of Dejerine-Sottas, and one case of Kugelberg-Welander's disease) and compared them with normal human muscle. In all the myopathies studied, a severe derangement of the respiratory control with variable derangement of oxidative phosphorylation was found. This supports the idea that a group of neuromyopathies shares the same biochemical lesion as the so-called mitochondrial myopathies, forming with them a group of myopathies which may be related through a similar biochemical lesion of varying degree. Alternatively, disturbance of mitochondrial functions in a number of myopathies could be considered as a non-specific finding.

Topics: Adenosine Diphosphate; Adolescent; Adult; Ascorbic Acid; Child; Female; Glutamates; Humans; Hypertrophy; Infant; Malates; Male; Middle Aged; Mitochondria, Muscle; Motor Neurons; Muscular Atrophy; Muscular Diseases; Myotonic Dystrophy; Neuromuscular Diseases; Oxidative Phosphorylation; Oxidative Phosphorylation Coupling Factors; Oxygen Consumption; Phosphates; Spinal Cord Diseases; Succinates

Topics: Adrenal Glands; Adrenalectomy; Animals; Ascorbic Acid; Diabetes Mellitus, Experimental; Female; Hypertrophy; Male; Mice; Rats

Topics: Analysis of Variance; Animals; Ascorbic Acid; Binding Sites; Body Weight; Castration; Estrogens; Female; Hypertrophy; Male; Organ Size; Pituitary Diseases; Pituitary Gland; Rats

1. Adrenocortical hyperactivity caused by a marked increase in circulating corticotrophin occurred in guinea-pigs on a diet deficient in ascorbic acid.2. Betamethasone prevented the rise in the blood ACTH concentration in scorbutic animals and also the increased steroid production per gramme adrenal tissue in vitro. It diminished the adrenal hypertrophy and partially suppressed the rise in plasma cortisol.3. Ninety minutes after the injection of ascorbic acid corticotrophin could no longer be detected in the plasma of scorbutic animals.4. Neither the survival time nor the weight loss was affected by betamethasone treatment.

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Betamethasone; Body Weight; Diet; Female; Guinea Pigs; Hydrocortisone; Hypertrophy; Time Factors

Topics: Alkaline Phosphatase; Aminopropionitrile; Animals; Ascorbic Acid; Calcification, Physiologic; Cartilage; Chick Embryo; Chondroitin; Collagen; Cortisone; Endoplasmic Reticulum; Glycogen; Hypertrophy; Lipids; Skull

Topics: Adrenal Glands; Adrenocortical Hyperfunction; Animals; Ascorbic Acid; Cholesterol; Dexamethasone; Hydrocortisone; Hypertrophy; Hypothalamo-Hypophyseal System; Hypothalamus; Male; Organ Size; Pituitary Gland; Pituitary-Adrenal System; Rats

Topics: Adrenal Glands; Adrenocortical Hyperfunction; Animals; Ascorbic Acid; Body Weight; Carbon Tetrachloride Poisoning; Female; Hypertrophy; Organ Size; Rats

Topics: Adrenal Glands; Adrenalectomy; Adrenocorticotropic Hormone; Animals; Ascorbic Acid; Carbon Isotopes; Cortisone; Drug Antagonism; Glycyrrhiza; Histamine; Hypertrophy; Male; Pharmacology; Phenylalanine; Pituitary Gland; Pituitary-Adrenal System; Plants, Medicinal; Prednisolone; Protein Biosynthesis; Rats

Topics: Adrenal Glands; Adrenocortical Hyperfunction; Animals; Ascorbic Acid; Atrophy; Diet; Drug Antagonism; Hypertrophy; Male; Rats; Testis; Tyrosine

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Ascorbic Acid; Histology; Hyperplasia; Hypertrophy; Lipid Metabolism; Metyrapone; Mineralocorticoid Receptor Antagonists; Pharmacology; Pituitary Diseases; Pituitary Gland; Research; Rodentia

Topics: Adrenal Glands; Adrenocortical Hyperfunction; Animals; Ascorbic Acid; Cholesterol; Diabetes Mellitus, Experimental; Histocytochemistry; Hypertrophy; Lipids; Rats

Topics: Adrenal Glands; Adrenalectomy; Adrenocorticotropic Hormone; Animals; Ascorbic Acid; Hypertrophy; Pituitary Diseases; Pituitary Gland; Pituitary Gland, Anterior; Rats; Stress, Physiological

Topics: Ascorbic Acid; Humans; Hypertrophy; Male; Prostate; Prostatic Hyperplasia; Vitamins