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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present paper examines the steroidogenic responsiveness of immature porcine Leydig cells in primary culture. Both testosterone (T) and dehydroepiandrosterone sulfate (DHAS) secretion were measured under basal conditions and after stimulation with human chorionic gonadotropin (hCG) (25 ng/ml). In medium supplemented with insulin, transferrin, epidermal growth factor (3H) and 0.1% calf serum, cells survived 3-5 days in culture. The production of steroids (under hCG stimulation) is poor on day 0-1 of the culture. On day 2-4 basal T and DHAS levels are 1.9 and 17.0 ng/10(6) cells/24 h. The addition of hCG stimulated T and DHAS production 19- and 6-fold respectively and the average productions were 37 and 109 ng/10(6) cells/24 h. Increasing the serum to 0.5% did not change the viability of the cultures, but increased hCG stimulated T and DHAS production (183 and 188 ng/10(6) cells/24 h). The addition of alpha-tocopherol (vitamin E) to 0.1% calf serum led to a 4-fold increase in stimulated T production (142 ng/10(6) cells/24 h) and maintained full cell viability for more than 5 days. Measurement of 3 beta-ol steroid dehydrogenase activity indicates that the amount of enzyme is 4 times higher at day 2 than at day 0 and 1 (with or without hCG), suggesting a spontaneous maturation of the cells in culture. This might explain the increased T production with time in culture. In cumulative experiments (24 h) the cells do not seem to be desensitized to hCG stimulation following prolonged exposure to 25 ng hCG since the daily steroid production is increasing with time in culture. However, kinetic studies show that steroidogenesis is not linear over a 24 h period. In cumulative experiments the steroid production stops between 12 and 16 h following hCG exposure (5 and 100 ng/ml) and resumes following a medium change. These results suggest that some inhibitory compounds are accumulated in the medium and are controlling the Leydig cell function. Moreover high doses of hCG (100 ng/ml) result in a lower production of steroids and an earlier plateau in the case of DHAS. These results demonstrate that porcine Leydig cells can live and differentiate in hormone- and vitamin-supplemented medium and that auto-feedback mechanisms inhibiting steroid accumulation take place under in vitro conditions.
Mol Cell Endocrinol 1983 Apr
PMID:Androgen production in primary culture of immature porcine Leydig cells. 622 Sep 34

Response of alveolar Type II (T-II) cells of male Sprague-Dawley weanling rats maintained on vitamin E (VE)-deficient and -supplemented diets to chlorphentermine (CP) treatment was evaluated. Ultrastructural and quantitative procedures were used to assess the T-II cell-drug interaction. Subjective examination of photomicrographs revealed numerous disrupted surfactant lamellar bodies in the CP-treated animals, as compared to fewer in controls. In addition, an unusual amorphous material was associated with these cells in drug-treated animals. Quantitative assessment confirmed the above subjective impression and revealed an increase in the size of T-II cells in treated rats. Morphometric evaluation showed that CP treatment significantly altered the volume density of cytoplasm, mitochondria, and rough endoplasmic reticulum (RER). Furthermore, a significant interaction between the diet and treatment with respect to volume fractions of mitochondria, RER, and Golgi complex was observed. The present study indicates that cytoplasmic components in T-II cells are altered as a result of CP treatment and that VE status of the animals influences the nature and extent of these alterations.
Exp Mol Pathol 1983 Aug
PMID:Chlorphentermine-induced alterations in the lungs of vitamin E-deficient and -supplemented rats: quantitative ultrastructural analysis of Type II Cell response. 630 43

Male Sprague-Dawley rats were maintained on diets containing 0.60, or 300 ppm vitamin E (VE) for 9 weeks with chlorphentermine (CP) or saline vehicle (SV) treatments administered over the last 3 weeks (20 mg CP/kg for one week and 30 mg CP/kg for subsequent 2 weeks or equivalent volume of saline vehicle). Spontaneous erythrocyte hemolysis averaged 68% for VE-deficient (0 ppm) and less than 9% for VE-supplemented (60 and 300 ppm) animals prior to saline and CP treatments. These values were not changed significantly by vehicle or drug administration. The lung-to-body weight ratios nearly doubled and the total lung phospholipid levels increased equivalently (three- to fourfold) in all three CP-treated VE groups as compared to corresponding SV controls. The levels of thiobarbituric acid-reactive material (TBA-RM), an index of lipid peroxidation, was increased in the lung tissue above SV controls in all dietary groups with the deficient group being the highest. There was no difference in the TBA-RM values of 60 and 300 ppm groups within each group. Quantitative morphometric analysis revealed that in the VE-supplemented groups, CP treatment caused a significant increase in the number of alveolar macrophage foam cells (FC) with a slight increase in the volume density of surfactant-like material (SLM). By comparison, there were fewer FCs but a larger quantity of SLM in the VE-deficient group. The results suggest that VE deficiency modifies the pulmonary response to CP resulting in lipid peroxidation-induced FC disintegration and the accumulation of SLM.
Exp Mol Pathol 1983 Jun
PMID:Chlorphentermine-induced alterations in the lungs of vitamin E-deficient and supplemented rats: 1. Biochemical and morphometric analysis of the pulmonary response. 685 9

Selected estimates of lipid peroxidation were analyzed in mouse quadriceps femoris muscle immediately after submaximal prolonged (9 hr) and exhaustive maximal running (2-3 hr), and at intervals 1-10 days afterward during the exercise-induced myopathy. Immediately after the two types of exertion no significant changes were observed in the concentrations of lipid peroxidation products (thiobarbituric acid (TBA) reactive substances, and lipofuscin) or in the estimates of autoxidation (spontaneous and Fe2+-induced autoxidations) and antioxidant (catalase, glutathione peroxidase, and vitamin E) capacities. The enzymatic estimate of exercise myopathy (beta-glucuronidase) increased considerably (2-6 days) after both types of exertion. Simultaneously, the lipid peroxidation rate of muscle homogenates in vitro increased markedly and in highly significant correlation with the activity of beta-glucuronidase. The concentrations of TBA reactants and lipofuscin as well as Fe2+-induced lipid peroxidation were not affected during exercise myopathy. The activities of catalase and glutathione peroxidase increased significantly after both exertions, while the concentration of vitamin E was unchanged. Exhaustive running of endurance-trained mice caused only slight signs of myopathy and no increase in the rate of lipid peroxidation in vitro.
Exp Mol Pathol 1983 Jun
PMID:Lipid peroxidation in exercise myopathy. 685 10

Vitamin E, a lipophilic antioxidant, has effectively inhibited the activation of cytokine-induced nuclear factor kB (NFkB). Since NFkB plays a critical role in the induction of an isoform of nitric oxide synthase (iNOS) gene by lipopolysaccharide (LPS), we investigated the effect of a vitamin E derivative, pentamethyl-hydroxychromane (PMC), which is an extremely potent inhibitor of NFkB activation, on the induction of nitric oxide (NO) synthesis and iNOS mRNA by LPS. PMC inhibited the LPS-stimulated induction of NO production in a concentration-dependent fashion in cultured J774 macrophages and rat vascular smooth muscle cells without evidence of cytotoxicity. However, the addition of PMC to J774 macrophages after the induction of iNOS did not inhibit NO production. Treatment of J774 macrophages with LPS resulted in a significant expression of iNOS mRNA, which was profoundly reduced by PMC. Data suggest that PMC inhibits the induction of iNOS by preventing iNOS gene expression through inhibition of NFkB activation.
Biochem Mol Biol Int 1995 Jan
PMID:Pentamethyl-hydroxychromane, vitamin E derivative, inhibits induction of nitric oxide synthase by bacterial lipopolysaccharide. 753 70

The free radical scavenging effect of "beta catechin", an antioxidant preparation containing green tea extract, ascorbic acid, sunflower seed extract, dunaliella carotene and natural vitamin E, was evaluated. Two techniques were used: electron spin resonance (ESR) spectrometry to measure radical-scavenging activity, and measurement of its effect on iron-induced lipid peroxidation in brain. A 0.05% solution of "beta catechin" completely scavenged 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals (6.1 x 10(15)spins/ml). A 10% solution of "beta catechin" completely scavenged superoxide (4.2 x 10(15) spins/ml) generated by the hypoxanthine-xanthine oxidase system. An undiluted solution of "beta catechin" scavenged about 90% of hydroxyl radicals (3.5 x 10(15) spins/ml) generated by the Fenton reaction. "beta catechin"s effect on the accumulation of thiobarbituric acid-reactive substances (TBARS) was evaluated from tissue obtained from the ipsilateral cortex of FeCl3-induced epileptic rats. Oral administration of "beta catechin" (1 or 2ml/kg body weight) both inhibited TBARS formation and increased the activity of superoxide dismutase (SOD) in the ipsilateral cortex 30 min after iron-salt injection into the left sensory motor cortex. These data suggest that "beta catechin" has an antioxidant effect and may have a prophylactic effect against aging and other neurological diseases related to free radical mechanisms.
Biochem Mol Biol Int 1995 Apr
PMID:Antioxidant effects of "beta catechin". 754 42

In the present study, we examined whether active oxygen formed in the process of 4-nitroquinoline 1-oxide (4NQO) reduction by DT-diaphorase could induce oxidative stress on the pulmonary nuclei. The rapid production of OH- radical-like species after the start of the 4NQO reduction was observed, and subsequent induction of nuclear lipid peroxidation occurred. In conjugation with this event, DNA damage estimated as DNA single strand breaks (DNA-SSB) increased in a time-dependent manner. The induction of this DNA damage was partially inhibited by mannitol or vitamin E treatment. These findings suggest that the active oxygen generated in the process of the 4NQO reduction can induce oxidative damage on the pulmonary nuclei.
Res Commun Mol Pathol Pharmacol 1995 Mar
PMID:Active oxygen generated in the process of carcinogen metabolism can induce oxidative damage in nuclei. 762 Aug 30

The relationship between the metabolism of alpha-tocopherol (alpha-T) (vitamin E) and that of ascorbic acid (vitamin C) was examined in cultured hepatocytes intoxicated with tert-butyl hydroperoxide (TBHP). Unlike vitamin E, the cellular content of vitamin C did not decline after overnight culturing of freshly prepared hepatocytes. In addition, this basal vitamin C content was not affected by the presence of alpha-T phosphate in the overnight culture medium. Supplementation of the overnight culture medium with vitamin C (10 microM to 10 mM) increased the cellular content of vitamin C by > 1 order of magnitude. Increasing the cellular content of ascorbate increased the protection against TBHP toxicity, with or without the presence of a physiological content of vitamin E. In vitamin E-supplemented cells, a loss of alpha-T occurred within 15 min of exposure to TBHP and before the decrease in cellular ascorbate content. The vitamin C content declined in parallel with the loss of cell viability. Supplementation of the overnight culture medium with increasing concentrations of ascorbate progressively spared the depletion of alpha-T while preventing the cell killing. Pretreatment with the ferric iron chelator deferoxamine or the antioxidant N,N'-diphenyl-1,4-phenylenediamine prevented the loss of ascorbate and the cell killing by TBHP in hepatocytes either sufficient or deficient in alpha-T. However, neither alpha-T nor ascorbate prevented the accumulation of DNA single-strand breaks caused by TBHP, indicating that these vitamins do not effectively scavenge the TBHP-derived radicals responsible for DNA damage. The data in the present study indicate that vitamins E and C act as independent antioxidants and that ascorbate does not regenerate alpha-T in cultured rat hepatocytes.
Mol Pharmacol 1995 Jul
PMID:Relationship of the metabolism of vitamins C and E in cultured hepatocytes treated with tert-butyl hydroperoxide. 762 78

The neonatal human Leydig cell undergoes a transient period of activation during the first months of life. The biological significance of this activation is unknown. Furthermore, little is known about the hormonal regulation of this biological process, even though it coincides with an elevation of LH levels in serum. In order to study the function of human prepubertal testicular culture cells, obtained during the neonatal period, a method for maintaining primary culture cells (isolated from testes collected at necropsy) in culture was developed. Within 24 h after death, testes were collected from 1-36-month-old subjects. Subjects were divided into two age groups, based on the presence or absence of fetal Leydig cells: 1-7-month-old infants (group 1) and 12-36-month-old children (group 2). Testes were digested with collagenase, and cells were seeded in multi-well dishes. Cells were grown in serum-free conditioned media supplemented with 5 mg/l vitamin C, 0.2 IU/l vitamin E and 10% fetal bovine serum for 2 days. Cells were then grown for an additional 4 days in serum-free media in the presence or absence of hLH (40 IU/l), hCG (135 IU/l), rh FSH (1.5 IU/l), rhGH (0.12 IU/l) or insulin (0.9 mumol/l). Concentrations of steroids in media were determined by RIA on day 6 of culture. In basal conditions cells of group 1 (n = 11) secreted more testosterone, androstendione, 17-hydroxyprogesterone, progesterone and dehydroepiandrosterone (mean +/- SE: 6.76 +/- 1.86, 7.37 +/- 1.82, 61.9 +/- 1.86, 5.75 +/- 1.74 and 8.51 +/- 3.23 pmol/10(6) cells/24 h, respectively) than cells of group 2 (n = 5) (2.95 +/- 1.15, 1.50 +/- 2.75, 1.44 +/- 2.75, 0.78 +/- 1.74 and 3.23 +/- 1.32, respectively). Under hLH stimulation, cells of group 1 increased testosterone, androstendione and 17-hydroxyprogesterone secretions (to 38.2 +/- 0.89, 13.5 +/- 1.17 and 51.7 +/- 3.23), while progesterone secretion remained unchanged (2.82 +/- 1.20). Cell response to rhFSH and rhGH was similar to that of hLH. On the other hand, medium collected from cultures of cells isolated from a Sertoli cell tumor was able to stimulate testosterone secretion in subcultures of control testicular cells in a way similar to that of hCG. In conclusion, (1) these prepubertal human testicular cells can be maintained in primary culture for several days keeping their in vivo steroidogenic potential; (2) cells isolated from young infants can respond to hLH in culture; (3) response to rhFSH is probably mediated by a paracrine factor; (4) response to rhGH is observed in the absence of gonadotropins.(ABSTRACT TRUNCATED AT 400 WORDS)
J Steroid Biochem Mol Biol 1995 Jun
PMID:Human prepubertal testicular cells in culture: steroidogenic capacity, paracrine and hormone control. 762 44

It is established that acetaminophen exhibits oxidative behaviour. The effects of acetaminophen (0.3-14.5 microM) on methemoglobin levels, superoxide dismutase and Na(+)-K+ ATPase activities of normal and vitamin E or vitamin C pretreated erythrocytes were investigated. In acetaminophen incubated erythrocytes, methemoglobin concentration and superoxide dismutase activity were increased in a dose and incubation-time dependent manner, the activity of Na(+)-K+ ATPase was decreased by acetaminophen treatment. Vitamin E (1mg/dl of erythrocyte suspension) or vitamin C (1mg/dl of erythrocyte suspension) provided partial protection of hemoglobin, superoxide dismutase and Na(+)-K+ ATPase against acetaminophen action. Vitamin E was more effective than vitamin C.
Biochem Mol Biol Int 1995 Apr
PMID:Effects of acetaminophen on methemoglobin, superoxide dismutase and Na(+)-K+ ATPase activities of human erythrocytes. 762 22


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