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T Lin

Publications and source records attributed to T Lin.

At least 91 records · Page 5Linked to original sources
PubMed1982

[Testosterone-estradiol binding globulin and sex steroids during pregnancy and at delivery].

Testosterone-estradiol binding globulin (TeBG), testosterone, estradiol-17 beta, index-T (testosterone not bound to TeBG) and index-E2 were determined during pregnancy, at parturition, in the umbilical artery and vein, and during postpartum periods. TeBG showed a rapid increase during the early pregnancy and then it reached a certain level at the mid pregnancy. At parturition, it decreased to about half of the late pregnancy. In the umbilical artery and vein the level was extremely low. Testosterone gradually increased from the early to the late pregnancy. However, index-T reached its lowest level during the 5th month of pregnancy. In the umbilical artery and vein testosterone exhibited a slightly lower level in comparison with the maternal blood but in contrast to this index-T exhibited five times higher level in the umbilical artery and vein than in the maternal blood. Estradiol-17 beta exhibited a linear increase from the early to the late pregnancy but index-E2 showed a sudden increase during the late pregnancy. The levels in the maternal blood at the parturition and in the umbilical artery and vein were compared: The estradiol-17 beta levels were maternal blood greater than umbilical vein greater than umbilical artery and the index-E2 levels were maternal blood .=. umbilical vein greater than umbilical artery.

Estradiol↗
PubMed1981

Direct inhibition of rat leydig cell function by tamoxifen.

The effects of tamoxifen on rat testicular steroidogenesis were studied using dispersed interstitial cells. Tamoxifen significantly inhibited LH-, and 8-bromo-adenosine 3',5'-monophosphate (8-bromo-cyclic AMP)-stimulated testosterone synthesis in a dose-dependent manner. Tamoxifen (10(-5)M) also reduced LH-stimulated cyclic AMP formation. The addition of equimolar concentrations of 17 beta-estradiol or tamoxifen separately to interstitial cells resulted in similar inhibition of LH-stimulated testosterone synthesis. When equimolar concentrations of 17 beta-estradiol and tamoxifen were added concomitantly to interstitial cells, the inhibition was additive. Present studies demonstrate that tamoxifen has direct inhibitory effects on testicular steroidogenesis: both at the plasma membrane resulting in decreased cyclic AMP formation and also at steps subsequent to cyclic AMP.

Animals↗
PubMed1981

The aging Leydig cell: 2. Two distinct populations of Leydig cells and the possible site of defective steroidogenesis.

Using metrizamide gradient centrifugation two populations of Leydig cells were found in both 60-90 day-old and 24 month-old rats. Cells from both Band 2 (B2) and Band 3 (B3) responded to LH stimulation with increased cyclic AMP formation; however, only B3 cells produced significant amounts of testosterone. Cells from both B2 and B3 of the old rats synthesized less cyclic AMP and testosterone than cells from their younger counterparts. In response to LH stimulation, 0.01 - 1.0 mIU/ml, no appreciable difference of cyclic AMP formation could be detected between young and old Leydig cells. Maximal testosterone production occurred when 1 mIU/ml LH was used. Only when LH concentration was increased to 10 and 100 mIU/ml, did young Leydig cells produce significantly more cyclic AMP than old Leydig cells. After addition of 5X10(-7)M of pregnenolone or progesterone to the incubation medium, both young and old Leydig cells produced comparable amounts of testosterone. These results demonstrate no impairment of old rat Leydig cells to synthesize testosterone from pregnenolone and progesterone.

Aging↗
PubMed1981

The aging Leydig cell: VII. Cytoplasmic estradiol receptors.

Plasma estradiol and cytosolic estradiol receptor levels of testes were determined in a group of young (2-3 months) and old (24 months) Sprague-Dawley rats. Estradiol binding sites for the young rats averaged 5.6 +/- 0.3 fmol/mg protein (x +/- SE, n=12), which was comparable to that of the old rats, 5.7 +/- 0.3 fmol/mg protein (n=12). Using Scatchard analyses, the association constants at equilibrium of estradiol receptor binding of the old and young rats were the same, 6.1 x 10 10 M-1. Plasma estradiol levels were also similar in both groups-19.6 +/- 2.8 pg/ml (n=14) for the young and 19.2 +/- 2.6 pg/ml (n=10) for the old rats. Our results suggest that impaired testosterone biosynthesis in old rats was not due to elevated plasma estradiol levels or to differences in testicular estradiol receptor content.

Aging↗
PubMed1981

Regulation of cyclic guanosine 3',5'-monophosphate in interstitial cells of the rat testis.

The present studies were performed to evaluate the role of luteinizing hormone (LH) and calcium on cyclic guanosine 3',5'-monophosphate (cyclic GMP) formation in rat testicular interstitial cells. Dose related increases were observed in both intra-and extra-cellular cyclic GMP when various concentrations of LH (1, 10, 100 mlU/ml) were added to the purified Leydig cells. Cyclic GMP was also increased significantly with calcium ionophore A23187 at concentrations of 0.1, 1 and 10 microgram/ml. Adding LH concomitantly with A23187 resulted in a synergistic response and greatly enhanced cyclic GMP formation. When interstitial cells were incubated in calcium-free medium with 1 mM EGTA, the effects of LH and 123187 on cyclic GMP formation were abolished. These data suggest that LH and A23187 can increase cyclic GMP formation in interstitial cells and this response requires extracellular calcium.

Animals↗
PubMed1981

Gossypol inhibits testicular steroidogenesis.

Gossypol, a compound isolated from cottonseed, has been used in the People's Republic of China as an antifertility agent in men. It was reported that gossypol is highly effective in reducing sperm count. Our study suggests that gossypol inhibits luteinizing hormone, 8-bromo-adenosine 3',5'-monophosphate-induced testosterone formation, and the conversion of pregnenolone to testosterone in isolated rat interstitial cells. Serum testosterone levels were also significantly reduced in rats after 1 week of treatment with gossypol. Oligospermia and azoospermia in men caused by gossypol may be secondary to decreased testosterone biosynthesis.

Animals↗
PubMed1981

Full recovery from severe orthostatic hypotension after vacor rodenticide ingestion.

A patient who had severe orthostatic hypotension secondary to ingesting Vacor, a rodenticide containing N-3 pyridilmethyl-N'-nitrophenyl urea (PNU), fully recovered from this initially disabling condition 11 months after poisoning. Initial treatments with elastic stockings, fludrocortisone acetate, and dihydroergotamine mesylate resulted in no obvious improvement of his orthostasis. Findings from a hemodynamic study performed with the patient was severely orthostatic suggested functional impairment of vascular adrenergic nerve terminals as a major lesion. A similar study after recovery from orthostasis showed that the baroreceptor reflex mechanism returned to normal. This report shows that initially severe and disabling orthostatic hypotension may not be a hopelessly permanent sequela of PNU intoxication and that a gradual, spontaneous full recovery from orthostasis is possible.

Adult↗
PubMed1980

The effects of cytochalasin B on testosterone synthesis by interstitial cells of rat testis.

The present study examined the effects of cytochalasin B on various steps in the luteinizing hormone (LH)-stimulated increase in testosterone synthesis by collagenase-dispersed interstitial cells of adult rat testis. Cytochalasin B at a concentration range of 0.1--50 microM inhibited the LH-stimulated increase in testosterone synthesis in a dose-dependent manner. Both intracellular and medium (released) testosterone levels were reduced, thus indicating that the decrease was not due to the accumulation of testosterone inside the cell as a result of cytochalasin B treatment. Cytochalasin B also inhibited the 8-bromocyclic AMP and pregnenolone-stimulated testosterone synthesis in a similar dose-dependent manner. Cytochalasin B at the two higher doses (10 and 50 microM) also inhibited the LH-stimulated generation of cyclic AMP by interstitial cells. However, this drug had no effect on basal testosterone synthesis except at the highest concentration added. Previous studies on adrenocorticotropic hormone (ACTH)- and LH-stimulated increase in glucocorticoid and testosterone synthesis in adrenal and Leydig cells, respectively, demonstrated that cytochalasin B or anti-actin inhibited the transport of cholesterol into mitochondria. The present studies suggest that cytochalasin B inhibits at least two additional steps in the LH-stimulated increase in testosterone synthesis: (1) the generation of cyclic AMP at the level of the plasma membrane, and (2) the conversion of pregnenolone to testosterone at the level of the smooth endoplasmic reticulum. It remains to be established whether these are direct effects of cytochalasin B, or whether they are mediated by disruption of microfilaments by cytochalasin B.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1980

The effects of calcium ionophore A23187 on interstitial cell steroidogenesis.

The present study was performed to evaluate the effects of calcium ionophore A23187 on adenosine 3',5'-monophosphate (cyclic AMP) and testosterone production in rat interstitial cells. Interstitial cells were incubated in Krebs-Ringer solution with varying amounts of luteinizing hormone, pregnenolone, or A23187. Cyclic AMP and testosterone were measured in the incubation medium after 4 h incubation. A23187 (0.01--10 microgram/ml) caused progressive increases of cyclic AMP formation (from 0.18 +/- 0.02 (S.E.) pmol/10(6) cells for the control of 0.42 +/- 0.02 pmol/10(6) cells, P less than 0.025), while testosterone production remained unaltered. When varying amounts of A23187 were added concomitantly with luteinizing hormone (5 IU/l), A23187 inhibited luteinizing hormone-induced steroidogenesis in a dose-dependent manner, but it had no effect on luteinizing hormone-induced cyclic AMP formation. When pregnenolone (10(-6) M) was added to the cells, testosterone formation increased from 1.50 +/- 0.22 to 8.46 +/- 1.65 ng/10(6) cells. A23187 (1 microgram/ml) had no discernable effect on the conversion of pregnenolone to testosterone. The main effect of increased cytosol calcium on steroidogenesis seems to be at the steps beyond adenylate cyclase-cyclic AMP. These results suggest that calcium is important for the conversion of cholesterol to pregnenolone, while the steps beyond pregnenolone are relatively independent of Ca2+.

Animals↗
PubMed1980

Direct inhibition of testosterone synthesis in rat testis interstitial cells by ethanol: possible sites of action.

The present in vitro studies using interstitial cells of adult rat testes demonstrated that ethanol inhibits LH- and 8-bromo-cyclic AMP-stimulated testosterone synthesis, pregnenolone- and progesterone-stimulated testosterone synthesis, and basal testosterone synthesis. However, the patterns of inhibition following exposure to 0.22 to 880 or 1100 mM ethanol were different. In general, the inhibition curves for LH-, 8-bromo-cyclic AMP-, pregnenolone- and progesterone-stimulated testosterone synthesis were biphasic, with a gradual slope from 0.22 to 220 mM ethanol, and a sharper slope with concentrations of ethanol greater than 220 mM. Basal testosterone synthesis was reduced only to 74% of control with ethanol concentrations up to 44 mM, and higher concentrations of ethanol reduced testosterone synthesis no further. The effect of ethanol on Lh-stimulated cyclic AMP accumulation showed an even different pattern: some of the lower concentrations of ethanol inhibited cyclic AMP accumulation, while higher levels of ethanol progressively increased cyclic AMP accumulation. These studies demonstrate that isolated interstitial cells are highly sensitive to the direct effects of ethanol; they also suggest that the principle site of ethanol inhibition may be at the level of the smooth endoplasmic reticulum where progesterone is converted to testosterone.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1980

The aging Leydig cell: 1. Testosterone and adenosine 3',5'-monophosphate responses to gonadotropin stimulation in rats.

Plasma testosterone levels before and after a single injection of hCG were significantly lower in 24-month old rats than 60--90 day old animals (p less than 0.001). Even with repeated hCG administration for three weeks, plasma testosterone levels of old rats could not be restored to levels present in unstimulated young rats. In response to in vitro LH and 8-bromo-cyclic AMP stimulation, purified young Leydig cells produced significantly higher amounts of testosterone than Leydig cells from old rats. Maximal testosterone formation of the young Leydig cells in response to LH was 42.0 +/- 6.88 ng/10(6) cells, while cells from old rats produced only 16.8 +/- 3.69 ng/10(6) cells (p less than 0.01). However, the dose of LH at which one half maximal response (ED50) occurred was 0.1 mIU/ml for young Leydig cells and 0.05 mIU/ml for old Leydig cells. Basal and 1.0 mIU LH-stimulated cyclic AMP formation were comparable in both groups, but cyclic AMP formation in response to 10 mIU of LH was significantly less in the old rats (p less than 0.05). Present results demonstrate impaired steroidogenic capacity of old rats both in vivo and in vitro. Decreased testosterone response in old rats most likely is the consequence of understimulation of Leydig cells by gonadotropin; however, there appear to be additional intrinsic defects in old Leydig cells.

Animals↗
PubMed1979

In vitro studies of the testis: the effect of LH on cyclic nucleotides.

This study evaluated the relationship between LH, cyclic AMP, cyclic GMP, and testosterone using in vitro incubation of decapsulated rat testes and sampling incubation medium. With added LH (1.0, 5.0, 100, and 500 mIU/ml) there were statistically significant increases in cyclic AMP at 5 mIU/ml or more LH, and progressively greater titers of this nucleotide were produced as LH was increased. For cyclic GMP all levels of added LH caused significant increments in titers of nucleotide; however, peak cyclic GMP concentrations occurred with 5 mIU/ml of LH. The addition of 10(-3) and 10-(4)M 8-bromo-cyclic AMP caused significant increases in testosterone production, while no changes in production of this androgen were found with 10(-3), 10(-4), or 10(-5)M 8-bromo-cyclic GMP. Neither cyclic AMP nor cyclic GMP titers were altered by the addition of 1 to 50 micrograms/ml of testosterone to medium bathing the rat testes. The dose response curves of cyclic AMP and cyclic GMP to LH are different. Progressive increments in added LH cause parallel increases of cyclic AMP and a biphasic change of cyclic GMP, 8-bromo-cyclic GMP does not cause testosterone generation, suggesting that cyclic GMP does not result in androgen synthesis. However, cyclic GMP may be involved in other Leydig cell functions.

Animals↗
PubMed1979

Plasma cyclic nucleotide levels in hyperthyroidism.

Plasma cyclic AMP and cyclic GMP levels were studied in a group of normal subjects and 10 subjects with hyperthyroidism. In the control group, mean plasma cyclic AMP levels were 15.3 +/- 1.3 nmol/l (SEM), and plasma cyclic GMP levels were 9.4 +/- 0.58 nmol/l (SEM). In untreated hyperthyroid subjects, both plasma cyclic AMP and cyclic GMP levels were significantly elevated above normal with mean values of 35.0 +/- 2.4 nmol/l (SEM) (P less than 0.001) and 14.7 +/- 0.2 nmol/l (SEM), (P less than 0.001), respectively. Six of the hyperthyroid subjects were re-studied when they became euthyroid; plasma cyclic nucleotide concentrations all fell within the normal range. To evaluate the relative contribution of triiodothyronine and thyroxine to elevated plasma cyclic nucleotide levels, two hyperthyroid subjects were treated with propylthiouracil and iodide. Plasma cyclic nucleotide levels were normalized when plasma triiodothyronine levels declined to normal range, at the time when plasma thyroxine levels were still elevated. These preliminary data suggest that increased triiodothyronine production is responsible for the increased cyclic nucleotide levels in hyperthyroidism.

Adult↗
PubMed1978

Effect of treadmill exercise on plasma and urinary cyclic adenosine 3'5'-monophosphate.

The effect of treadmill exercise on plasma and urinary cyclic adenosine 3'5' monophosphate levels (cyclic AMP) was studied in twelve healthy subjects. Plasma cyclic AMP levels were found to be markedly elevated without significant changes in urinary cyclic AMP or cyclic AMP/creatine ratio. Most likely altered plasma glucagon and catecholamine levels were responsible for these changes.

Adult↗
PubMed1977

Circadian rhythms in the urinary excretion of cyclic 3',5'-adenosine monophosphate (cyclic AMP) and cyclic 3',5'-guanosine monophosphate (cyclic GMP) in human subjects.

Significant circadian rhythns in urinary excretion of cyclic AMP, cyclic GMP, creatinine, 17-hydroxycorticosteroids and inorganic phosphorus were demonstrated in three normal subjects (two males and one post-menopausal female) who collected serial 4-h specimens for periods of 33, 22, and 14 days, respectively. Peak excretion of the above substances occurred, respectively, at approximately 1500-1700, 2300-0200, 1700-1800, 1100-1300, and 1800-2200 h. The estimated amplitudes of the rhythms expressed as a percentage of the mean 4-h excretion rate were 12-13%, 9-13%, 9-15%, 30-78% and 22-26%, respectively. With the possible exception of cyclic GMP, all of the observed rhythms appeared to be sinusoidal, with normal periods of 24 h. The rhythms in both cyclic AMP and creatinine excretion, but not in the remaining substances may be explained largely in terms of the known rhythm in glomerular filtration rate. The factors responsible for the rhythm in cyclic GMP excretion are unknown.

17-Hydroxycorticosteroids↗