PubMed Health⌕ Search

Biomedical subjects

G Csaba

Publications and source records attributed to G Csaba.

At least 55 records · Page 3Linked to original sources

Effect of vitamin D(3) treatment in the neonatal or adolescent age (hormonal imprinting) on the thymic glucocorticoid receptor of the adult male rat.

Single neonatal treatment with 25 microg vitamin D(3) significantly decreased the thymic glucocorticoid receptor density (B(max)) of 6-week-old male rats. In females, a similar treatment did not cause any changes. Single vitamin D(3) treatment (50 microg) during adolescence (i.e. 6-week-old animals) significantly increased the glucocorticoid receptor density in adult (10-week-old) males. No significant changes in receptor affinity (K(d)) could be observed. Considering that in earlier experiments similar neonatal treatments influenced bone mineral mass and sexual behavior, the hormonal imprinting effect of vitamin D(3) and its harmful effect on the development of other members of the steroid receptor superfamily, seems to be unquestionable.

Aging↗

Effect of digoxin imprinting in adolescence on the sexual behavior of adult rats.

Four-time 3 micrograms digoxin treatment of male rats at puberty (in six weeks old rats) significantly increased the libido of rats (number of intromissions) and reduced the number of ejaculations, two months after the treatments (in three and a half months old rats). In female rats the Meyerson index and lordosis quotient were not significantly decreased. The experiment calls attention to the wide-ranging imprinting effect of digoxin which was also demonstrated earlier after prenatal (maternal) treatment. The experiment also supports the male sexual potency influencing effect of digoxin treatment, previously supposed in men.

Aging↗

Direct and transgenerational effect of benzpyrene treatment at adolescent age on the uterine estrogen receptor and thymic glucocorticoid receptor of the adult rat.

Hormonal imprinting develops perinatally at the first encounter between the maturing receptor and the target hormone, helping the normal accomplishment of receptor maturation. In the presence of hormone excess or foreign molecules able to bind to the maturing receptor, faulty imprinting takes place, which disturbs the normal receptor function for life. Earlier experiments demonstrated that the effect of faulty perinatal benzpyrene imprinting of the steroid hormone receptors is transmitted to the progeny generations. In certain organs which are maturing later (such as the uterus) imprinting can be executed at adolescence. In the present experiments pubertal benzpyrene imprinting caused a durable decrease in female's estrogen receptor density. The transgenerational effect of this type of imprinting was also studied. The pubertal imprinting of the parents was transgenerationally transmitted to the offspring generation in which--without further treatment--the density (Bmax) of the uterine estrogen receptors was significantly higher than that in the controls. There were measurable effects neither in the affinity (Kd) of uterine estrogen receptors nor in the Kd and Bmax of the male thymus glucocorticoid receptors. The experiments call attention to the profound and comprehensive imprinting effect of the environmental pollutant benzpyrene.

Animals↗

Effects of tumor necrosis factor alpha (TNF alpha) on the phospholipid metabolism of Tetrahymena pyriformis.

The effect of (0.05 ng ml-1 and 0.1 ng ml(-1)) TNF alpha on the phospholipid metabolism of Tetrahymena pyriformis was studied. The amount of phosphatidyl choline (PC), phosphatidyl inositol (PI), phosphatidic acid (PA), phosphatidyl ethanolamine (PE), diacylglycerol (DAG), arachidonic acid (AA) and ceramide was higher, but the phosphatidyl inositol 4 phosphate (PIP) and phosphatidyl inositol bis-phosphate (PIP2) as well, as sphingomyelin (SM) content was lower in TNF alpha-treated cells than in the controls. In the culture medium (secreted forms) this situation was reversed. There were differences in the results gained by incorporation of [3H]-palmitic acid or 32P into the phospholipids. To control the functional effects of TNF alpha in Tetrahymena, the rate of cell division, the condensation of chromatin, the viability of cells and morphometrical values have been studied. The cytokine reduced cell growth, altered morphometric indices and increased chromatin condensation, however cell viability was not influenced. The results demonstrate the effects of TNF alpha at a low level of evolution, what is realized by changes in the phospholipid metabolism participating in signalling pathways.

Animals↗

Induction of digoxin-like material production, and the digoxin binding in the unicellular organism Tetrahymena by digitoxin.

Thin layer chromatographic, and laser-confocal microscopic analyses with a monoclonal antibody to digoxin also displaying high affinity to digoxigenin, were used to determine the presence and localization of cardioactive glycosides. Tetrahymena pyriformis was found to possess digitoxigenin-like material, but digoxin, digitoxin, digoxigenin, gitoxin and lanatoside C were not detected. Digitoxin treatment elicited the appearance of a digoxin-like material in the progeny generations. Digoxin was taken up by untreated Tetrahymena, especially strongly 24 h after digitoxin treatment. While the cardenolide was localized in vesicles of the cell body in untreated Tetrahymena, the engulfed digoxin appeared in the epiplasmic layer and also in the cilia after digitoxin pretreatment. Digoxin pretreatment did not increase digoxin uptake. These data indicate that Tetrahymena has: (1) the capacity to discriminate between closely related molecules; (2) the ability to induce digoxin-like material production; and/or (3) enzymes that can effect a digitoxin-digoxin transformation.

Animals↗

Presence and localization of histidine decarboxylase enzyme (HDC) and histamine in Tetrahymena pyriformis.

Histidine decarboxylase (HDC) enzyme and its function under hormonal influences were studied in a low level of phylogeny. HDC protein is present in the unicellular ciliate Tetrahymena and its expression was not altered by insulin or histamine treatment. Starvation for 24 h enormously decreased the quantity of histamine in the cells. However, insulin influenced the activity of the HDC enzyme, demonstrated by the seven-fold quantity of histamine in the starved cells after insulin treatment. Insulin also increased the uptake of histamine from the tryptone-yeast extract medium. HDC was found in different parts of the cytoplasm, mainly in the periphery (epiplasm) of the cells. The experiments demonstrated the uptake and synthesis of histamine by Tetrahymena as well as the possibility of hormonal regulation of HDC activity.

Animals↗

Steroid hormone (hydrocortisone, oestradiol and testosterone) uptake, storage or induced synthesis in tetrahymena.

After cyclodextrin-coated 10(-6) m steroid hormone treatment for 3 days (hormonal imprinting), Tetrahymena cells and their media were analysed by radioimmunoassay for the same hormone and for the presence of the other two. In the absence of hormone treatment, the cells contained no detectable levels of the three steroids. By 2 days in fresh medium following exposure of cells to a 72 h pretreatment of each specific hormone, correspondingly high quantities of hydrocortisone and oestradiol, but lesser quantities of testosterone, were found in both the media and the cells. One week after treatment only traces of hydrocortisone were found, exclusively within the cells themselves. Oestradiol was present in measurable quantities in both cells and media, whereas testosterone was only present in the medium. The presence of the other two hormones to the one used in the pretreatment were not usually present, except that when testosterone had been given, some oestradiol was also detected at 48 h, suggesting Tetrahymena has a functional cytochrome P(450)aromatase.

Animals↗

Chemotaxis and chemotactic selection induced with cytokines (IL-8, RANTES and TNF-alpha) in the unicellular Tetrahymena pyriformis.

Three representative cytokines interleukin (IL-8), RANTES and tumour necrosis factor alpha (TNF-alpha) have a concentration-dependent chemotactic effect on the unicellular Tetrahymena. Maximal effective concentrations of IL-8 (1 ng/ml) and RANTES (75 ng/ml) are in the same range as in mammals, which indicates an evolutionary background of physiological effects elicited. Progeny generations of cells selected for their affinity to cytokines (IL-8 and TNF-alpha) show an enhanced positive chemosensory reaction to the cytokines. The changed reaction of these cells to the chemoattraction of the culturing medium was also observed. The results call attention to the presence of cytokine-dependent processes at a low phylogenetic level.

Animals↗

Neonatal vitamin E treatment induces long term glucocorticoid receptor changes: an unusual hormonal imprinting effect.

Single neonatal vitamin E treatment significantly altered the affinity (Kd) of thymic glucocorticoid receptors in male adolescent and adult rats. In six weeks old animals the affinity increased (and there is a tendency for an increase in receptor density), in twelve weeks old animals the affinity decreased. The thymic glucocorticoid receptors and uterine estrogen receptors of female animals were not influenced at all. Thousandfold tocopherol did not compete with labeled dexamethasone for their receptors, suggesting that neonatal vitamin E imprinting effect was not done at direct receptorial level.

Animals↗

Imprinting of thymic glucocorticoid receptor and uterine estrogen receptor by a synthetic steroid hormone at different times after birth.

1. Single allylestrenol treatment (hormonal imprinting) of 3-day old rats reduced the density of thymus glucocorticoid receptors and increased the density of uterus estrogen receptors at adult age. 2. Similar treatment of 7-, 14-, or 28-day old animals did not alter the binding capacity of the receptors of the adult animals at all. 3. In 3-day-old animals, the direction of imprinting was similar to the prenatal imprinting of the thymus glucocorticoid receptor (reduction), whereas neonatal treatment of uterine estrogen receptors decreased receptor density, and imprinting on the 4th day increased it. This means that the imprintability persists only to the 4th day; its consequence can be changed. 4. The experiments demonstrate that hormonal imprinting can be provoked by allylestrenol not only pre- or neonatally, as was done in previous experiments, but also a few days later. The imprintability was lost between the 4th and 8th day of life.

Age Factors↗

Fetal digoxin treatment enhances the binding capacity of thymic glucocorticoid receptors in adult female rats.

1. Hormonal imprinting is provoked in the perinatal critical period in the presence of the appropriate hormone or molecules similar to it. As a consequence of hormonal imprinting, the developing receptor finishes its maturation normally (in the presence of the adequate hormone) or abnormally (under the effect of foreign molecules that are able to bind to the receptor). 2. Digoxin--which has a steroid character--caused faulty imprinting by treatments at the 15th, 17th and 20th days of pregnancy. In the adult (3-month-old) animals, the density of thymic glucocorticoid receptors was significantly elevated, whereas the density of uterine estrogen receptors was not, without any change in receptor affinity. 3. The experiments call attention to the steroid receptor imprinting effect of fetal digoxin treatment that must be considered in regard to this treatment at this period and later in regard steroid treatments.

Animals↗

Effect of fetal digoxin exposure (imprinting) on the sexual behavior of adult rats.

1. Digoxin exposure of rat fetuses at the 15th, 17th and 19th day of pregnancy by treating the mother (with 9 microg digoxin altogether) caused alterations in the sexual behavior of adult rats (3-month-old males and six-month-old ovariectomized and hormone-treated females). 2. The number of active males was significantly higher in the treated group and ejaculation as well as multiple ejaculation occurred only here. Females also were more receptable after fetal digoxin treatment. It is known from the literature that long-term digoxin treatment in adult age influences (reduces) the male sexual activity in humans. In the rat, the opposite effect was observed after fetal treatment. 3. The experiments call attention to the prolonged effect of fetal digoxin exposure caused by the treatment of the mother.

Animals↗

Effect of neonatal glucocorticoid treatment on bone mineralization of adult nontreated, dexamethasone-treated or vitamin D3-treated rats.

1. Single neonatal dexamethasone (DEX) treatment significantly decreased the body weights of 5-month old male rats. There was no significant difference in females. 2. Bone mineral density (BMD) of neonatally DEX-treated male rats and bone mineral content (BMC) of double DEX-treated (neonatally and in adult age) males were reduced. 3. BMD and BMC calculated to body weight were highly significantly increased after neonatal or double DEX treatment in males. In females only BMC/body weight was elevated after double DEX treatment. 4. Adult vitamin D treatment completely compensated for the changes caused by single or double DEX treatment. 5. The results call attention to the imprinting effects of neonatal glucocorticoid treatment, which were manifested in changes of body weight and bone mineral mass. At the same time the gender-dependence of this phenomenon was demonstrated.

Aging↗

Unspecific binding capacity of androgen receptors in the rat uterus.

Rat uterine cytosol receptor homogenate binds estradiol and testosterone alike. Saturation and displacement studies were done with these two hormones. Testosterone displaced only testosterone while estradiol displaced estradiol as well as testosterone. The experiments call attention to the unspecific binding capacity of rat uterine androgen receptors.

Animals↗

Testosterone and progesterone level alterations in the adult rat after retinoid (retinol or retinoic acid) treatment (imprinting) in neonatal or adolescent age.

Newborn rats were treated with a single dose of vitamin A (retinol), or with three doses of retinoic acid (in the 1st, 3rd and 5th days). Serum testosterone and progesterone level was measured in the four months old male and female rats, respectively. Retinol significantly decreased both hormone levels, however retinoic acid decreased the progesterone level only. In the second part of the experiments adolescent rats (in the 6th and 7th week after birth) were treated and measured similar to the newborns. In this case retinol significantly diminished testosterone level, without influencing the progesterone level. Retinoic acid decreased testosterone level and elevated progesterone level. The results demonstrate the long lasting effects of retinoid treatments at a neonatal or adolescent age, pointing also to the differences in the direction of the effects. Considering that previously the receptorial and sexual-behavioral effects of perinatal vitamin A treatments were observed, the experiments call attention to such harmful influences of perinatal vitamin A treatments, which are not manifested in morphological alterations.

Aging↗

Transgenerational effect of a single neonatal benzpyrene treatment on the glucocorticoid receptor of the rat thymus.

Hormonal imprinting is provoked perinatally by the appropriate hormone on its receptor, causing a life-long adjustment of the connection between the two participants. Faulty imprinting is caused by the presence of molecules similar to the hormone in this critical period, which results in a persistent alteration of the receptor. In the present experiment the transgenerational imprinting effect of a steroid-like environmental pollutant, benzpyrene, on the receptor binding capacity of filial thymic dexamethasone and uterine estrogen receptors was studied. The receptor density (Bmax) of the thymic glucocorticoid receptors of the males was reduced up to the third (F2) generation. In females this reduction was observed only in the F1 generation of treated animals. There was no change in receptor affinity (Kd). Uterine estrogen receptors were not subjected to transgenerational imprinting. The experiments demonstrate (1) the possibility of the transgenerational transmission of imprinting effect, (2) the differences of steroid receptors in different organs, and (3) the differences of male's and female's reactions from this aspect. The results call attention to the dangers of perinatal aromatic hydrocarbon exposition to the progeny generations.

Animals↗

Effect of single neonatal vitamin D3 treatment (hormonal imprinting) on the bone mineralization of adult non-treated and dexamethasone treated rats.

Hormonal imprinting (the first encounter between the hormone and receptor after birth) is needed for the normal development of receptor. Presence of the appropriate hormone in excess, or its absence, as well as presence of hormone-like molecules able to bind to the maturing receptor in this time, can cause faulty imprinting. In this experiment the effect of neonatal treatment with a single dose of 0.05 mg cholecalciferol (vitamin D3) was studied by bone densitometry. The treatment caused significant decrease of body weight in 3-month old females and also significant reduction of bone mineral density (BMD) and bone mineral content (BMC) in males. Dexamethasone treatment of 3-month old rats for 10 days increased BMD in males and BMC in females without affecting body weight. The double treatment (vitamin D neonatally and dexamethasone when adult) decreased the body weight of both sexes and increased BMD in males, and BMC, BMD/bw and BMC/bw in both sexes, related to the control or the only vitamin D treated groups. Considering the hormonal imprinting effect of neonatal vitamin D treatment at glucocorticoid receptorial level in other experiments, similar effects also can be supposed for vitamin D itself, manifested in the changes of bone mineralization.

Animals↗

Effect of retinoid (vitamin A or retinoic acid) treatment (hormonal imprinting) through breastmilk on the glucocorticoid receptor and estrogen receptor binding capacity of the adult rat offspring.

Hormonal imprinting occurs perinatally when the developing receptor and the appropriate hormone meet each other. The presence of related molecules in this critical period causes misimprinting. Ligands bound to a member of the steroid-thyroid receptor superfamily can disturb the normal maturation of other members of the family, which is manifested in altered binding capacity of the receptor and decreased or increased response of the receptor-bearing cell for life. Excess or absence of the hormone also can cause misimprinting. Treatments once a week for 3 weeks of nursing rat mothers with 6 mg/animal all-trans retinol/dose caused faulty imprinting manifested in significantly reduced density (Bmax) of thymic glucocorticoid receptor in male and female adult progenies alike. 0.03 mg all-trans retinoic acid treatment of nursing mothers was ineffective. Receptor affinity (Kd) was unchanged in both cases as well, as the binding values of uterine estrogen receptors. The results of the experiment call attention to the transmission of imprinter molecules by breastmilk to the progenies, which can cause lifelong alterations at receptorial level and points to the human health aspect. Possible reasons for the differences between retinol and retinoic acid effects and in the sensitivity of receptors are discussed.

Animals↗