Biomedical subjects

J Arunakaran

Publications and source records attributed to J Arunakaran.

At least 37 records · Page 2Linked to original sources

PubMed2003

Effects of estradiol and progesterone on vertebral collagen, glycosaminoglycans and phosphatases in ovariectomized adult rats.

Vertebral collagen, glycosaminoglycans (GAGs), tartrate-resistant acid phosphatase (TRAP) and alkaline phosphatase (ALP) were measured in ovariectomized (ovx) adult Wistar rats treated with estradiol (E 2 ) (10 micro g/kg BW for 35 days on alternate days, and progesterone (P 4 ) (140 micro g/kg BW for 35 days on alternate days) in E 2 + P 4 treated rats. P 4 given alone or in combination with E 2 significantly increased the levels of collagen in the vertebral bone. Neither ovx nor E 2 treatment altered the concentration of collagen in these rats. Administration of E 2 or P 4 significantly decreased the concentration of hyaluronic acid (HA), but remaining unaffected when a combination of these steroids was given. In contrast to their effect on HA, E 2 and P 4 each significantly increased the levels of chondroitin sulfate (CS) in the vertebral bone. The specific activity of ALP was decreased after ovx. E 2 and P 4 alone or in combination also registered a significant decrease in the activities of ALP and TRAP. The results suggest that E 2 and P 4 each exert definite effects on vertebral bone turnover in ovariectomized rats.

Acid Phosphatase↗

PubMed2003

The role of luteinizing hormone and prolactin in the regulation of insulin receptors in Leydig cells of the adult rat.

The role of luteinizing hormone (LH), prolactin and their combination in the regulation of insulin receptors in Leydig cells was studied. Leydig cells were isolated from adult male Wistar rats and measurement of insulin binding and internalization was done by incubating the cells with a saturating concentration of 125I-insulin in the presence or absence of different doses of unlabeled LH/insulin. LH exposure (100 and 200 ng dose) caused a significant increase in Leydig cell surface and internalized insulin receptor concentrations. Prolactin at all doses was ineffective in inducing a significant change in insulin receptor concentration. Under basal condition, Leydig cell surface binding of 125I-insulin was greater than the internalization at 34 degrees C but at 4 degrees C, surface binding remained lower than that at 34 degrees C with negligible internalization. Internalization of insulin receptors was measured by incubating the cells at 4 degrees C for 16h and then rapidly incubating at 34 degrees C for various time intervals (60, 120, and 180 min). LH/PRL or LH + PRL did not induce any significant change in the internalization of 125I-insulin at 60 and 120 min. The rate of internalization was greater at 120 min in basal as well as LH/PRL exposed Leydig cells, compared to 60 min of incubation. Prolactin alone did not evoke any appreciable change in internalization of 125I-insulin compared to basal at all three time points tested. Total and acid soluble release of 125I-insulin recorded a significant increase in Leydig cells exposed to LH, which was marginally potentiated when prolactin was added along with LH. Monensin treatment of Leydig cells prevented the recycling of insulin receptors to the cell surface and thereby suppressed the surface binding and enhanced the internalized 125I-insulin. Under cycloheximide treatment, neither surface bound nor internalized 125I-insulin recorded a significant change compared to their respective basal values. It is concluded from the present study that LH has dose-dependent biphasic effects on insulin receptors in Leydig cells by modulating the internalization and intracellular processing of hormone-receptor complexes but prolactin has no such effects.

Animals↗

PubMed2003

Effect of polychlorinated biphenyl, Aroclor 1254 on rat epididymis.

BACKGROUND & OBJECTIVES: Polychlorinated biphenyls (PCB), the synthetic chlorinated organic compounds, are known to decrease thyroid function, sperm count and fertility, and increase the risk of testicular cancer may cause serious effect on male reproduction. The objective of the present study was to study the effect of PCB, Aroclor 1254 on rat epididymal structure and function. METHODS: Adult male albino rats were treated ip with Aroclor 1254, 200 microg/kg body weight for 15 and 30 days. Serum levels of testosterone, estradiol, total triiodothyronine (T3), thyroxine (T4) and thyroid stimulating hormone (TSH) were measured by radioimmunoassay. The epididymal weight, sperm count, and caudal epididymal sialic acid, glyceryl phosphoryl choline (GPC) were also investigated. Histological studies were done on caput and caudal epididymal regions. RESULTS: Serum testosterone showed no change, but estradiol levels increased in 30 days treated animals, T3 and T4 levels decreased and TSH levels increased in both 15 and 30 days treated animals. Body weight, epididymal weight, sialic acid, GPC and sperm count were decreased only in 30 days Aroclor treated group. INTERPRETATION & CONCLUSION: The results suggested that Aroclor 1254 treatment for 15 and 30 days induced hypothyroidism in rats, but epididymal functions were altered only at 30 days treatment. The adverse effect of Aroclor 1254 (PCB) on epididymis might be due to indirect action through hormonal regulation.

Animals↗

PubMed2001

Prolactin and Leydig cells: biphasic effects of prolactin on LH-, T3- and GH-induced testosterone/oestradiol secretion by Leydig cells in pubertal rats.

The effect of rat prolactin (rPRL) on basal and LH-, GH- and T3-mediated testosterone and oestradiol secretion was studied in pubertal rat Leydig cells. Purified Leydig cells were cultured for 24 h at 37 degrees C in a medium containing 4% foetal calf serum (FCS). The medium was then replaced with fresh medium containing different concentrations of rPRL (5-400 ng/mL) for 48 h at 34 degrees C without FCS. rPRL increased testosterone secretion by Leydig cells at doses of 50-400 ng and maximum stimulation was observed at a dose of 200 ng. Oestradiol secretion was parallel to that of testosterone except at low doses (5-50 ng/mL). To assess the modulatory effect of rPRL on LH-, GH- and T3-induced Leydig cell testosterone and oestradiol secretion, minimum (50 ng) and maximum (200 ng) effective doses of rPRL were co-administered with LH (25/100 ng), GH (10/50 ng) and T3 (25/50 ng). Co-administration of rPRL (50/100 ng) with T3 (25/50 ng) decreased testosterone secretion. While co-administration of T3 (25 ng) decreased rPRL-induced oestradiol secretion, the latter was unaltered at a dose of 50 ng T3. A minimum effective dose of rPRL (50 ng) plus LH (25 ng) stimulated both testosterone and oestradiol secretion. While a maximum effective dose of rPRL (200 ng) did not alter LH (25 ng)-induced testosterone and oestradiol secretion, it inhibited testosterone secretion induced by 100 ng LH and increased oestradiol secretion. Both doses of rPRL (50, 200 ng) plus GH (10/50 ng) inhibited testosterone secretion when compared with testosterone secretion induced by either GH or PRL alone and stimulated oestradiol secretion. The present in vitro study indicates that rPRL stimulates both testosterone and oestradiol secretion by Leydig cells and that this effect can be modulated by LH, GH and T3.

Animals↗

PubMed2001

Differential effect of hyperthyroidism on rat epididymal glycosidases.

The impact of hyperthyroidism on epididymal glycosidases was studied in albino rats. Hyperthyroidism was induced in Wistar rats aged 30 days by daily injection of T4 (25 microg/100 g body weight/day intramuscularly) for 30 or 60 days; control rats were injected with vehicle (alkaline saline, pH 7.8). One set of hyperthyroid rats was reverted to euthyroid status by withdrawing T4 treatment after 30 days of hyperthyroidism. To asses the direct effect of thyroid hormone on epididymal hexosaminidases, caput, corpus and cauda tissues were stimulated with 25, 50 or 100 ng/mL T3 for 24 h, after an initial culture of 24 h. The activity of beta-glucosidase decreased in caput, corpus and cauda epididymis of hyperthyroid rats. beta-Galactosidase activity increased in the caput epididymis irrespective of the duration of hyperthyroidism. While a similar decrease occurred in the corpus and cauda epididymis in the 30 day hyperthyroid group, an opposite trend was observed in 60 day hyperthyroid rats. Caput beta-N-acetylglucosaminidase activities increased at both time points, whereas activity decreased in the corpus and cauda in 30 day, but increased in 60 day hyperthyroid rats. Hyperthyroidism consistently increased caput and corpus beta-N-acetylgalactosaminidase activity irrespective of the duration. Cauda epididymal beta-N-acetylgalactosaminidase activity was decreased in 30 day and increased in 60 day hyperthyroid rats. Hyperthyroidism induced changes in caput beta-galactosidase, beta-N-acetylgalactosaminidases, corpus beta-N-acetylglucosaminidase and cauda beta-N-acetylgalactosaminidase which were irreversible while the remaining actvities were brought back to normal when T4 treatment was withdrawn. In vitro studies showed that T3 stimulates epididymal hexosaminidases (beta-N-acetylglucosaminidase and beta-N-acetylgalactosaminidase) irrespective of the dose. These data suggest that thyroid hormones have a specific and direct influence on glycosidases in specific regions of the epididymis.

Animals↗

PubMed2000

Thyroidectomy modulates rat prostatic monosaccharides.

Earlier studies have shown that thyroid hormones play an important role in glycoprotein metabolism in the prostate. In this paper, hypothyroidism induced changes in prostatic glycoprotein-associated monosaccharides and fructose concentrations were studied in 30-day-old peripubertal rats. Hypothyroidism was induced by total surgical thyroidectomy and confirmed by radioimmunoassay (RIA) of thyroid hormones and thyroid stimulating hormone (TSH). Animals were killed after 30 and 60 days post-thyroidectomy. To test the direct effect of thyroid hormones on prostatic monosaccharides, prostatic tissue was incubated for 24 h at 37 degrees C with 25, 50 or 100 ng/mL T3. Ventral prostatic hexosamines and sialic acid concentrations were significantly decreased in hypothyroid rats aged 30 and 60 days, whereas fucose concentration was increased at 30 days but decreased at 60 days in hypothyroid rats. In the case of the dorsolateral prostate, hypothyroidism enhanced the concentration of hexosamines but caused a decrease in levels of fucose, sialic acid and fructose, irrespective of the duration of hypothyroidism. Concentrations of fucose, fructose and hexosamines in the anterior prostate were decreased and sialic acid concentration was increased in 60-day hypothyroid rats. In in vitro studies, the concentrations of fucose, sialic acid and hexosamines were significantly increased in all three prostatic lobes irrespective of the T3 dose with which they had been incubated. A consistent increase in fructose concentration was observed in anterior and dorsolateral prostates when incubated with different doses of T3 stimulation. It is concluded that the influence of hypothyroidism on prostatic monosaccharides seems to be specific for each sugar in different lobes of the prostate. These results clearly show that thyroid hormones differentially regulate prostatic glycoprotein metabolism.

Animals↗

PubMed2000

Influence of streptozotocin-induced diabetes and insulin treatment on the pituitary-testicular axis during sexual maturation in rats.

Effects of streptozotocin (STZ)-diabetes and insulin treatment on the functioning of pituitary-testicular axis during sexual maturation was studied. Prepubertal (30 days old) and pubertal (50 days old) male Wistar rats were made diabetic by a single injection of STZ. A group of diabetic rats was given insulin (3U/100 g b.wt./day in 2 equally divided doses), 3 days after STZ treatment. Prepubertal and pubertal rats of all groups were killed on postnatal days 51 and 71, respectively. STZ-diabetes caused marked reduction in serum LH, FSH, prolactin, testosterone and testicular interstitial fluid testosterone as well as the activities of Leydig cellular steroidogenic enzymes (3beta-and 17beta-hydroxysteroid dehydrogenases). Insulin treatment to diabetic rats maintained these changes at control range except FSH and prolactin in prepubertal rats. The results indicate that (i) diabetes-induced steroidogenic lesions in Leydig cells represent a direct consequence of dysfunctioning of pituitary-testicular axis, (ii) the adverse effects of diabetes on pituitary-testicular functions are influenced by age of its induction and (iii) optimum insulin level is essential for the acquisition of Leydig cellular steroidogenic efficacy during sexual development.

17-Hydroxysteroid Dehydrogenases↗

PubMed2000

Growth hormone directly stimulates testosterone and oestradiol secretion by rat Leydig cells in vitro and modulates the effects of LH and T3.

The modulatory effect of GH on basal, LH and T3 mediated secretion of testosterone and oestradiol by purified rat (60 day old) Leydig cells was studied in vitro. Percoll gradient purified Leydig cells (1 x 10(3)) were cultured for 48 hours at 34 degrees C in a medium containing different concentrations of rat GH (5-400 ng/mL), after an initial culture for 24 hours at 37 degrees C. GH increased testosterone and oestradiol secretions in a dose dependent manner. While testosterone secretion reached the saturation point with 50 ng GH, oestradiol secretion reached the saturation point with 150 ng GH, followed by diminished secretions. Co-administration of minimum (10 ng) effective does of GH with minimum (25 ng) or maximum (100 ng) effective doses of oLH significantly decreased the testosterone secretion. However, an increased secretion of testosterone was observed when maximum effective doses of rGH (50 ng) and oLH (100 ng) were co-administered. Minimum effective (25 ng) or maximum effective (50 ng) doses of T3 inhibited GH mediated secretion of testosterone in vitro. Oestradiol concentration in the culture medium increased when either dose of rGH was co-administered with the minimum or maximum effective doses of oLH. T3 50 ng augmented the secretion of oestradiol by Leydig cells in the presence of GH. These results indicate that GH acts as a gonadotrophin to stimulate testosterone and oestradiol secretions by Leydig cells, and that it modulates LH or T3 induced secretion of these steroids, depending on the intensity of their stimulation.

Animals↗

PubMed2000

T3 directly stimulates basal and modulates LH induced testosterone and oestradiol production by rat Leydig cells in vitro.

The effect of T3 on basal and LH mediated synthesis and secretion of testosterone and oestradiol by puberal rat Leydig cells was studied in vitro. Percoll gradient purified Leydig cells (1 x 10(3)) were cultured for 48 hours at 34 degrees C in a medium containing a range of 5-400 ng/mL concentration of T3 or ovine LH after 24 hours initial culture at 37 degrees C. T3 increased testosterone and oestradiol secretions in a dose dependent manner which reached the saturation point with 50 ng dose. While the minimum effective dose of T3 (25 ng) potentiated the stimulatory effect of the minimum effective dose of LH (25 ng) on testosterone secretion, it suppressed the effect of the saturation dose of LH (100 ng). Fifty ng T3 quelled the stimulatory effect of either dose of LH. Both doses of T3 increased oestradiol secretion, irrespective of the dose of LH. Addition of androstenedione (500 ng/mL) to the culture medium enhanced 25 ng T3 induced testosterone and oestradiol secretions. While androstenedione potentiated the stimulatory effect of T3 (25 ng) on LH (25 ng) induced testosterone and oestradiol secretions, it reversed the inhibitory effect of 50 ng T3 on LH mediated testosterone secretion which was accompanied by a decrease in oestradiol secretion. Puromycin (35 microg/mL) suppressed the stimulatory effect of T3 on basal and LH mediated testosterone and oestradiol production. Taken together, the present results indicate a direct stimulatory effects of T3 on basal production of testosterone and oestradiol by Leydig cells and its modulatory effect on LH mediated steroidogenic activity varies depending upon the intensity of LH stimuli.

Androstenedione↗

PubMed2000

Transient neonatal hypothyroidism alters plasma and testicular sex steroid concentration in puberal rats.

The stimulatory and inhibitory effects on testicular steroidogenesis of transient neonatal hypothyroidism from day 1 postpartum through different postnatal developmental events on testis at puberal age (60 days old) were studied in vivo. Hypothyroidism was induced in neonates by feeding the lactating mother or directly with 0.05% methimazole (MMI) through drinking water from the day of parturition to 10, 15, 30, 40 and 60 days, and were killed at day 60 postpartum. Plasma and testicular interstitial fluid (TIF) progesterone, testosterone, dihydrotestosterone (DHT) and estradiol concentrations were assessed. Testis weight and volume significantly increased in rats subjected to 10 and 15 days of hypothyroidism, decreased in rats subjected to 30, 40 and 60 days of hypothyroidism. A consistent increase in Leydig cell number was seen in puberal rats subjected to transient neonatal hypothyroidism but decreased in 60 days hypothyroid rats. Peritubular myoid cell number was consistently decreased in all experimental rats. Leydig cell diameter decreased consistently in all experimental groups. Persistent hypothyroidism (60 days hypothyroid) consistently decreased both plasma and TIF sex steroids. In transient hypothyroid rats, progesterone concentration decreased in both plasma and TIF. Transient hypothyroidism from birth to day 10 postnatal age maintained normal titre of plasma testosterone, whereas a significant increase in TIF testosterone concentration was evident when compared with controls. All other groups of rats subjected to transient neonatal hypothyroidism had consistently low titres of plasma and TIF testosterone. Plasma DHT concentrations in rats subjected to transient neonatal hypothyroidism remained unaltered. However, TIF DHT increased in 10 days

Animals↗

PubMed1999

Effects of piperine on testis of albino rats.

Piperine was administered to mature male albino rats at doses of 5 and 10 mg/kg body weight, p.o., respectively, for 30 days. Only a 10 mg dose of piperine treatment caused a significant reduction in the weights of testis and accessory sex organs. Histological studies revealed that piperine at a 5 mg dose caused partial degeneration of germ cell types, whereas at a 10 mg dose, it caused severe damage to the seminiferous tubule, decrease in seminiferous tubular and Leydig cell nuclear diameter and desquamation of spermatocytes and spermatids. Correlated to the structural changes, a fall in caput and cauda epididymal sperm concentrations was also evident. A 10 mg dose of piperine also caused a marked increase in serum gonadotropins and a decrease in intratesticular testosterone concentration, despite normal serum testosterone titres.

Abortifacient Agents, Steroidal↗

PubMed1999

Effects of piperine on the lipid composition and enzymes of the pyruvate-malate cycle in the testis of the rat in vivo.

Effects of piperine at two oral doses (5 and 10 mg/kg body weight for 30 days) on the lipid composition and some lipogenic enzymes of the rat testis were studied. Piperine treatment depleted the total lipid content which was mainly due to the diminution of the total phospholipid concentration. All the classes of phospholipids were decreased markedly following high dose piperine treatment. In contrast, a marked increase in total cholesterol and cholesterol ester was evident with a concomitant fall in free cholesterol. A similar trend was found for the total glyceride glycerol and its fractions. Total glyceride glycerol and triacyl glycerol showed a significant increase at the expense of diacyl glycerol in rats treated with the high dose of piperine. Lipogenic enzymes, malate dehydrogenase (MDH), malic enzyme (ME) and isocitrate dehydrogenase (ICDH) were inhibited by the high dose and only MDH and ME activities were inhibited by the low dose treatment.

Administration, Oral↗

PubMed1999

Effects of ethanol treatment on epididymal secretory products and sperm maturation in albino rats.

Alcoholics are often associated with fertility disturbances with low sperm count and impaired sperm motility. Spermatozoa attains forward motility and fertilizing capacity during their transit through the epididymis. Epididymal secretory products form a suitable microenvironment, which favors sperm maturation. To study the effects of ethanol on epididymal sperm maturation, ethanol (3 g/kg body weight as 25%, v/v) was given by gastric intubation twice daily for 30 days, and in another group, rats given treatment for 30 days were withdrawn of treatment for a further period of 30 days to assess the reversibility of ethanol-induced changes. Serum and epididymidal testosterone and dihydrotestosterone (DHT), epididymidal tissue and sperm carnitine, acetyl carnitine, glycerylphosphoryl choline (GPC), and sialic acid were studied along with epididymidal sperm count and cauda epididymidal sperm motility. Ethanol treatment significantly reduced the epididymal tissue/sperm carnitine, acetyl carnitine, GPC, and sialic acid, suggesting its adverse effect on these secretory products. Impaired cauda epididymidal sperm motility and fertility (in vivo) of ethanol-treated rats imply the defective sperm maturation. All these changes were reverted back to normalcy after withdrawal of ethanol treatment, indicating the transient effects of ethanol. In conclusion, it is evident that ethanol has an adverse effect on sperm maturation, which may be affected due to the decrease in serum/epididymal testosterone and DHT level and epididymal secretory products.

Acetylcarnitine↗

PubMed1998

Prostate-thyroid axis: stimulatory effects of ventral prostate secretions on thyroid function.

BACKGROUND: Endocrine cells of the prostate secrete thyrotropin (TSH)-releasing hormone (TRH), TRH- and TSH-like peptides, and growth factors. Propylthiouracil- and methimazole-induced hypothyroidism increased prostatic levels of TRH in rats as in hypothalamus, whereas thyroxine (T4) replacement decreased TRH. From these reports, we inferred the existence of a prostate-thyroid axis. METHODS: The influence of the prostate on the thyroid gland was studied in albino rats. Ventral prostate was surgically removed on day 31 postpartum. The animals were sacrificed on day 60 postoperation. Serum thyroid hormones were assayed by radioimmunoassay (RIA). For in vitro studies, normal thyroid and ventral prostate glands were cocultured with or without thyroid-stimulating hormone (TSH) antibody, to assess the direct influence of prostatic secretions on thyroid hormone secretion. RESULTS: Serum total and free T4 and triiodothyronine (T3) were significantly reduced in ventral prostatectomized rats. Histological analysis of the thyroid showed that the diameters of the peripheral and middle follicles, colloid epithelial cells, and nuclei were increased in prostatectomized rats, indicating hypothyroid status. Total T3 and T4 were significantly elevated in the culture medium when thyroid and prostate were cocultured, irrespective of the presence of TSH antibody. CONCLUSIONS: The present study suggests that ventral prostatic secretions have a stimulatory role on the thyroid gland.

Aging↗

PubMed1998

Impact of altered thyroid hormone status on prostatic glycosidases.

The impact of hyper- and hypothyroidism on prostatic glycosidases was investigated. Hyper-thyroidism was induced by administering L-thyroxine (25 micrograms/100 g body weight/day) for 60 days and hypothyroidism was induced by total thyroidectomy. To test the direct influence of thyroid hormones, prostatic lobes were incubated with different concentrations (10, 25 and 50 ng/mL) of T3 and beta-N-acetylglucosaminidase and beta-N-acetylgalactosaminidase were assayed. Serum levels of thyroid hormones, oestradiol and testosterone increased in hyperthyroid, and decreased in hypothyroid rats. TSH decreased in hyperthyroid, and an opposite trend was seen in thyroidectomized, rats. Prostatic [anterior (coagulating glands), dorsolateral and ventral prostates] beta-glucosidase, beta-galactosidase, beta-N-acetylglucosaminidase and beta-N-acetylgalactosaminidase activities increased uniformly in hyperthyroid, and decreased in thyroidectomized, rats. In vitro studies showed a dose-dependent stimulatory effect of T3 on beta-N-acetylglucosaminidase and beta-N-acetylgalactosaminidase in all three lobes of the prostate. From the present study, it is concluded that hyperthyroidism augments and hypothyroidism inhibits prostatic glycosidases and T3 has a direct stimulatory effect on these enzymes.

Animals↗

PubMed1998

Interaction of estradiol, progesterone and corticosterone on uterine connective tissue degrading enzymes.

The impact of ovarian hormones and corticosterone acetate on uterine connective tissue degrading enzymes were studied in mature albino rats. Ovariectomy resulted in a significant increase in the activities of alpha- and beta-galactosidases and glucosidases in the uterus. Administration of estradiol to ovariectomized rats brought back the activities of alpha-galactosidase and alpha-glucosidase to normalcy. While beta-galactosidase and beta-glucosidase were significantly decreased. Administration of progesterone to ovariectomized rats resulted in the increase of alpha- and beta-galactosidases and glucosidases. Administration of corticosterone to ovariectomized rats produced a further increase in alpha- and beta-galactosidases and glucosidases in the uterus. Adrenalectomy in ovary intact rats produced a decrease in alpha-galactosidase however, beta-glucosidase was significantly increased. Administration of corticosterone to ovary intact rats significantly increased the activities of alpha- and beta-galactosidases, while alpha- and beta-glucosidases were found to be decreased. Ovariectomy resulted in a significant increase in the activities of cathepsin-D and cathepsin-E. Administration of estradiol to ovariectomized rats brought back the activity of cathepsin-D to normalcy, whereas cathepsin-E was significantly increased. Administration of progesterone as well as estradiol to ovariectomized rats significantly increased the levels of cathepsin-E, however, cathepsin-D was brought back to normalcy. Administration of corticosterone to ovariectomized rats as well as ovariectomy + adrenalectomy significantly increased the activity of cathepsin-D and cathepsin-E. Adrenalectomy significantly decreased the activity of cathepsin-D, while administration of corticosterone increased the cathepsin-D and cathepsin-E in the uterus. Therefore, these results suggest that estradiol is a potent ovarian steroid protecting the extra cellular matrix components. The effect of progesterone appears to modulate and act hand in hand with estradiol. Corticosterone appears to have an opposite effect to that of estradiol.

Adrenalectomy↗

PubMed1995

Preliminary study of androgen, thyroid & adrenal status in alcoholic men during deaddiction.

To evaluate the status of the testes, thyroid, and adrenals in male alcoholics during the period of voluntary abstinence and therapy, chronic male drinkers undergoing a 4 wk inpatient deaddiction programme in a social hospital were recruited. Levels of a few serum and urinary hormones/metabolites viz., serum testosterone, total triiodothyronine (T3) and thyroxine (T4) and urinary total 17-ketosteroids (17-KS), estrone, estradiol, and 17-hydroxy corticosteroids (17-OHCS) were assessed in alcoholics thrice during the treatment programme at hospital i.e., on the zero (day of admission), 10th, and 20th day and compared to those of non-alcoholic controls. Alcoholics registered elevated serum total T3, and reduced total T4 and testosterone levels at admission, which persisted even after 20 days of the rehabilitative programme. Markedly high urinary levels of total 17-KS, estrone, and 17-OHCS were observed on zero day of admission. Urinary estrone and 17-OHCS, unlike total 17-KS, showed a trend to return to the normal range during the 20 days period. Urinary estradiol levels, however, recorded no significant alteration. The results of this preliminary study are suggestive of alcohol-induced perturbations on the functional integrity of the testes, thyroid, and adrenal in male alcohol addicts, wherein 20 days period of total alcohol abstinence and rehabilitative programme failed to reverse alcohol-induced hypoandrogenization and altered thyroidal status, but only partially restored certain biochemical events associated with the excretion of steroid metabolites.

17-Hydroxycorticosteroids↗

PubMed1994

Ethanol induced changes in prostatic lipid profiles of albino rats.

Alcohol induced changes in the ventral and dorsolateral prostatic lipid profiles were studied. The results obtained from the present study indicate that alcohol consumption leads to significant alterations in the ventral and dorsolateral prostatic lipids. An increase in the ventral prostate total cholesterol and total glyceride glycerol was observed, but a reverse trend was seen in total phospholipid. However total lipids remained unaltered. Dorsolateral prostatic total lipids, glyceride glycerol and phospholipids were increased but a decrease in total cholesterol was observed. Withdrawal of ethanol treatment for a period of 30 days brought back most of the changes to normalcy. The abnormalities in lipid profiles of both ventral and dorsolateral prostates may be responsible for the altered semen quality prevalent in chronic alcoholics.

Alcoholism↗