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M M Aruldhas

Publications and source records attributed to M M Aruldhas.

79 records · Page 5Linked to original sources

Effect of corticosterone on rat epididymal lipids.

Corticosterone-induced changes in serum hormone profiles and the lipid composition of the caput and cauda epididymidis were studied. The analysis was conducted in both unwashed and washed (free from fluids and spermatozoa) epididymal tissues. Corticosterone treatment significantly depressed serum prolactin and testosterone but gonadotropins were unaltered. In the unwashed caput region, lipid analysis showed a significant decrease in total lipids, as well as in cholesterol, phospholipid, and the phosphatidyl inositol, phosphatidyl choline, and phosphatidyl ethanolamine fractions. However, in the unwashed cauda region, the total lipid and cholesterol content was not altered while total phospholipid and phospholipid fractions were significantly decreased. On the other hand, in the washed caput and cauda regions, corticosterone induced a significant increase in total lipid, glyceride, and the mono, di, and triglyceride fractions, leaving total phospholipid and its fractions unaltered. Following 20-day withdrawal of corticosterone treatment, all lipid classes returned to normal along with serum hormone profiles. Our findings imply that an excess of corticosterone influences epididymal lipids. These changes in the epididymal lipid pattern probably are reflected in fertility disorders in patients with glucocorticoid excess.

Animals↗

Interactions of androgens and prolactin in the seminal vesicles of mature bonnet monkeys, Macaca radiata. I. Nucleic acids and phosphatases.

The effects of prolactin (PRL), bromocriptine, testosterone propionate (TP), dihydrotestosterone (DHT), and the combinations of these androgens with PRL or bromocriptine on nucleic acids (RNA and DNA) and phosphomonoesterases (acid and alkaline phosphatase) of the seminal vesicles of castrated mature bonnet monkeys were studied. Castration decreased body weight, and seminal vesicle organ weight, nucleic acids and acid and alkaline phosphatases. TP/DHT replacement to castrates restored body weights and seminal vesicle DNA to normal and markedly increased the weight, RNA content and acid and alkaline phosphatase activities of the seminal vesicles. PRL did not alter body weight and increased the weight of the seminal vesicles, and their RNA content and phosphomonoesterase activities. PRL + TP/DHT enhanced all parameters. Bromocriptine given alone decreased body weight and acid phosphatase. Bromocriptine given along with TP/DHT suppressed the stimulatory influence of these androgens on most of the parameters studied. The results of the present study suggest that PRL has a specific stimulatory effect on seminal vesicle growth and function, that the presence of PRL is essential for androgen action, and that PRL acts synergistically with androgens.

Acid Phosphatase↗

Impact of neonatal onset hypothyroidism on Sertoli cell number, plasma and testicular interstitial fluid androgen binding protein concentration.

The impact of neonatal onset hypothyroidism from day 1 postpartum through different postnatal developmental events on rat testis was 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 birth and were killed at day 10, 15, 30, 40 and 60 postpartum. Hypothyroidism was confirmed by radioimmunoassay of thyroid hormones and TSH. Sertoli cell number, plasma and testicular interstitial fluid (TIF) androgen binding protein (ABP) concentration was quantified. Sertoli cell number was consistently decreased in all hypothyroid rats. Plasma ABP was also decreased irrespective of the duration of hypothyroidism. Unlike plasma ABP, TIF ABP concentration in hypothyroid rats increased at day 10, and 15 postpartum and decreased in other age groups. Plasma FSH level was increased significantly in all hypothyroid groups. The present investigation points out that suppression of T3 during the critical period of Sertoli cell proliferation affects their number and functional activity.

Aging↗

Duration-dependent effect of transient neonatal hypothyroidism on sertoli and germ cell number, and plasma and testicular interstitial fluid androgen binding protein concentration.

The impact of transient neonatal hypothyroidism on growth and function of puberal testis during different milestones of postnatal testicular development was studied in Wistar rats. Rat pups were made hypothyroid for 10, 15, 30, 40 and 60 days of postnatal age from birth by providing 0.05% (W/V) methimazole (MMI) in the drinking water of the mother, from day 1 postpartum till weaning (25 days postpartum) and thereafter in the drinking water. Control rats were raised without MMI treatment. Sertoli cell number and its function was assessed on day 60 postpartum. Sertoli cell number increased consistently in 10, 15, 30 and 40 days transient hypothyroid rats but decreased in rats subjected to continuous hypothyroidism from birth to 60 days postpartum. Rats subjected to continuous hypothyroidism from birth showed spermatogenic arrest at puberty and had only a single layer of spermatogonia. Transient neonatal hypothyroidism for 10 (or) 15 days from birth increased spermatocytes (pachytene and zygotene), spermatids (elongated and round) whereas, that of 30 and 40 days decreases the number of germ cells. Plasma androgen binding protein (ABP) concentration decreased in puberal rats belonging to all groups, whereas the testicular interstitial fluid (TIF) concentration of ABP increased significantly in 10 and 15 days hypothyroid rats while it decreased in all other groups. These findings indicate that the mitogenic activity of Sertoli cell is increased irrespective of the duration of transient neonatal hypothyroidism. However, the functional activity of Sertoli cells (ABP production) in these puberal rats varies depending upon the postnatal period at which the animals were in hypothyroid state.

Aging↗

Impact of neonatal hypothyroidism on Leydig cell number, plasma, and testicular interstitial fluid sex steroids concentration.

We have previously demonstrated that neonatal and transient neonatal hypothyroidism modulates Leydig, Sertoli, and germ cell numbers, sex steroids and androgen binding protein concentration. The present study was undertaken to study the effect of neonatal onset hypothyroidism on Leydig and peritubular myoid cell numbers, plasma and testicular interstitial fluid (TIF) sex steroid concentration at different age groups of Wistar rats. Hypothyroidism was induced by giving 0.05% methimazole (MMI) to lactating mothers or directly to the male pups from day 1 postpartum through days 10, 15, 30, 40 and 60 postpartum. To confirm hypothyroidism, plasma thyroid hormones and TSH were assayed. Plasma and TIF testosterone, progesterone, dihydrotestosterone (DHT) and estradiol were assayed by radioimmunoassay. Leydig cell number in hypothyroid rats were less than the age-matched controls. The diameter of Leydig cells in hypothyroid rats was smaller than the controls but 10 days old hypothyroids alone had larger than control rats. A significant decrease of peritubular myoid cell number was observed in 30, 40 and 60 days hypothyroid rats and increased in 10 and 15 days hypothyroidism. Hypothyroid rats had elevated level of plasma LH and decreased GH (except day 10 postpartum). Plasma PRL level was increased in 10 and 15 days hypothyroid rats and an opposite effect was observed in 40 and 60 days hypothyroidism. Plasma testosterone, DHT and estradiol were decreased in all hypothyroid rats. However, plasma progesterone level in hypothyroid rats was significantly higher at days 10, 30, and 40 postpartum and an opposite effect was seen in 15 and 60 days experimental groups. TIF testosterone and progesterone titre showed a consistent decrease in hypothyroid rats irrespective of the duration. In hypothyroid rats, TIF DHT levels decreased significantly in days 10, 40 and 60 postpartum. However, it increased in days 15 and 30 postpartum. Except at day 10 postpartum, the level of TIF estradiol in hypothyroid rats was significantly less than their age matched controls. Our data clearly indicate that neonatal onset hypothyroidism adversely affect Leydig cell proliferation along with impaired steroidogenesis.

Aging↗

Progesterone induced modulations of serum hormonal profiles in adult male and female rats.

The impact of progesterone on serum hormonal profiles in the presence and absence of gonads was studied in adult male and female albino rats. Progesterone was administered intramuscularly for 30 days at a dose of 1 mg/100g body weight/day. Serum testosterone, estradiol and prolactin titres decreased in male and female rats with intact gonads given progesterone. While the levels of both luteinizing hormone (LH) and follicle stimulating hormone (FSH) decreased in male rats with intact gonads, only FSH decreased in female rats. The inhibitory effect of progesterone on serum estradiol, LH, FSH and prolactin persisted even after gonadectomy in male rats. This persistent inhibitory effect of progesterone was also seen on serum testosterone, FSH and prolactin levels of female rats. Ovariectomy modified progesterone action on LH, as is evident from the decreased levels of LH observed only in ovariectomized rats given progesterone. While progesterone had no effect on serum T3 and T4 in male rats, gonadectomy altered the levels of T3 and T4 in male and female rats. Progesterone increased the levels of T3 and decreased the levels of T4 in ovariectomized rats. Growth hormone (GH) and thyroid stimulating hormone (TSH) levels seem to be resistant to changes in progesterone titre, irrespective of the sex and gonadal status. The present data suggest the existence of a sex specific effect of progesterone on gonadotrophins. The data on T3, T4 and TSH reveals that progesterone has no effect on the pituitary thyroid axis in the presence of gonads.

Animals↗

Influence of castration and testosterone propionate on prostatic and seminal vesicular lipids in mature monkeys.

The effect of castration and administration of testosterone propionate (TP) has been studied in mature monkeys in relation to prostatic and seminal vesicular lipids to castrates on prostatic and seminal vesicular lipids were studied in mature monkeys. Castration decreased prostatic total lipid, total phospholipids and total glyceride glycerols. Among neutral lipid classes only diacyl glycerol was decreased due to castration. Similarly among phospholipid classes, phosphatidyl choline and ethanolamine were decreased. A marked decrease in the seminal vesicular total lipid, total phospholipids, total cholesterol and total glyceride glycerol were observed due to castration. Mono and diacyl glycerols and phosphatidyl choline and ethanolamine also registered a significant decrease after castration. Administration of TP to castrates brought back all the lipid classes to normal level which showed a decrease due to castration. However, TP treated to castrates on both seminal vesicles and prostates had no effect on other classes of lipids which were unaltered by castration. The present study reveals that lipid metabolism in the male accessory sex organs is under androgenic control. Nevertheless, the influence of testicular androgen is specific to different classes of lipids as a number of phospholipids and neutral lipid classes were resistant to castration or administration of TP.

Animals↗