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Biomedical subjects

H F Huang

Publications and source records attributed to H F Huang.

At least 55 records · Page 3Linked to original sources
PubMed1989

Multiple sites of action of the vitamin D endocrine system: FSH stimulation of testis 1,25-dihydroxyvitamin D3 receptors.

1,25-Dihydroxyvitamin D [1,25(OH)2D] receptors exist in numerous unexpected tissues. These include, for example, rat lung, heart, testis, and uterus, but not prostate and bladder. The issues of 1,25(OH)2D effects on and receptor location in the testis were addressed by (a) physiological and pharmacological manipulations of tubule cell types and (b) histological examination of testes of vitamin D-deficient rats. FSH treatment in hypophysectomized adult rats increased 1,25(OH)2D receptor levels by 135% (P less than 0.01). Busulfan treatment reduced testis receptor levels by 35% (P less than 0.05) after 35 days (maximum effect), and the effect was reversed after recovery (85 d). Cryptorchidism for 5 or 50 days resulted in modest (33%, P less than 0.05) or substantial (79%, P less than 0.001) reductions in receptor levels. Only the FSH treatment and 50 days cryptorchidism reduced receptor levels in the residual tissue. The testes of vit. D-deficient rats showed incomplete spermatogenesis and degenerative changes. Although interpretation is complicated by the intricate communication among testis cell types, these data suggest that the Sertoli cell is a primary site of action of 1,25(OH)2D in the testis. Moreover, these data indicate that 1,25(OH)2D receptor function in the testis relates to germ cell division/maturation, although this may be an indirect effect via the Sertoli cells.

Animals↗
PubMed1989

Characterization of cis-platinum-induced Sertoli cell dysfunction in rodents.

The present study examined the effects of dosage and frequency of cis-platinum administration on various aspects of Sertoli cell function and its correlation with the status of spermatogenesis in rats 1 and 9 weeks after the initial drug administration. Adult male Sprague-Dawley rats were administered cis-platinum (10 mg/kg) intraperitoneally as a single dose or as five daily doses of 2 mg/kg. Electron microscopic observation of testicular tissues fixed in the presence of lanthanum revealed that cis-platinum administration resulted in leakage of the Sertoli cell tight junctions. This occurred as early as 24 hr after the five daily injections, and persisted at least 40 days. Testicular androgen-binding protein (ABP) content was not significantly affected by either treatment regimen after 1 or 9 weeks of recovery. On the other hand, serum ABP values were significantly elevated after 9 weeks of recovery. In addition, the increased sodium and decreased potassium concentrations in seminiferous tubular fluid noted in cis-platinum-treated animals were also indicative of abnormal Sertoli cell secretory function. Degeneration of spermatogenic cells was noted as early as 5 days after the last drug administration; and partial restoration of spermatogenesis was noted after 40 days of recovery. We conclude that in rats both morphological and biochemical properties of Sertoli cells are affected by cis-platinum administration. These changes in Sertoli cell function may be responsible for the cis-platinum-induced impairment of spermatogenesis in these animals.

Androgen-Binding Protein↗
PubMed1989

Modification of Sertoli cell functions in vitamin A-deficient rats.

FSH binding and cAMP responses to FSH in Sertoli cell-enriched testes were not affected by the vitamin A (retinol) status of the animals. These results indicate that changes in Sertoli cell functions during vitamin A deficiency are independent of FSH-Sertoli cell interactions. Concentrations of serum androgen binding protein (ABP) in vitamin A-deficient rats were consistently higher than those of control animals throughout the study period. The accumulation of testicular fluid after efferent duct ligation, an indication of Sertoli cell secretory function, was normal in vitamin A-deficient rats at least until 70 days of age, but declined thereafter. ABP concentrations in seminiferous tubular fluid of vitamin A-deficient rats increased transitorily during the 70-80-day age period but returned to normal by 90 days. The increment of ABP in seminiferous tubular fluid after efferent duct ligation, and ABP concentrations in interstitial fluid were consistently lower in vitamin A-deficient rats. The higher serum ABP in vitamin A-deficient rats therefore cannot be explained by an increase in the permeability of Sertoli-cell tight junctions or basement membrane.

Androgen-Binding Protein↗
PubMed1988

Partial prevention of procarbazine induced germinal cell aplasia in rats by sequential GnRH antagonist and testosterone administration.

The present study examined the feasibility of using a combination of gonadotropin releasing hormone antagonist (GnRH-A) and testosterone in the prevention of procarbazine induced germinal aplasia. Daily injections of GnRH-A or vehicle were given to adult male rats for 21 days prior to procarbazine (PCB) administration and continued until 2 days after the second of two doses of procarbazine (200 mg/kg i.p.) given 1 week apart. One group of rats receiving GnRH-A and PCB was given s.c. two 5-cm testosterone capsule (TC) implants (inside diameter, 3.5 mm) immediately following the second dose of PCB. Eight weeks after the last PCB treatment, more than 99% of the seminiferous tubular cross-sections of rats receiving PCB alone were devoid of spermatogenic activity. Spermatogenesis in PCB injected animals receiving GnRH-A pretreatment alone was abortive but was partially preserved when exogenous testosterone was given following PCB administration. At 16 weeks, spermatogenesis was absent in all PCB treated animals and was only observed in less than 1% of the tubular cross-sections of the PCB treated rats receiving GnRH-A pretreatment alone. On the other hand, active spermatogenesis was noted in 68% of the tubular cross-sections, and complete spermatogenesis was noted in four of the five PCB treated rats receiving both GnRH-A pretreatment and subsequent TC implantation. At the time of sacrifice, testicular testosterone concentrations in animals receiving TC implants were below 10% of normal levels, while both serum and testicular testosterone content were increased in PCB treated animals with or without GnRH-A pretreatment. Concomitantly, testicular androgen binding protein content remained suppressed and serum androgen binding protein was elevated, indicating a prolonged defect in Sertoli cell function. These lesions were prevented by GnRH-A pretreatment. The present study demonstrates that GnRH-A pretreatment and subsequent TC implantation resulted in restoration of complete spermatogenesis in adult male rats given a 400-mg/kg cumulative dose of PCB. It is postulated that GnRH-A may ameliorate PCB induced Sertoli cell dysfunction and/or stimulate the number of spermatogonia to provide more proliferating cells ready for repopulation of the germinal epithelium following PCB injury. The differentiation of these spermatogonia was further supported by exogenous testosterone through certain unknown local mechanisms, resulting in the completion of spermatogenesis.

Androgen-Binding Protein↗
PubMed1988

Disruption of sustentacular (Sertoli) cell tight junctions and regression of spermatogenesis in vitamin-A-deficient rats.

The relationship between the intactness of sustentacular (Sertoli) cell tight junctions and the status of spermatogenesis was examined in rats fed a vitamin-A-deficient diet after weaning (VAD rats). Both serum and testicular retinol concentrations of the VAD rats declined to a nadir by 80 days of age. At this time, it was observed that Sertoli cell tight junctions of the VAD animals were intact and complete spermatogenesis was maintained. Leakage in Sertoli cell tight junctions, as demonstrated by the presence of lanthanum in the adluminal compartment of the seminiferous epithelium, was first observed in 90-day-old VAD rats. Severe regression of spermatogenic cells was noted in 100-day or older VAD animals. These results suggest that severe germ cell loss observed during chronic vitamin A deficiency may result from abnormal intratubular environment due to the disruption of the blood-testis barrier.

Animals↗
PubMed1988

Dissociation of qualitative and quantitative effects of the suppression of testicular testosterone upon spermatogenesis.

The present study examined the quantitative and qualitative effects of suppressed testicular testosterone concentration upon spermatogenesis. Adult male rats were given sc implants of 0.5- to 5-cm long testosterone filled silastic capsules (TC) for 10 weeks. Testicular testosterone concentrations were suppressed to below 5% of the control level in rats receiving 1.5- to 5-cm TC implants. Spermatogenesis was arrested at early spermatids in rats given 1.5-cm TC implants, but was maintained in those given 3- or 5-cm TC implants. The number of A1 spermatogonia was 10-15% higher in rats bearing 0.75- to 1.5-cm TC implants, while a 5-15% reduction in preleptotene spermatocytes was noted in rats receiving 1.5-cm or longer TC implants. Linear regression analysis revealed a significant negative correlation between the number of A1 spermatogonia and the percent yield of preleptotene spermatocytes. This result illustrates the presence of a negative feedback mechanism in the regulation of A1 spermatogonia. The lack of a correlation between the quantitative changes in germ cell number and the hormonal states suggests that factors or local mechanisms independent of the concentration of hormones are involved in the regulation of germ cell differentiation.

Androgen-Binding Protein↗
PubMed1988

Effect of sexual maturity on testicular injury subsequent to procarbazine administration in rats.

The present study examined the effect of age on various aspects of Leydig cell and Sertoli cell function in Sprague-Dawley rats administered procarbazine. Procarbazine was administered intraperitoneally to Sprague-Dawley rats aged 14, 24, and 60 days in 3 weekly injections of 200 mg/kg. Animals were sacrificed 1 week after the last injection. Severe impairment of spermatogenesis was evident in all animals. Sertoli cell function, as assessed by total testicular ABP content, was not significantly different between procarbazine-treated animals and controls in any age group. On the other hand, procarbazine administration resulted in a 60% reduction in total intratesticular testosterone content in the 14-day-old rats but not in the 24- or 60-day-old animals. Serum testosterone was significantly reduced by 50% in the group of 14-day-old animals but not in the other age groups. Serum LH values were not significantly changed from control levels in any age group. Testicular content of Fe, Zn, Mn, and Cn were unaltered by procarbazine administration in any age group. Since serum LH and testicular cation content were not affected by procarbazine treatment, the significant decreases in serum and testicular testosterone in 14-day-old animals after procarbazine administration may indicate a direct age-dependent effect of procarbazine on Leydig cell function.

Animals↗
PubMed1987

Restoration of spermatogenesis by high levels of testosterone in hypophysectomized rats after long-term regression.

In order to correlate the levels of intratesticular testosterone and the status of spermatogenesis, the present study examined the spermatogenic responses of mature chronically hypophysectomized (HPX) rats to different regimens of testosterone (T) replacement, i.e. implantation of a 2 X 5 or 6 X 5 cm long testosterone capsule (TC), or injection of 25 mg or 100 mg of testosterone enanthate (TE) every 4 days for 90 days. These regimens restored the testicular testosterone of the HPX rats to 25-96% of that measured in normal control rats. The testis weight of untreated HPX rats was below 30% of the normal control values. It was restored to 60-80% of control values in the TC implanted rats and to 50% in those receiving TE injection. Complete spermatogenesis of HPX rats was restored in those receiving TC implants and 100 mg TE injections. It was incomplete in those given 25 mg TE injections. Quantitative evaluation of germ cells revealed that spermatogonial populations of HPX rats were restored to 70 and 50% of the normal levels in rats receiving TC implants and TE injection, respectively. Differentiation of these cells resulted in the population of preleptotene spermatocytes to the same extent as those observed in spermatogonia. The yield of spermatids in both TC- and TE-treated HPX rats was below 50% of normal controls. Ratios between two successive generations of germ cells in stage VII epithelium revealed both dosage and regimen effects upon the yield of meiotic cells and spermatids. These results suggest that both T concentration and the mode of T availability to the testis may be important for specific steps of germ cell development in different stages of the cycle of the seminiferous epithelium. The results of the present study demonstrate that as little as 25% of normal testicular T concentration is sufficient to support all stages of spermatogenesis. Failure to restore a normal germ cell number even in the presence of a normal testicular T concentration suggests the need of other factors for quantitative spermatogenesis. Furthermore, despite a higher testicular T concentration achieved by TE injections, the restoration of spermatogenesis was less pronounced by this regimen. This finding suggests that the consistency of testicular T may also be important for normal spermatogenesis.

Animals↗
PubMed1986

Suppression of the intratesticular testosterone is associated with quantitative changes in spermatogonial populations in intact adult rats.

To investigate the interactions between testosterone and FSH on quantitative aspects of spermatogenesis, intact adult rats were implanted sc with 0.5- to 50-cm long testosterone-filled silastic capsules (TC) for 8 weeks. Serum testosterone levels were suppressed slightly in rats bearing 1-cm TC implants but were elevated 6- to 30-fold when 5 cm or longer TC implants were used. These changes in serum testosterone were associated with a biphasic, dose-dependent response in testicular testosterone concentrations, reaching a minimum of 10-15% of the control values in rats bearing the 1- or 5-cm TC implants, but rebounding to 80% when 50-cm long TC implants were used. Meanwhile, serum FSH was comparably suppressed by 40-70%. Complete spermatogenesis was observed in all experimental animals with the exception of three rats with 1-cm TC implants in which elongated spermatids were absent or reduced in number. Enumeration of various cell types in the basal compartment of whole mounted seminiferous tubules revealed a 20% increase in type A1 spermatogonia in rats with the 1-cm TC implants. On the other hand, a 15-20% reduction in type B spermatogonia and preleptotene spermatocytes was noted in rats receiving 5-cm or longer TC implants. These results demonstrate that complete spermatogenesis can be maintained in intact animals in the presence of 10-15% of the normal testicular testosterone concentration. Failure to maintain normal testis weight, testicular testosterone concentration, or germ cell number at a 30-fold increase in serum testosterone demonstrates that high levels of serum testosterone may not be beneficial for quantitative spermatogenesis. Furthermore, both quantitative and qualitative differences were observed in different phases of spermatogenesis in the presence of comparable serum FSH and testicular testosterone concentrations. These results suggest that factors other than these two hormones are also involved in the regulation of spermatogenesis.

Animals↗
PubMed1984

Alteration of free sulphydryl content of rat sperm heads by suppression of intratesticular testosterone.

Subcutaneous injections of testosterone propionate to adult male rats at a dose of 2.5 or 10 mg/kg body weight, 3 times per week for 7 weeks, resulted in a 75% reduction in serum LH and more than 50% reduction in intratesticular testosterone concentration, but serum FSH levels remained unchanged. The free -SH content, measured as iodo[14C]acetamide binding, increased by 70-100% in testicular sperm heads after suppression of testicular testosterone, and by 25-30% in caput epididymal sperm heads but was decreased by 70-80% in cauda epididymal sperm heads. These results demonstrate an alteration in the oxidative state of sperm nuclear basic proteins, suggesting incomplete nuclear maturation. These changes may be specific for the suppression of intratesticular testosterone, thus illustrating the androgen dependency of sperm head maturation. The contrast effects noted between the iodo[14C]iodoacetamide binding by the caput and the cauda epididymal sperm heads indicate that testosterone propionate treatment may affect the mechanisms regulating the oxidation of the sulphydryl residues in sperm heads during epididymal transit. This alteration may not directly relate to the tissue androgen concentrations.

Animals↗
PubMed1984

Pituitary-testicular interrelationships during germinal involution in the vitamin A deficient rat.

Pituitary-testicular relationships in mature male rats were investigated during the period of germinal involution after the induction of vitamin A deficiency (VAD). Vitamin A deficiency caused a decrease in testicular weight, a gradual increase in the incidence of delayed spermiation, increased phagocytosis of spermatids and pyknosis of germ cell nuclei in rats aged 80 to 110 days. Both basal and gonadotrophin releasing hormone (GnRH)-stimulated serum FSH concentrations were increased by 100 days of age. During the same period, the per cent increment in GnRH-stimulated FSH secretion, pituitary FSH concentration and LH secretion remained unchanged. These results suggest that the increased serum FSH may mark specifically an alteration in the germinal epithelium. By 140 days of age, spermatogenic activity in the rats with VAD was limited to the spermatogonial proliferations so that only Sertoli cells, spermatogonia and preleptotene spermatocytes remained. At this time hypersecretion of FSH persisted while the per cent increment of GnRH-stimulated FSH secretion decreased. Concomitantly, basal and GnRH-stimulated LH concentrations were also increased in the presence of normal serum testosterone. These results indicate that a complete cessation of spermatogenesis beyond preleptotene spermatocytes is associated with a change in the secretion of both FSH and LH. The relationship between serum LH and testosterone was normal until at least 110 days of age. By 140 days the ratio between basal LH and basal testosterone, and between total LH and total testosterone, after GnRH administration, increased in the rats with VAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Failure of spermatid release under various vitamin A states - an indication of delayed spermiation.

Vitamin A deficiency (VAD) was induced in male Sprague-Dawley rats by feeding them a vitamin A-deficient diet after weaning and subsequently supplementing their diet with retinoic acid. The serum vitamin A levels of these rats were at a minimum by 60 days of age. Although spermatogenesis can proceed normally during the early phase of vitamin A deficiency, a small number of late spermatids were not released from the seminiferous epithelium at the end of Stage VIII of the cycle of the seminiferous epithelium but rather at a later stage. This observation suggests a delay in spermiation. This delayed spermiation was noted as early as 50 days of age and persisted in rats even after 60 days of vitamin A replacement. These results demonstrate that in rats the timing of spermiation can be retarded by vitamin A deficiency. Although the mechanisms causing this delay in spermiation are not known, the vitamin A-deficient rat provides a useful model system for studies on the regulation of spermiation.

Animals↗