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Background: The objective of this study was to determine the effect of active immunization against LHRH on the growth characteristics and histology of subcutaneously implanted tumors of the androgen-sensitive Dunning R3327-PAP and androgen-independent R3327-AT2.1 rat prostate adenocarcinoma sublines., Results: We herein demonstrate that 1) active immunization with an LHRH-diphtheria toxoid-conjugate (LHRH-DT) leads to the downregulation of gonadotropins and testosterone and consequently the atrophy of testosterone-dependent organs such as the testes, prostate, and androgen-sensitive Dunning R3327-PAP tumors, 2) growth inhibition of Dunning R3327-PAP tumors is caused by suppression of cell division rather than by an increase in cell death and is associated with an increase of the tumor stroma content, and 3) volume increase of the androgen-independent Dunning R3327-AT2.1 tumor is slightly but significantly reduced, indicating a local stimulatory LHRH loop within this tumor cell line.

Testicular minces were utilized to study the effect of gossypol on testosterone production. Testosterone production was assessed in both control nd gossypol treated groups after 0 to 4 hours incubation in the presence of hCG. Media testosterone was measured by radioimmunoassay. Gossypol did not alter testosterone production when present in incubates at the concentrations of 3.5 x 10(-5) M, 7 x 10(-5) M and 3.5 x 10(-4) M. Preincubation of testis mince with gossypol (7 x 10(-6) M, 7 x 10(-5) M, 3.5 x 10(-4) M) for 1 to 4 hours did not alter subsequent hCG induced testosterone production in mature rats. Testosterone production however, was inhibited in immature rat testis when the whole testis was incubated for 4 hours with different concentrations of gossypol (7 x 10(-6) M, 7 x 10(-5) M, 3.5 x 10(-4) M). In vivo testosterone production was not inhibited in the immature rat testis 24 hours after oral administration of gossypol (100 mg/kg).

The effects of a combination of medroxyprogesterone acetate and testosterone enanthate, on the exocrine and endocrine testicular function were examined in adult men. The treatment was carried out with 2 different regimens and lasted for 8 months. Group I received an initial injection of 1000 mg medroxyprogesterone acetate and 500 mg testosterone enanthate followed by monthly maintenance dose of 150 mg medroxyprogesterone acetate and 500 mg testosterone enanthate. In group II, after an initial high dose of 1000 mg medroxyprogesterone acetate and 250 mg testosterone enanthate treatment was given as biweekly injections of 75 mg medroxyprogesterone acetate and 250 mg testosterone enanthate. Complete spermatogenic arrest of variable duration was achieved in all 9 subjects enrolled. Restoration of spermatogenesis occurred in both groups, in a few cases during the treatment, and there was a delay of full recovery of sperm counts up to 5 months after cessation of therapy. None of the subjects enrolled in this study complained of decrease in libido or change in sexual behaviour. Clinical evaluation and measurements of various urine and serum components revealed no significant changes during the treatment period. The dosage and the different administration schedule of the hormone combination described here was inadequate to maintain azoospermia in all subjects during treatment.

Testosterone proprionate in form of eye drops will not be absorbed. A good absorption takes place following the administration of testosterone containing nasal drops in the form of an emulsion of pure testosterone. A quick, significant testosterone increase but of only short duration takes place. Unpleasant side effects were not observed. This treatment may be clinically applicable to male patients in the climacteric period.

A potential male contraceptive approach was evaluated in clinical trials involving monthly injections of depot medroxyprogesterone acetate and either subdermal implants of testosterone propionate or monthly injections of testosterone enanthate. Pregnancies occurred in partners of 9 men with recent sperm counts of 10 million/ml or below. In 5 of the 9 instances, the sperm counts were less than 1 million/ml. It appears that male contraceptive methods involving spermatogenic suppression may require attainment and maintenance of azoospermia. The pregnancy rate cannot be calculated, because the extent of other contraceptive use is uncertain. There were no spontaneous abortions. 6 pregnancies were carried to term, and all progeny were normal, based on physical examination at birth or 3 months after birth.

This paper is a historic review of two studies of the treatment of cryptorchidism. One was concluded 20 years ago with native LHRH, while the other took place 14 years ago and involved one of the potent LHRH analogues. The first study was initiated at the end of 1971-at a time when the different modes of action of the decapeptide were by far not evaluated to the full extent they are now-and included ten prepubertal boys with undescended testes aged five to ten years. The treatment consisted of intramuscular application of 20 micrograms LHRH once daily for three weeks. Additionally, three boys, five, seven and nine years of age, also presenting undescended testes underwent an LHRH test with intravenous bolus application of 200 micrograms. In all three subjects, a 2.5-fold increase in plasma testosterone was observed 20 min after the bolus. The treatment group showed neither a rise in LH nor in testosterone at the end of therapy. Testicular descent was achieved in six out of six boys with bilateral and in 2/4 with unilateral undescended testes. These good results might be based on the fact that six boys had retractile rather than actually undescended testes. In the second study started in 1978, 18 boys, three to 12 years of age with either unilateral or bilateral cryptorchidism, were treated with a synthetic LHRH analogue ("D-Leu 6, Des-Gly-10 LHRH ethylamide") applied intranasally. The peptide prepared in an aqueous solution was administered in the form of nose drops.(ABSTRACT TRUNCATED AT 250 WORDS) [ABSTRACT FROM AUTHOR]