The aim of this study was to establish whether a rise in plasma carnitine and testosterone stimulates carnitine uptake in the epididymis. Three groups of rats were injected SC with testosterone enanthate (2.35, 2.40, and 3 mg/kg body weight, respectively, three times a week for 4 weeks) and compared to controls. All three doses proved effective and induced a rise in the weight of the seminal vesicles and prostate, thus reflecting a rise in plasma androgen levels. Testosterone enanthate reduced both testicular weight and the number of spermatozoa in the testes. It raised the level of blood carnitine by 40% in group 1 and by 150% in groups 2 and 3, but the carnitine concentration in the epididymal fluid did not change. These results suggest that the system of carnitine transport across the epididymis is saturated, and that it is not activated by a rise in plasma testosterone.

1 In pregnant rats, chronic NO-synthase inhibition induces the development of a pre-eclamptic syndrome, characterized by an increase in maternal blood pressure, a loss of vascular refractoriness to pressor stimuli, a reduction in litter size and a decrease in pups (and maternal) weight. We investigated whether a NO-donor, molsidomine, administered during NO synthase inhibition, could restore a normal pregnancy.2 Pregnant rats were given daily, starting from day 14 of gestation, saline (controls), or L-NAME (50 mg kg-' d-'), or molsidomine (15 or 30 mg kg-' d-'), or the L-NAME + molsidomine combinations. Maternal blood pressure and body weight, litter size, pups weight and vascular reactivity to pressor stimuli (angiotensin II, noradrenaline, electrical stimulation of the spinal cord) were investigated. 3 L-NAME alone, as compared to controls, increased maternal blood pressure, reduced litter size (-59%), increased foetal reabsorptions (+ 625%) and decreased foetal weight (-10%). Vascular reactivity to pressor stimuli was enhanced. 4 Molsidomine alone, as compared to controls, dose-dependently decreased maternal blood pressure but had no effect on vascular reactivity and, whatever the dose, on foetal outcome. 5 The L-NAME-molsidomine combinations dose (of molsidomine)-dependently limited the rise in maternal blood pressure induced by L-NAME alone but unexpectedly, dose-dependently and significantly worsened pregnancy evolution, e.g., at 30 mg kg-'d-': litter size (-80%), foetal reabsorptions (+ 1025%), foetal weight (-24%). Vascular reactivity to pressor stimuli was paradoxically further enhanced. 6 Thus, in a chronic NO deprivation-induced model of pre-eclampsia in rats, molsidomine, possibly because of its hypotensive action, worsens the foetal outcome, which questions the usefulness of NOdonors in pre-eclamptic women.

BACKGROUND Hormonal treatments lasting 2–6 months inhibit spermatogenesis in men and have been proposed as germ cell protection against anticancer therapy. Because it is unthinkable to delay anticancer treatments, the authors investigated the protection afforded against irradiation of rats by 22 days of hormonal pretreatment. METHODS Adult Sprague–Dawley rats were assigned to an untreated control group (C) or to one of 5 treatments: medroxyprogesterone acetate plus testosterone only (M), 3 or 5 gray of irradiation (R3 and R5), or hormonal treatment prior to 3 or 5 gray of irradiation (MR3 and MR5). Mating trials were conducted 1, 24, 45, 65, 86, and 109 days after treatment. At 122 days, genital organ weights, testis histology, and epididymal spermatozoa were evaluated. RESULTS Irradiation reduced sperm production and had a clastogenic effect on postmeiotic germ cells. No protective effect of steroid treatment was observed. Moreover, testis weight, tubule diameter, the repopulating index, and the sperm head count decreased more in the MR5 group than in the R5 group. Mating tests showed decreases in positive vaginal smears and fertility at both 45 and 65 days, and an increase in resorption at 109 days. CONCLUSIONS These results indicate that hormonal pretreatment potentiates irradiation damage to germ cells, especially stem cells, as regards survival and genomic alterations, probably because of increased lipoperoxidation of late spermatids. Cancer 1999;85:1313–22. © 1999 American Cancer Society.