Pharmacokinetics of zinc tannate after intratesticular injection.

Forty-eight sexually mature male rats were injected intratesticularly with either 1, 3, or 6 mg zinc tannate (Kastrin) or with saline (as control). Zinc localized only in low concentration in primary spermatocytes and could not be detected in spermatogonia, Sertoli cells, spermatids, or spermatozoa. Forty-eight hours after injection of 1 mg Kastrin, zinc was accumulated in the spermatogonia and primary spermatocytes while, after injection of 3 mg, zinc was preferentially localized in Sertoli cells and spermatids; however, zinc was observed in the spermatids and spermatozoa 48 h after injection with 6 mg, and germ cells lost their identity and were fragmented after 1 week.

Pulmonary vascular changes in young and aging rats exposed to 5,486 m altitude.

Young (YNG) and middle-aged (MA) male rats were exposed to 5,486 m for durations ranging from 1 to 42 days to determine the effect of age on the progression of polycythemia, right ventricular hypertrophy (RVH), lung vascular muscularization, and pulmonary vascular responsiveness. Other rats were exposed for 42 days at 5,486 m and were then allowed to recover at 1,520 m for periods up to 42 days. The progression and subsequent regression of polycythemia and RVH with altitude exposure were similar for YNG and MA rats.

Chemical sympathectomy and serotonin inhibition reduce monocrotaline-induced right ventricular hypertrophy in rats.

Young male rats were administered monocrotaline (40 mg/kg, s.c.) either after chemical sympathectomy with 6-hydroxydopamine (6-OHDA, 100 mg/kg), after serotonin synthesis inhibition with p-chlorophenylalanine (PCPA, 500 mg/kg), or after saline injection.

Density and ultrastructure of mast cells in lung vessels of aging rats exposed to and recovering from chronic hypoxia.

A decrease in pulmonary vascular responsiveness in aging animals during exposure to chronic hypoxia has been previously reported; however, morphological documentation is lacking. Lungs from young (3-5 months) and aging (12-14 months) Sprague-Dawley rats, exposed to and recovering from chronic hypoxia, were morphometrically analyzed at the light-microscopic level for changes in perivascular mast cells, and at the electron-microscopic level for cellular alterations. While young rat lungs showed proliferation of mast cells around elastic and muscular pulmonary arteries and arterioles, perivascular mast cell density in lungs of aging rats was significantly greater than in young rat lungs.

Changes in pulmonary alveolar macrophages in rats exposed to oxides of zinc and nickel.

Pulmonary alveolar macrophages (PAM) from rats exposed to a single dose of ZnO or NiO showed distinct changes in size and ultrastructure. ZnO exposure brought about considerable reduction in the size of the cells, which can be distinguished into two types of macrophages. The macrophages contained a prominent nucleolus, several primary and secondary lysosomes, membrane formations, electron dense structures, and small dense mitochondria.

Effect of LHRH on cyproterone-acetate-injected adenohypophyses of castrated mice.

Luteinizing hormone releasing hormone (LHRH)-treated adenohypophyses from castrated, cyproterone acetate-injected adult male mice were studied with transmission electron microscopy (TEM). LHRH-treated luteinizing hormone (LH) gonadotrophs (types a and b) in castrated mice showed accumulation of secretory granules at the capillary pole, dilated Golgi apparatus and extensive rough endoplasmic reticulum (RER) profiles. Following treatment, granular content in LH type-a gonadotrophs was decreased and profiles of secretory granules were seen in the intercellular and perivascular spaces.

Ultrastructural changes in rat alveolar macrophages exposed to oxides of copper and cadmium.

The morphological effects of single intratracheal injections of copper oxide (CuO) and cadmium oxide (CdO) (5 mg) on rat alveolar macrophages were studied. Rats sacrificed after a one week recovery period showed distinct morphological changes induced by CuO and CdO. Copper oxide induced hypertrophy of both the alveolar macrophages as well as the epithelial lining.

Glycogen localization in pulmonary vascular smooth muscle of chronically hypoxic rats.

The pulmonary trunk, muscular arteries, and arterioles of male Sprague-Dawley rats exposed to simulated high altitude hypoxia (380 mm Hg) for six weeks were studied for glycogen localization. As early as three days exposure time, glycogen particles were mobilized in the smooth muscle cells of muscular arteries and arterioles. Weekly sacrifice of animals showed increasing preferential accumulation of glycogen, near the sarcoplasmic reticulum, in the subsarcolemmal region, adjacent to micropinocytotic vesicles, and near the mitochondria in the smooth muscle cells of muscular arteries and arterioles.

Fine structural changes in pulmonary veins of chronically hypoxic mice.

The pulmonary veins of male Swiss albino mice, exposed to simulated high altitude (380 mm Hg) for four weeks were studied for structural alterations. Endothelial cells contained invaginated nuclei and an accumulation of vesicles on the adluminal surfaces. In the subendothelial region, cells which contained filaments and dense bodies were noted.

Altered vascular responsiveness in isolated perfused lungs from aging rats.

Systemic vascular hyporesponsiveness has been well documented in aged rats, but a similar decreased vasoreactivity of the pulmonary vasculature has not been reported. Isolated lungs from young (3-5 months) and middle-aged (12-14 months) rats were perfused with whole blood and challenged alternately with alveolar hypoxia, angiotensin II, and 5-hydroxytryptamine. Hypoxic pulmonary vasoconstriction was less in the aging rats during both 5-min and 10-min hypoxic exposures.

Effect of cyproterone acetate on adenohypophysis of castrated mice.

Pituitaries from castrated male mice injected with cyproterone acetate were examined ultrastructurally. LH gonadotrophs showed two types: (a) those containing a dilated RER, a hypertrophied Golgi, and decreased granular content; and (b) those presenting an electron lucent cytoplasm and a nonhypertrophied RER. Following cyproterone acetate treatment both LH cell types showed increased RER cisternal hypertrophy and absence of Golgi membranes.

The effect of cyproterone acetate on the mouse adenohypophysis. II. Gonadotrophs and somatotrophs.

The adenohypophyses of adult male C57BL/6J mice pituitaries injected with cyproterone acetate for four weeks were examined with the electron microscope. The gonadotrophs showed an accumulation of the hormone-containing granules, and a noticeable decrease in the amount of rough endoplasmic reticulum. The somatotrophs exhibited proliferated profiles of rough endoplasmic reticulum, hypertrophied Golgi apparatus, and a slight decrease in the GH-containing granules.

Effect of cyproterone acetate on mouse adenohypophysis. I. The adrenocorticotrophs.

The adenohypophyses of adult male C57BL/6J mice pituitaries injected with cyproterone acetate for four weeks were examined with the electron microscope. The adrenocorticotrophs of the adenohypophysis showed an absence of the 200-nm granules that were lined along the plasma membrane, a decrease in profiles of rough endoplasmic reticulum, sparse distribution of ribosomes, and flatten Golgi membranes. It is believed the antiandrogen cyproterone acetate inhibited ACTH synthesis and release and that this was responsible for adrenocortical atrophy.

Effect of cyproterone acetate on structure of adrenal cortex in hypophysectomized, ACTH treated mice.

Hypophysectomized adult male C57BL/6J mice injected with 0.08 mg/g of cyproterone acetate showed large aggregates of cellular lipid as well as nodular formations in the zona fasciculata of the adrenal cortex. Daily ACTH injections (10 IU) reversed the atrophic changes noted above.

Effect of castor oil and benzyl benzoate used as a vehicle for antiandrogens on the adrenal cortex.

The use of benzyl benzoate as a vehicle constituent in administering cyproterone acetate caused morphological changes detectable at the ultrastructural level in the adrenal cortex. Xastor oil and benzyl benzoate in a 4:1 ratio caused intracellular as well as intercellular changes. In the zona fasciculata there were alterations in mitochondrial shape, size, and matrix.

The innervation of the mouse adrenal cortex.

The fine structure of the mouse adrenal cortex was examined with the electron microscope for the presence of neural elements. Several axon terminals containing mostly clear vesicles (60 nm) were noted in the vicinity (250 nm) of the capsular fibroblasts. In the subcapsular region, myelinated as well as unmyelinated fibers were commonly found.

Effect of cyproterone acetate on the structure of the adrenal cortex.

Adult male C57 BL/6J mice injected with 0.08 mg/g of cyproterone acetate showed an increase in cellular lipid content in the zona fasciculata and zona reticularis of the adrenal cortex. In the perimedullary region, densely staining cells aggregated to form scattered nodules.

Effect of cyproterone acetate on adrenal cortex of castrated mice.

Castrated adult male C57BL/6J mice displayed a wide perimedullary zone (secondary X-zone) whose cells were characterized by proliferated rough and smooth endoplasmic reticulum and elongated mitochondria with lamellar cristae. Castrated mice which received 0.08 mg/g of cyproterone acetate showed a much inhibited secondary X-zone at the light microscopic level, while at the ultrastructural level the perimedullary cells lacked the proliferated rough and smooth endoplasmic reticulum as well as the elongated mitochondria.