Seminal vesicle

Rodent 5-7-day Hershberger assay change in weight of prostate and seminal vesicles in castrated rats. 

Seminal vesicle. An organ in which a portion of the seminal fluid is retained. 

No studies were located that examined reproductive function in animals after inhalation exposure to endosulfan. However, routine gross and histopathological examination of the reproductive organs (testes, epididymides, seminal vesicles, prostate, ovaries, and uterus) of rats exposed (nose-only) to concentrations of endosulfan of up to 2 mg/m for 6 hours/day, 5 days/week for a total of 21 out of 29 days revealed no adverse effects (Hoechst 1984c). 

Metastatic spread can occur by local extension, lymphatic drainage, or hematogenous dissemination.17 Lymph node metastases are more common in patients with large, undifferentiated tumors that invade the seminal vesicles. The pelvic and abdominal lymph node groups are the most common sites of lymph node involvement (Fig. 89-1). Skeletal metastases from hematogenous spread are the most common sites of distant... 

Cp No seminal vesicle involvement, T3 (Tumor extends through the prostatic capsuled... 

C2 Seminal vesicle involvement, T4 (Tumor is fixed or invades adjacent structures... 

Radical prostatectomy Surgical removal of the entire prostate and the seminal vesicles. 

Incubation of BP with arachidonic acid and ram seminal vesicle micro-somes, a rich source of PGH synthase, produces 1,6-, 3,6-, and 6,12-quinones as the exclusive products of oxidation (Figure 2) (18). 

Addition of RNA or DNA prior to oxidation of BP by PGH synthase results in substantial nucleic acid binding (17,21). Addition of RNA five minutes after initiation of oxidation leads to no covalent binding (17). This implies that the quinones do not bind to nucleic acid but rather a short-lived intermediate in their formation does. Arachidonic acid oxygenation in ram seminal vesicle microsomes is complete within two min, which suggests that the reactive intermediate is generated concurrently with PGH2 The structures of the nucleic acid adducts have not been elucidated so the identity of the reactive intermediate is unknown. 

Figure 2. Products of BP oxidation by arachidonic acid and ram seminal vesicle microsomes.

In contrast to the results with BP, incubation of BP-7,8-dihydrodiol with ram seminal vesicle microsomes and arachidonate generates a species that is strongly mutagenic to Salmonella strains TA98 and TA100 (Figure 3) (22). Formation of the mutagen is inhibited by... 

Figure 3. Induction of mutation in Sj typhimurium TA98 by BP-7,8-dihydrodiol, arachidonic acid, and ram seminal vesicle microsomes. Concentration dependence on BP-7,8-dihydro-diol. (Reproduced with permission from Ref. 22. Copyright 1978 Academic.)...

Table I. Relative Yields of Diastereomeric Adducts From Anti-diol Epoxide Plus Polyguanylic Acid Compared to Adducts Generated During Metabolism of BP-7,8-dihydrodiol by Ram Seminal Vesicles in the Presence of Arachidonic Acid...

Support for this conclusion is provided by the hydroperoxide specificity of BP oxidation. The scheme presented in Figure 6 requires that the same oxidizing agent is generated by reaction of h2°2/ peroxy acids, or alkyl hydroperoxides with the peroxidase. Oxidation of any compound by the iron-oxo intermediates should be supported by any hydroperoxide that is reduced by the peroxidase. This is clearly not the case for oxidation of BP by ram seminal vesicle microsomes as the data in Figure 7 illustrate. Quinone formation is supported by fatty acid hydroperoxides but very poorly or not at all by simple alkyl hydroperoxides or H2C>2. The fact that... 

Figure 7. Dependence of BP oxidation by ram seminal vesicle micro-somes on the concentration of different hydroperoxides. Abbreviations used are 20 4, arachidonic acid 15-HPEA, 15-hydroperoxy-eicosatetraenoic acid t-BuOOH, t-butyl hydroperoxide. The structure is PGG2 is given in Figure 1.

Peroxyl radicals are the species that propagate autoxidation of the unsaturated fatty acid residues of phospholipids (50). In addition, peroxyl radicals are intermediates in the metabolism of certain drugs such as phenylbutazone (51). Epoxidation of BP-7,8-dihydrodiol has been detected during lipid peroxidation induced in rat liver microsomes by ascorbate or NADPH and during the peroxidatic oxidation of phenylbutazone (52,53). These findings suggest that peroxyl radical-mediated epoxidation of BP-7,8-dihydrodiol is general and may serve as the prototype for similar epoxidations of other olefins in a variety of biochemical systems. In addition, peroxyl radical-dependent epoxidation of BP-7,8-dihydrodiol exhibits the same stereochemistry as the arachidonic acid-stimulated epoxidation by ram seminal vesicle microsomes. This not only provides additional... 

Dyck, M.K., Gagne, D., Ouellet, M., Senechal, J.-F., Belanger, E., Lacroix, D., Sirard, M.-A., and Pothier, F. 1999. Seminal vesicle production and secretion of growth hormone into seminal fluid. Nature Biotechnology 17, 1087-1090. 

The brain, like the seminal vesicles, is able to reduce testosterone to 5a-dihydrotestosterone (DHT) and, like the placenta, the brain aromatizes testosterone to estradiol (Fig. 52-4). Neither conversion occurs equally in all brain regions. The aromatization reaction is discussed below. Regional distribution of 5a-reductase activity toward testosterone in rat brain reveals that the highest activity is found in the midbrain and brainstem, intermediate activity is found in the hypothalamus and thalamus, and the lowest activity is found in the cerebral cortex [1]. The pituitary has higher 5a-reductase activity than any region of the brain, and its activity is subject to changes as... 

Androgenic deficiency in male rats given a single oral dose of 15 pg 2,3,7,8-TCDD/kg BW was evident as early as 2 days posttreatment, with persistence up to 12 days. These deficiencies may account for male reproductive pathology and dysfunction in rats treated with overtly toxic doses of TCDD. Findings included depression in plasma testosterone concentrations, as well as decreased weight of seminal vesicles (by 68%), ventral prostate gland (by 48%), testes, and epididymis (Moore et al. 1985). 

Men with disease fixed or invading adjacent structures other than the seminal vesicles (T4) are at very high risk for recurrence. Androgen ablation should be initiated at diagnosis instead of waiting for the onset of symptoms. 

Prenatal and postnatal exposures to fenvalerate reduced prostate and seminal vesicle weights and plasma testosterone levels in male rats [55], A chronic study showed no adverse effects on reproductive tissues at a high dose level of 1,000 ppm [142]. In vivo and in vitro studies with rats and mice suggested that fenvalerate may affect male and female reproduction, possibly due to calcium transport alteration [143-146], One paper reported that fenvalerate affected human sperm count and sperm motility of male workers who were exposed to fenvalerate in a pesticide factory [147]. 

W15. Williams-Ashman, H. G., Banks, J., and Wolfson, S. K., Jr., Oxidation of polyhydric alcohols by the prostate gland and seminal vesicle. Arch. Biochem. Biophys. 72, 485-494 (1957). 

In contrast, no reproductive effects were observed in male Sprague-Dawley rats exposed to 500 ppm -hexane 22 hours a day for 6 months (IRDC 1981). No treatment-related lesions were noted in any of the reproductive tissues examined (seminal vesicles, prostate, testis, epididymis). Similar results were reported in both sexes of weanling Fischer 344 rats exposed to up to 10,000 ppm -hexane 6 hours a day, 5 days a week for 13 weeks (Cavender et al. 1984). No treatment-related histopathologic lesions were present in any of the following reproductive tissues ovaries, uterus, oviducts, vagina, cervix, seminal vesicles, prostate, testis, or epididymis. 

Thyroid gland Hematopoietic system Adrenal gland Pancreas Seminal vesicle Urinary tract Lymphatic system... 

---