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Arch Toxicol. 2002 Jul;76(7):423-9. Epub 2002 Jun 13.
Effects of butyl paraben on the male reproductive system in mice.

Oishi S.

Department of Toxicology, Tokyo Metropolitan Research Laboratory of Public Health, 3-24-1 Hyakunin-cho, Shinjuku-ku, Tokyo 169-0073, Japan. oishokyo-eiken.go.jp

Parabens are alkyl ester compounds of p-hydroxybenzoic acid widely used as preservatives in foodstuffs, cosmetics, toiletries and pharmaceuticals. These compounds are known to exert a weak estrogenic activity in estrogen receptor assays in vitro and in uterotrophic assays in vivo. In this paper, we have shown that butyl paraben had an adverse effect on the male mouse reproductive system and that it damaged the late steps of spermatogenesis in the testis. Butyl paraben was administered to 4-week-old Crj:CD-1 mice assigned to groups of eight animals, at doses of 0.01%, 0.10%, and 1.00% in the diet for 10 weeks. The average butyl paraben intake from the calculated food consumption was 14.4+/-3.60, 146+/-35.9, and 1504+/-357 mg/kg per day for the 0.01%, 0.10%, and 1.00% dietary butyl paraben groups, respectively. There were no treatment-related effects of butyl paraben on the liver, ventral prostates, seminal vesicles, and preputial glands (both in terms of absolute weight and relative to body weight) in any of the study groups. Both the absolute and relative weights of the epididymides were significantly higher in 1.00% group when compared with controls. A dose-dependent decrease of both round and elongated spermatid counts in stages VII-VIII seminiferous tubules was observed, and the elongated spermatid counts were significantly lower in all of the treated groups. The numbers of spermatogonia and spermatocytes did not differ from control values. The serum testosterone concentration decreased in a dose-dependent fashion and was significant at 1.00%. These data demonstrated that butyl paraben can exert an adverse effect on the male reproductive system at doses that are well below those of the accepted daily intake (ADI) in Japan.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12111007&dopt=Abstract

Urol Res. 2002 Jul;30(3):195-8. Epub 2002 Jun 04.
Therapeutic strategy after microsurgical varicocelectomy in the modern assisted reproductive technology era.

Fujisawa M, Dobashi M, Yamasaki T, Okada H, Arakawa S, Kamidono S.

Division of Urology, Department of Organs Therapeutics, Kobe University Graduate School of Medicine, 7-5-2 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan. masated.kobe-u. ac.jp

In this study, we searched for prognostic factors at preoperative examination for the improvement in spermatogenesis of patients undergoing varicocelectomy.Eighty patients with varicocele testis underwent microsurgical varicocelectomy. Before surgery, the seminogram, testicular volume, varicocele grade, and serum FSH, LH, testosterone, prolactin, and estradiol were evaluated. Postoperatively, semen analysis was performed every 3 months. We assessed the associations between the preoperative variables and postoperative seminogram improvement. 0f 80 patients, 37 showed improvement, usually by 6 months. Patient age, duration of sterility, testicular volume, sperm motility, morphology, semen volume, serum LH, testosterone, prolactin, and estradiol showed little difference between responders and non-responders. A small left testis, or a grade III varicocele decreased the likelihood of improvement. Patients with a sperm count of 10-20 x 10(6)/ml were significantly more likely to respond to varicocelectomy than those with sperm counts <5 x 10(6)/ml. Patients with elevated FSH were less likely to respond, as were those with a Johnsen score below 6. Varicocelectomy alone is unlikely to improve sperm counts of patients with a sperm count below 5 x 10(6)/ml, high FSH, small left testes, or Johnsen scores below 6. In conclusion, for couples in this situation, assisted reproductive technology coupled with varicocelectomy should be proposed.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12111184&dopt=Abstract

Prostate. 2002 Jul 1;52(2):130-8.
Association of polymorphisms within androgen receptor, 5alpha-reductase, and PSA genes with prostate volume, clinical parameters, and endocrine status in elderly men.

Schatzl G, Madersbacher S, Gsur A, Preyer M, Haidinger G, Haitel A, Vutuc C, Micksche M, Marberger M.

Department of Urology and Ludwig-Boltzmann-Institute for Research of Prostate Diseases, University of Vienna, Austria.

BACKGROUND: The aim of this study was to assess the impact of polymorphisms of three genes within the androgen pathway on prostate volume, clinical parameters, and endocrine status. METHODS: Elderly men with lower urinary tract symptoms underwent clinical and endocrine work-up. In parallel, polymorphisms within the 5alpha-reductase gene (SRD5A2 V89L and A49T), the androgen receptor gene (AR; number of CAG repeats), and the prostate specific antigen (PSA) gene (A --> G substitution at position-158) were determined by polymerase chain reaction and restriction-length polymorphism analysis by using DNA from peripheral blood. RESULTS: A total of 190 men (66.5 +/- 9.2 yr) were analyzed. The number of CAG repeats within the AR and the PSA polymorphism revealed no associations to clinical and endocrine parameters. Individuals carrying the mutated SRD5A2 A49T allele (5.3% of the total population) had larger prostates (54.1 vs. 39.3 ml), higher PSA levels (12.2 vs. 4.3 ng/ml), and a 35% reduction in prostatic stroma/epithelial cell ratio. Men with the mutated SRD5A2 V89L gene had lower testosterone levels. CONCLUSIONS: In contrast to prostate cancer, polymorphisms within AR and PSA genes do not seem to be of importance for benign prostatic hyperplasia. Polymorphisms within the 5alpha-reductase gene are interesting biomarkers for the development of benign prostatic hyperplasia and benign prostatic enlargement. 2002 Wiley-Liss, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12111704&dopt=Abstract

J Cell Biochem. 2002;86(1):107-17.
Progesterone attenuates the inhibitory effects of cardiotonic digitalis on pregnenolone production in rat luteal cells.

Chen JJ, Chien EJ, Wang PS.

Department of Physiology, Schools of Life Science and Medicine, National Yang-Ming University, Shih-Pai, Taipei 11221, Taiwan, Republic of China.

Previous studies have shown that digoxin decreases testosterone secretion in testicular interstitial cells. However, the effect of digoxin on progesterone secretion in luteal cells is unclear. Progesterone is known as an endogenous digoxin-like hormone (EDLH). This study investigates how digitalis affected progesterone production and whether progesterone antagonized the effects of digitalis. Digoxin or digitoxin, but not ouabain, decreased the basal and human chorionic gonadotropin (hCG)-stimulated progesterone secretion as well as the activity of cytochrome P450 side chain cleavage enzyme (P450scc) in luteal cells. 8-Br-cAMP and forskolin did not affect the reduction. Neither the amount of P450scc, the amount of steroidogenic acute regulatory (StAR) protein, nor the activity of 3beta-hydroxysteroid dehydrogenase (3beta-HSD) was affected by digoxin or digitoxin. Moreover, in testicular interstitial and luteal cells, progesterone partially attenuated the reduction of pregnenolone by digoxin or digitoxin and the progesterone antagonist, RU486, blocked this attenuation. These new findings indicated that (1) digoxin or digitoxin inhibited pregnenolone production by decreasing the activity of P450scc enzyme, but not Na(+)-K(+)-ATPase, resulting in a decrease on progesterone secretion in rat luteal cells, and (2) the inhibitory effect on pregnenolone production by digoxin or digitoxin was reversed partially by progesterone. In conclusion, digoxin or digitoxin decreased progesterone production via the inhibition of pregnenolone by decreasing P450scc activity. Progesterone, an EDLH, could antagonize the effects of digoxin or digitoxin in luteal cells. 2002 Wiley-Liss, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12112021&dopt=Abstract

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