Disease relevance of Sperm Count

• The control animal developed azoospermia after 4 months of treatment with cyclophosphamide, and serum testosterone increased while sperm count decreased [1].
• The results indicated that HST-1/FGF-4 significantly reduced the apoptotic death of germ cells and prevented testicular weight loss and sperm count reduction [2].
• In contrast, the Benchmark Dose approach can provide estimates of the magnitude of sperm count reduction at a regulatory level, and the Quantitative Risk Estimation approach can provide estimates of exposure-induced infertility [3].
• In mice, DEHP at 1/6 LD50 significantly depressed body weight gain for up to 12 weeks after treatment, and reduced epididymal sperm number by 4 weeks [4].
• Evaluation of chlorambucil toxicity on the reproductive system was based on penile and testicular size, serum testosterone values, and sperm count [5].

High impact information on Sperm Count

• FINDINGS: In two men with ejaculate sperm counts of 40 000-100 000 per mL, we detected Y-chromosome deletions in leucocyte DNA similar in location to those previously reported in azoospermic individuals [6].
• Testicular biopsies in 3 men with high titres of antibodies and very low sperm-counts which became normal with prednisone showed adequate spermatogenesis; however, focal round-cell infiltration of seminiferous tubules was observed in 1 case [7].
• 18 other men with normal sperm-counts were given one or more courses of methylprednisolone 96 mg/day for 7 days [7].
• All 5 patients who received testosterone became azoospermic or severely oligospermic during treatment but had a normal sperm count 6 months after the discontinuation of therapy [8].
• MEASUREMENTS: Sperm counts, serum follicle-stimulating hormone levels, and serum luteinizing hormone levels were measured before, during, and after treatment with cyclophosphamide alone or cyclophosphamide plus testosterone [8].

Chemical compound and disease context of Sperm Count

• Higher FSH levels and lower sperm counts correlated inversely in the cryptorchidism group, while luteinizing hormone, testosterone and other results of semen analysis did not differ [9].
• Although body weight gain was depressed, none of the other measurements taken (epididymal sperm count, fructolytic activity of spermatozoa, relative weights of the reproductive organs, concentration of fructose in coagulating glands and fertility in relation to females impregnated, conceiving and litter size) was affected [10].
• Although the group of 16 subjects was small, all were men with long-standing infertility that had been refractory to previous treatments such as exogenous injections of human chorionic gonadotropin and varicocelectomy; 10 of the 16 men (62.5%) showed improvement in sperm counts within 2 to 5 months of starting clomiphene [11].
• The increase in infertility was calculated for a proportional reduction of all sperm counts within a population and for a group of workers exposed to dibromochloropropane [12].
• Azoospermia or severe oligospermia was found in 13 of 17 patients receiving cyclophosphamide with or without colchicine, whereas the sperm count was almost normal in six patients treated with colchicine alone and in four patients receiving neither drug (control patients) [13].

Biological context of Sperm Count

• In other sterile lines, TK was expressed at a lower level and sperm counts were normal but sperm motility was greatly reduced [14].
• However, inactivation of the Arl4 gene resulted in a significant reduction of testis weight and sperm count by 30 and 60%, respectively, without reduction of litter size or frequency [15].
• To test this hypothesis, we typed the Y chromosome in a group of Danish men with known sperm counts and compared the haplotype distribution with that of a group of unselected Danish males [16].
• The presence of this transgene [and thus the interspecies hybrid (i.e. mouse alpha:human FSHbeta hormone)] in the background of mouse FSHbeta deficiency completely restored the testis size, sperm number, and motility defects to levels comparable to those seen in control male mice [17].
• Reconstitution of male csfmop/csfmop mice with either circulating T in the adult or circulating CSF-1 throughout the postnatal period completely restored viable sperm numbers and significantly restored sexual behavior [18].

Anatomical context of Sperm Count

• We measured immunoreactive epidermal growth factor (EGF) by a homologous RIA in seminal plasma (SP) from 31 fertile and 52 infertile men to determine the relationship between SP EGF levels and total sperm count in the ejaculates [19].
• Bmp4 heterozygous males on a largely C57BL/6 background show compromised fertility due to degeneration of germ cells, reduced sperm counts, and decreased sperm motility [20].
• Uterine hypoplasia and impaired folliculogenesis were observed in the female, and decreased sperm count and decreased motility with histological abnormality of the testis were observed in the male [21].
• Furthermore, insulin treatment (1 U/mouse/day) of diabetic mice restored the submandibular gland, plasma EGF concentrations, and sperm counts to normal levels [22].
• Leptin-treated males had significantly elevated serum levels of FSH, increased testicular and seminal vesicle weights, greater seminal vesicle epithelial cell height, and elevated sperm counts compared to controls [23].

Associations of Sperm Count with chemical compounds

• At the highest doses of procarbazine (400 mg/kg) that caused a 56% decrease in sperm count, equimolar doses of N-acetylcysteine coadministered with procarbazine caused only a 17% decrease in sperm count, and equimolar doses of ascorbate coadministered with procarbazine caused only a 13% decrease in sperm count [24].
• Procarbazine causes dose-dependent decreases in sperm count after a single i.p. injection in (C57BL/6 X DBA/2)F1 male mice [24].
• There was an inverse correlation between basal serum 17 beta-estradiol (E2) levels and total sperm count (r = -0.87; P less than 0.05) [25].
• No correlation, however, could be established between testicular androgen levels and spermatogenic status (P greater than 0.30) or sperm counts (P greater than 0.60) [26].
• Serum T and DHT levels and sperm number significantly increased in all groups [27].

Gene context of Sperm Count

• When three or more seminal fluid samples collected 1 month apart were available from the same individual, the coefficient of variation was 10.0 +/- 1.26% (+/- SE) for IGFBP-3 by RIA vs. 73.3 +/- 11.2% for sperm counts in the same samples [28].
• Tenr mutant males have a reduced sperm count, and Tenr-/- sperm show a decrease in motility and an increase in malformed heads [29].
• Epididymal sperm count and sperm motility were greater in 12-week-old rescued mice than in age-matched Dax1-deficient mice [30].
• In addition, disruption of hsf2 resulted in reduced female fertility; however, despite ubiquitous expression in the testes and markedly reduced testis size and sperm count, only a small reduction in fertility was apparent in hsf2(-/-) male mice [31].
• We therefore conclude that the deletion of the DAZ1/DAZ2 gene doublet in five out of our 63 oligozoospermic patients (8%) is responsible for the patients' reduced sperm numbers [32].

Analytical, diagnostic and therapeutic context of Sperm Count

• It is recommended that all males with reduced or absence sperm counts seeking assisted reproductive technologies be screened for deletions of the Y chromosome [33].
• Moreover, sperm counts were significantly greater in the resveratrol-treated rats (24.8 +/- 3.30 x 10(7)) than in the control group (14.1 +/- 0.80 x 10(7)), but sperm quality did not differ [34].
• Insulin treatment of the diabetic rats restored serum gonadotropins, reproductive organ weight, sperm counts and motility, and seminal fructose to control levels [35].
• Although decreased sperm counts and serum testosterone levels have been found in men with occupational lead exposure, animal experiments suggest that fertility may be impaired at blood lead levels that have no apparent effect on reproductive hormone levels or sperm concentration [36].
• In male mice, epididymal sperm numbers, seminal vesicle weights, and androgen levels declined more dramatically after castration [37].

References