Conversion from spermatogonia to spermatocytes: Extracellular cues and downstream transcription network.

Spermatocyte (spc) formation from spermatogonia (spg) differentiation is the first step of spermatogenesis which produces prodigious spermatozoa for a lifetime. After decades of studies, several factors involved in the functioning of a mouse were discovered both inside and outside spg. Considering the peculiar expression and working pattern of each factor, this review divides the whole conversion of spg to spc into four consecutive development processes with a focus on extracellular cues and downstream transcription network in each one. Potential coordination among Dmrt1, Sohlh1/2 and BMP families mediates Ngn3 upregulation, which marks progenitor spg, with other changes. After that, retinoic acid (RA), as a master regulator, promotes A1 spg formation with its helpers and Sall4. A1-to-B spg transition is under the control of Kitl and impulsive RA signaling together with early and late transcription factors Stra8 and Dmrt6. Finally, RA and its responsive effectors conduct the entry into meiosis. The systematic transcription network from outside to inside still needs research to supplement or settle the controversials in each process. As a step further ahead, this review provides possible drug targets for infertility therapy by cross-linking humans and mouse model.

Chestnut polysaccharides benefit spermatogenesis through improvement in the expression of important genes.

Recently there has been a continuing worldwide decrease in the quality of human spermatozoa, especially in spermatozoa motility and concentration. Many factors are involved in this decline, and great efforts have been made to rescue spermatogenesis; however, there has been little progress in the improvement of sperm quality. Chestnuts are used in traditional Chinese medicine; their major active components are chestnut polysaccharides (CPs). CPs have many biological activities but their effects on spermatogenesis are unknown. The current investigation was designed to explore the impact of CPs on spermatogenesis and the underlying mechanisms. We demonstrated that CPs significantly increased sperm motility and concentration (4-fold and 12-fold, respectively), and improved seminiferous tubule development by increasing the number of germ cells after busulfan treatment. CPs dramatically rescued the expression of important genes and proteins (STRA8, DAZL, SYCP1, SYCP3, TNP1 etc.) in spermatogenesis. Furthermore, CPs increased the levels of hormone synthesis proteins such as CYP17A1 and HSD17ß1. All the data suggested that CPs improved the testicular microenvironment to rescue spermatogenesis. With CPs being natural products, they may be an attractive alternative for treating infertile patients in the future. At the same time, the deep underlying mechanisms of their action need to be explored.

Can maternal exposure to paracetamol impair reproductive parameters of male rat offspring?

Paracetamol is a widely used medication during gestation and lactation periods for the treatment of pain and fever. Several studies have shown that exposure to paracetamol can increase the incidence of cryptorchidism and decrease testosterone production. Therefore, the present study aimed to evaluate if maternal treatment with paracetamol during gestation and gestation/lactation periods can alter reproductive and behavioral parameters in male offspring. Female Wistar rats were treated daily by gavage with water or paracetamol (350 mg/kg/day) during gestation (CTRG and PARG) or gestation/lactation periods (CTRGL and PARGL). There were significant differences in histomorphometry (increased volume and total length of the seminiferous tubules) and weight of testes (PARG group) and copulatory behavior and testosterone levels (PARG and PARGL groups) at PND 120. Therefore, the present study showed that maternal exposure to paracetamol has an impact on the reproductive system and sexual behavior of male adult offspring suggesting an impaired in sexual hypothalamic differentiation at the beginning of the development of the brain.

Maternal vitamin B12 deficiency affects spermatogenesis at the embryonic and immature stages in rats.

To evaluate the role of cobalamin (Cbl) on spermatogenesis, the effect of dietary vitamin B(12) deficiency on early spermatogenesis was histologically investigated in male fetuses and newborns in the first filial generation (F(1) males) of rats. There was no difference in the number of gonocytes and supporting cells of Sertoli in the gonad in male fetuses on day 16 of gestation and in the testes in F(1) males at 0 days of age between vitamin B(12)-deficient (VB12-D) and vitamin B(12)-supplemented (VB12-S) groups. However, at 21 days of age, a decreased number of spermatogonia and no spermatocytes were observed in the VB12-D group. Numerous TUNEL positive cells were located among spermatocytes of the spermatogenic epithelium. The ultrastructural features examined using transmission electron microscopy were considered to be indicative of apoptosis. The incidence of seminiferous tubules having apoptotic cells was 51.5% in the VB12-D group. At 60 days of age, aplasia of the spermatids and spermatozoa was detected in the VB12-D group. In the connective tissue between the seminiferous tubules, many interstitial Leydig cells and blood vessels were observed in the VB12-D group, as compared with the VB12-S group. These changes produced by vitamin B(12) deficiency can be reversed by providing a VB12-S diet after weaning at 21 days of age. From these findings, such a vitamin B(12) deficiency during gestation and lactation could affect the germ cells and especially damage spermatocytes in F(1) male rats, which indicates that Cbl may be an essential constituent in the meiosis of spermatogenesis.

Effect of dietary selenium and vitamin E on spermatogenic development in boars.

An experiment involving a total of 61 crossbred boars evaluated the effects of dietary Se and vitamin E on spermatogenic development at various stages of sexual development and the prostaglandin F2alpha (PGF2alpha) content in the seminal vesicle and prostate glands at 18 mo of age. The experiment from 5.4 to 9 mo of age was conducted as a 2 x 2 factorial in a randomized complete block design. Dietary Se at 0 or .5 ppm was the first factor and vitamin E at 0 or 220 IU/kg diet was the second. From 9 to 18 mo of age, a group of sexually active and inactive boars was a third factor. Treatment diets were fed from weaning (28 d of age) to the end of the experiment. Three boars per treatment group at 5.4 (105 kg BW), 6.2 (130 kg BW), and 9.0 (150 kg BW) mo of age were killed and the testes collected. From 9 to 18 mo of age, three boars from each dietary treatment group were used for semen collection, and another set of three to four boars from each treatment group remained sexually inactive. At 18 mo, both sets of boars were killed and their testes, prostates, and seminal vesicles were collected. The testis at each age was evaluated for sperm reserve numbers and germ and Sertoli cell populations. At 5.4 or 6.2 mo of age, testicular sperm reserves were not affected by dietary Se (P > .15), at 9.0 mo of age there was a trend for a higher (P < .10) number of sperm reserves, and by 18 mo of age the Se-fed boars had higher (P < .01) numbers of sperm reserves. Vitamin E had no effect (P > .15) on testicular sperm reserves at any age period. Boars fed dietary Se had a greater number of Sertoli cells (P < .01) and round spermatids (P < .01) at 6.2 mo of age, but by 18 mo of age the boars fed Se had more Sertoli cells (P < .05), more secondary spermatocytes (P < .01), and more round spermatids (P < .05). Vitamin E did not affect Sertoli or germ cell populations at the various ages. Boars at 18 mo of age had lower PGF2alpha concentrations in the prostate (P < .05) and seminal vesicles (P < .01) when vitamin E was fed, whereas Se had no effect. Sexually active boars had lower PGF2alpha concentrations in the seminal vesicles (P < .01) than sexually inactive boars, but there was no effect (P > .15) of sexual activity on the number of Sertoli cells, primary or secondary spermatocytes, or round spermatids. Our results indicate that Se has a role in establishing the number of boar spermatozoal reserves and Sertoli cells, whereas supplemental vitamin E did not affect these criteria.