OBJECTIVESTo evaluate the relationship between sperm apoptosis and male infertility.

METHODSPercentage of apoptotic sperm (PAS) in spermatozoa of fertile and infertile men were tested by flow cytometry (FCM).

RESULTSSperm apoptosis had happened in all different people. PAS in fertile and infertile group was (4.28 +/- 1.66)% and (18.67 +/- 8.55)% respectively, and difference was significant between two groups (P < 0.01). There was negative correlation between PAS and semen volume, sperm density, percentage of forward motility, percentage of normal morphology (P < 0.01).

CONCLUSIONSThere was very close relationship between sperm apoptosis and male infertility. FCM used to test sperm apoptosis is rapid, accurate, objective and reliable to analyse sperm functions and male fertility.

Apoptosis ; Flow Cytometry ; Humans ; Infertility, Male ; pathology ; Male ; Spermatozoa ; pathology

Teratozoospermia is one of the important factors contributing to male infertility, and its pathogenesis is not yet clear. Recent years have witnessed some progress in the researches on sperm morphology, and some genes have been confirmed to be correlated with spermatogenesis. Aiming to provide some evidence for the pathogenesis of teratozoospermia, this paper reviews the relevant literature in the past five years addressing such special teratozoospermia as globozoospermia, nuclear vacuoles, decapitated spermatozoa, excessive residual cytoplasm, dysplasia of the fibrous sheath, and primary ciliary dyskinesia, and elaborates on the molecular genetic mechanisms of DPY19L2, AR, PRM1, GBA2, PCI, CREM, TH2A, TH2B, ODF1, Cntrob, OAZ-t, HOOK1, SPEM1, GAT1, PRSS21, 15-LOX, Sptrx, AKAP3, AKAP4, DNAI1, DNAH5, RSPH4A, TXNDC3, CCDC39, LRRC6, LRRC50, KTU and so on. Meanwhile, this review also presents an overview on the latest advances in assisted reproductive technology and its outcomes in the treatment of teratozoospermia patients in order to provide a theoretical basis for the diagnosis and treatment of male infertility.
Humans ; Infertility, Male ; genetics ; Male ; Membrane Proteins ; genetics ; Spermatozoa ; pathology

Globozoospermia, as a severe teratozoospermia caused by gene mutations, is a rare congenital disease with main clinical manifestations of the round head of sperm and abnormality or absence of acrosome, and its precise mechanism is not yet clear. Studies show that the pathogenic genes associated with globozoospermia include SPATA16, PICK1, GOPC, Hrb, Csnk2a2 and bs. This paper outlines the progress in the studies of molecular genetics of globozoospermia, aiming to contribute to the molecular diagnosis and mechanism investigation of the disease.
Acrosome ; Humans ; Infertility, Male ; genetics ; pathology ; Male ; Mutation ; Spermatozoa ; abnormalities

OBJECTIVETo study the relationship between the testis volume and types of spermatogenic cells derived from testicular biopsy in patients with azoospermia or cryptozoospermia.

METHODSWe collected testicular pathological biopsies from 492 infertile patients with azoospermia or cryptozoospermia reported in our hospital, classified them according to the testicular histological classification methods in WHO Manual for Standardized Investigation, Diagnosis and Management of the Infertile Male, and analyzed the relationship of the testis volume with the results of semen analyses and testicular histology.

RESULTSOf the 492 cases, 90.5% (445/492) were azoospermia and 9.5% (47/492) cryptozoospermia; mature spermatozoa were present in the seminiferous tubules in 17.9% (88/492) but absent in 42.9% (211/492), and Sertoli cell-only syndrome indicated in 39.2% (193/492); the testis volume was < or = 10 ml in 38.6% (190/492) and < or = 5 ml in 7.9% (39/492). Cryptozoospermia was detected in 14.8% (13/88) of those with mature spermatozoa in the seminiferous tubules, in 11.4% (24/211) of those without, and in 5.2% (10/193) of those with Sertoli cell-only syndrome, with a significantly lower rate in the latter group than in the former two (P < 0.05).

CONCLUSIONSpermatogenesis of the testis may be focal and difficult to be completely reflected by a single testicular biopsy, and it may exist even if the testis volume is significantly below the reference value. The indications for testicular biopsy should not be improperly expanded. The WHO testicular histological classification methods have provided a convenient and effective guidance for further clinical examinations and establishment of a protocol.

Adult ; Azoospermia ; pathology ; Biopsy ; Humans ; Male ; Middle Aged ; Semen Analysis ; Spermatogenesis ; Spermatozoa ; pathology ; Testis ; pathology

OBJECTIVETo examine the semen quality and the sperm morphology in infertile men with varicocele.

METHODSSemen from 98 infertile men with varicocele were studied and those of 130 normal semen donors were taken as the control. Semen analysis was performed based on the methods described in the WHO manual and sperm morphology was evaluated by WHO criteria.

RESULTSA significantly reduced percentage of normal morphologic sperm and of forward progression were found in patients with varicocele comparing with those of the control (P <0.001). The head defects were observed as the predominant type of sperm malformation.

CONCLUSIONThe varicocele increases malformed sperm in ejaculates, which may result from impaired male fertility by varicocele. Sperm morphologic assessment with WHO criteria provides a sensitive and practical measurement of sperm damage in infertile men with varicocele.

Adult ; Humans ; Infertility, Male ; complications ; pathology ; Male ; Semen ; Spermatozoa ; abnormalities ; pathology ; Varicocele ; complications ; pathology

Patients with non-obstructive azoospermia was once considered to be infertile due to impaired testicular spermatogenesis and consequent absence of sperm in the ejaculate. With the advent of intracytoplasmic sperm injection (ICSI), various testicular sperm retrieval techniques have been introduced recently, including fine needle aspiration, testicular sperm extraction, microdissection testicular sperm extraction, and so on. A large number of studies show that sperm can be retrieved in non-obstructive azoospermia patients, even in those with Klinefelter syndrome, because of the existence of isolated regions of spermatogenic tissue within the testis. 2010 EAU guidelines on male infertility recommend testicular sperm extraction or microdissection testicular sperm extraction for sperm retrieval from non-obstructive azoospermia. However, compared with testicular sperm extraction, the latter has a higher sperm retrieval rate with minimal postoperative complications. This article presents an overview on the prediction, operative procedure, sperm retrieval rate and postoperative complications of microdissection testicular sperm extraction.
Azoospermia ; pathology ; Humans ; Klinefelter Syndrome ; pathology ; Male ; Microdissection ; Sperm Retrieval ; Spermatozoa ; Testis ; pathology

Globozoospermia syndrome is a rare teratozoospermia, with an incidence of less than 0.1%. It is characterized by round sperm head, absence of acrosome, and messy sperm body and tail, but without other special clinical features. The absence of acrosome could reduce the activation ability of oocytes, and consequently decrease their fertilization ability. The assisted reproductive technique remains the only means for such patients to produce offspring. The pathogenesis of globozoospermia syndrome is not yet clear, though it is found to be related with 4 genes in the mouse and 1 on the human autosome. This article gives an overview on the clinical features, pathogenesis and genetics of globozoospermia syndrome, as well as the fertilizability and reproductivity of such patients.
Animals ; Humans ; Infertility, Male ; etiology ; genetics ; pathology ; Male ; Mice ; Sperm Head ; pathology ; Spermatozoa ; pathology

Acephalic spermatozoa syndrome (ASS) is one of the most severe spermatogenic failures of all infertility in men. The cognition of ASS has experienced a tortuous process. Over the past years, with the in-depth understanding of spermatogenesis and the emergence of new genetic research technologies, the unraveling of the genetic causes of spermatogenic failure has become highly active. From these advances, we established a genetic background and made significant progress in the discovery of the genetic causes of ASS. It is important to identify pathogenic genes and mutations in ASS to determine the biological reasons for the occurrence of the disease as well as provide genetic diagnosis and treatment strategies for patients with this syndrome. In this review, we enumerate various technological developments, which have made a positive contribution to the discovery of candidate genes for ASS from the past to the present. Simultaneously, we summarize the known genetic etiology of this phenotype and the clinical outcomes of treatments in the present. Furthermore, we propose perspectives for further study and application of genetic diagnosis and assisted reproductive treatment in the future.
Humans ; Infertility, Male/pathology* ; Male ; Membrane Proteins/genetics* ; Mutation ; Spermatogenesis/genetics* ; Spermatozoa/pathology*

OBJECTIVETo evaluate the relationship between sperm motility parameters and sperm morphology.

METHODSSeven hundred and eighty-three semen samples were tested. Sperm motility parameters were analyzed by computer-aided sperm analysis (CASA) , and sperm morphology assessed by automated sperm morphology analyzer (ASMA). The cases were classified based on the World Health Organization criteria. Morphologically 241 of the samples were normal and the other 542 abnormal.

RESULTSVCL, WOB, VAP of the morphologically abnormal group were significantly higher than those of the normal group (P < 0.05, P < 0.001), while MAD, LIN, STR of the abnormal group were significantly lower (P < 0.05, P < 0.001). There were significant positive correlations between the morphologically normal sperm rates and MAD, LIN, WOB, STR, and a significant negative correlation between the morphologically normal sperm rate and ALH.

CONCLUSIONMorphological abnormality of sperm is often accompanied with weak motility, which is probably attributed more to some factors that coact on both sperm motility and morphology than to the influence of sperm morphological abnormality on sperm motility.

Adult ; Humans ; Infertility, Male ; pathology ; physiopathology ; Male ; Sperm Count ; Sperm Motility ; Spermatozoa ; pathology

AIMTo evaluate the long term effect of experimental cryptorchidism on germ cell apoptotic rate and testicular sperm content in adult rats.

METHODSBilateral cryptorchidism was created in 40 adult male Sprague-Dawley rats by surgically manipulating the testes into the abdominal cavity and closing the internal inguinal ring. The rats were sacrificed and the testes removed 6 hours and 2, 4, 7, 21, 28 and 56 days after cryptorchidism. Germ cell apoptosis was quantified by means of TUNEL assay and apoptosis was confirmed using transmission electron microscopy.

RESULTSThe rate of apoptosis peaked at 4 days of cryptorchidism and then progressively declined to a nadir at 14 days of cryptorchidism. At 56 days of cryptorchidism, the germinal epithelium was largely depleted by the apoptotic process and only a few mature sperm were seen within the testis. At this point, a few tubules were seen to be repopulating with primary spermatocytes and the level of germ cell apoptosis began to increase marginally. Testicular sperm count (TSC) began to decline rapidly at day 7 of cryptorchidism. Only a few mature sperm were found in the testes of rats following 56 days of cryptorchidism. Multinucleated giant cells (MGC) were most numerous within the seminiferous tubules at day 4. At day 7, 35 % of MGCs were TUNEL positive. At all subsequent time points, however, MGCs fail to stain positive for apoptosis. This resumption of increased apoptosis coincided with the appearance of a population of primary spermatocytes in some seminiferous tubules. Moreover, there was not a corresponding increase in the number of mature sperm after 56 days of cryptorchidism.

CONCLUSIONThe decline in germ cell apoptosis after 4 days of cryptorchidism can be attributed to be the result of an overall depletion of germ cells. It appears that after a prolonged cryptorchidism (56 days), there is a limited resumption of spermatogenesis presumably as a result of a decrease in the maturing germ cells undergoing programmed cell death.

Animals ; Apoptosis ; Cryptorchidism ; pathology ; Male ; Rats ; Rats, Sprague-Dawley ; Seminiferous Tubules ; pathology ; Sperm Count ; Spermatozoa ; pathology ; Testis ; pathology