Biology Reference
In-Depth Information
reported sperm centrosome dysfunctions as a cause of infertility or abortive
embryonic development. More recently, Sathananthan et al. (
2001
) identified
structural alterations in sperm centrioles of infertile men, including disorganization
or loss of centriolar triplets, loss or abnormal positioning of proximal centrioles,
and intrusion of mitochondria within centrioles. Hewitson et al. (
1997
) and Rawe
et al. (
2008
) have also suggested that centrosomal anomalies are responsible for
defective sperm aster formation or microtubule elongation in human post-ICSI
fertilization failures.
Injection of isolated sperm tails (containing the proximal centriole) into oocytes
results in the formation of sperm asters (Van Blerkom and Davis
1995
). In later
studies it was demonstrated that the use of heterologous ICSI systems (human-
bovine, human-rabbit) provide objective information on the capacity of sperma-
tozoa to elicit normal aster development and constitute a novel tool to examine
sperm centrosomal function of infertile men (Terada et al.
2002
,
2004
; Yoshimoto-
Kakoi et al.
2008
). Using this technique sperm centrosomal failures were reported
in teratozoospermia and globozoospermia (Nakamura et al.
2002
; Terada et al.
2010
), the rate of sperm aster formation from infertile men was found to be lower
than that from fertile individuals (Rawe et al.
2002
), and Hinduja et al. (
2010
)
communicated that centrosome proteins centrin, a and c-tubulin, were reduced in
oligoasthenozoospermic patients. As a consequence of these observations efforts to
develop in vitro methods to restore defective sperm centrosomal function in
humans are underway (Nakamura et al.
2005
; Terada et al.
2010
).
In summary, centriolar and centrosomal abnormalities are involved in failed
fertilizations or abnormal development of the embryo. However, all these reports
derive from experimental observations or laboratory studies after post-ICSI
fertilization failures and do not identify diagnostic categories of clinical value in
human infertility. We and others have described a human syndrome of genetic
origin in infertile men with systematic teratozoospermia.
In 1987 we published a paper entitled Lack of a Head in Human Spermatozoa
from Sterile Patients: a Syndrome Associated with Impaired Fertilization (Chemes
et al.
1987b
). Three adult males were reported who suffered from primary sterility
and presented a characteristic sperm defect that repeated in all semen samples
examined. Most spermatozoa (75-100 %) presented with minute ''heads'', no
larger than 1 lm in diameter and negative for the Feulgen reaction, which indi-
cated lack of sperm heads. Two main abnormal configurations could be observed.
Some forms had cephalic ends with minute spherical thickenings containing sperm
centrioles and connecting pieces followed by normally structured midpieces and
flagella (Fig.
2.4
d). The other type was similar but without midpieces. In a second
publication, we documented the findings in 10 patients, the largest series published
to date (Chemes et al.
1999
). A third abnormal variety could be observed in which
heads were present but abnormally attached to midpieces, with no linear alignment
with the sperm axis (Figs.
2.4
c, e). The angles between heads and tails were up to
180. Normally formed spermatozoa amounted to no more than 1 %. Immature
spermatids in semen showed their flagellum-middle piece complexes abnormally
related or completely divorced from nuclei.
