PDF《Function in Bulls》

Zhu and Setchell 2004);

this sensitivity has been well documented in mice (Meistrich et al. 1973), bulls (Vogler et al. 1991), humans (Levine et al. 1990) and rams (Mieusset et al. 1991). Elevated testicular?epididymal temperature (because of scrotal insulation) has deleterious e?ects on sperm morphology (Vogler et al. 1993;

Barth and Bowman 1994), motility (Brito et al. 2004;

Fernandes et al. 2008;

Newton et al. 2009), viability (Vogler et al. 1991;

DeJarnette et al. 2000), sperm fertilizing capacity and developmental competence of resulting embryos (Thun- dathil et al. 2000, 2001a,b;

Walters et al. 2005b, 2006;

Fernandes et al. 2008). Speci?c sperm abnormalities emerge at consistent intervals after scrotal insulation (Barth and Bowman 1994;

Acevedo 2001;

Walters et al. Reprod Dom Anim

47 (Suppl. 4), 170C177 (2012);

doi: 10.1111/j.1439-0531.2012.02072.x ISSN 0936-6768 ?

2012 Blackwell Verlag GmbH 2005a;

Fernandes et al. 2008;

Newton et al. 2009);

the type of abnormality corresponds with where germ cells are in the spermatogenic process when testicular tem- perature was increased (Hales et al. 2005). Furthermore, the appearance of morphologically abnormal sperm was consistently accompanied by reduced sperm motility. Because sperm use ATP from mitochondrial oxidative phosphorylation to support motility (Ruiz-Pesini et al. 1998), perhaps heat stress has a direct e?ect on germ cell mitochondria. Abnormal sperm fail during various steps of gamete interaction, depending on the nature of the abnormality (Thundathil et al. 1998, 1999, 2000, 2001a,b). Further- more, apparently normal sperm coexisting in a semen sample with a high percentage of abnormal sperm have impaired sperm function. Some forms of abnormal sperm can penetrate the oocyte and initiate fertilization, but the resulting zygotes fail at various stages of preimplantation development (Thundathil et al. 2000, 2001a, b;

Walters et al. 2005a). Some of these impaired sperm functions may be due to the e?ects of elevated testicular tempera- tures on sperm DNA (Steinberger 1991;

Sailer et al. 1997;

Banks et al. 2005), sperm proteins or both. Effect of increased testicular temperature on expression pattern of sperm proteins Scrotal insulation induces abnormal spermatogenesis and impairs sperm function. Because sperm DNA is transcriptionally inactive, sperm functions are regulated by proteins already present in sperm without additional protein synthesis. Therefore, we hypothesized that elevated testicular temperature alters the content of proteins in sperm, impairing their function. To test this hypothesis, we used scrotal insulation to induced abnormal spermatogenesis in Holstein bulls, with pre- and post-insulation sperm compared for expression of sperm proteins (Newton et al. 2009). Whereas expression of Hexokinase-1, the a-4 subunit of Na+ ?K+ -ATPase and the testicular isoform of angio- tensin converting enzyme (tACE) were decreased, expression of tissue inhibitor metalloprotease-2 (TIMP-2) was higher in morphologically abnormal sperm. Tissue inhibitor metalloprotease-2 is abundant in epididymal ?uids (Belleanne ? ea et al. 2011) and the equilibrium between the production of proteinases and proteases and their inhibitors (e.g. TIMP-2) is critical for sperm maturation in the epididymis (Me?tayer et al. 2002). Perhaps proteinases and proteases arising from the damaged membrane of abnormal sperm increase TIMP-2 production in an attempt to preserve the membrane integrity, which may account for the increase in TIMP-2 content seen in insulated bulls compared with their controls. Similarly, there was a signi?cant decrease in PH-20 (a sperm adhesion molecule (SPAM1) implicated in zona-pellucida binding;