Download e-book for iPad: Clínicas Veterinarias de Norteamérica 2008. Volumen 38 Nº 5: by Gary Landsberg, Debra Horwitz

By Gary Landsberg, Debra Horwitz

ISBN-10: 8445819879

ISBN-13: 9788445819876

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Additional info for Clínicas Veterinarias de Norteamérica 2008. Volumen 38 Nº 5: Medicina de pequeños animales. Aplicaciones prácticas y nuevas perspectivas en conducta veterinaria

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This is achieved by the progressive replacement of nuclear histones with small positively charge proteins known as protamines. In eutherian mammals the proteins have evolved to contain cysteine residues that participate in the creation of intermolecular and intramolecular cross-links during epididymal transit that reinforce the compaction of the chromatin and render the DNA highly resistant to damage. 2 DNA Damage in Sperm 35 Interestingly, metatherian mammals do not possess cysteine-rich protamines, and as a result their spermatozoa do not undergo this post-testicular phase of nuclear remodeling.

The situation is complex because the degree of oxidative stress experienced by the spermatozoa will depend on the number and type leukocytes present in the ejaculate, when they entered the seminal compartment, whether the leukocytes are activated and, if so, when and how they are activated (Aitken and Baker 1995). Every human ejaculate contains a small number of leukocytes (in the order of 2–5 × 104/ml) that appear to be in a free radical-generating, activated state (Aitken et al. 1995; Aitken and Baker 2013).

Of course, smoking is not the only lifestyle or environmental factor that can influence levels of oxidative DNA damage in spermatozoa—another is paternal age. As males age, there is a downregulation of DNA repair genes (particularly BER), and levels of oxidative DNA damage in spermatozoa increase (Paul et al. 2011) such that a man aged over 35 will have three times the levels of DNA damage in his spermatozoa as a male below this age (Singh et al. 2003). One of the major consequences of this age-dependent increase in sperm DNA damage is a linear increase in the mutational load carried by the progeny over a paternal age range that stretches from 15 to 45 (Kong et al.

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Clínicas Veterinarias de Norteamérica 2008. Volumen 38 Nº 5: Medicina de pequeños animales. Aplicaciones prácticas y nuevas perspectivas en conducta veterinaria by Gary Landsberg, Debra Horwitz


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