Abstract:
:The selenoenzyme phospholipid hydroperoxide glutathione peroxidase (PHGPx) is regarded as the major molecular target of selenodeficiency in rodents, accounting for most of the histopathological and structural abnormalities of testicular tissue and male germ cells. PHGPx exists as a cytosolic form, mitochondrial form, and nuclear form (nPHGPx) predominantly expressed in late spermatids and spermatozoa. Here, we demonstrate that mice with a targeted deletion of the nPHGPx gene were, unlike mice with the full knockout (KO) of PHGPx, not only viable but also, surprisingly, fully fertile. While both morphological analysis of testis and epididymis and sperm parameter measurements did not show any apparent abnormality, toluidine blue and acridine orange stainings of spermatozoa indicated defective chromatin condensation in the KO sperm isolated from the caput epididymis. Furthermore, upon drying and hydrating, KO sperm exhibited a significant proportion of morphologically abnormal heads. Monobromobimane labeling and protein-free thiol titration revealed significantly less extensive oxidation in the cauda epididymis when compared to that in the wild type. We conclude that nPHGPx, by acting as a protein thiol peroxidase in vivo, contributes to the structural stability of sperm chromatin.
journal_name
Mol Cell Bioljournal_title
Molecular and cellular biologyauthors
Conrad M,Moreno SG,Sinowatz F,Ursini F,Kölle S,Roveri A,Brielmeier M,Wurst W,Maiorino M,Bornkamm GWdoi
10.1128/MCB.25.17.7637-7644.2005subject
Has Abstractpub_date
2005-09-01 00:00:00pages
7637-44issue
17eissn
0270-7306issn
1098-5549pii
25/17/7637journal_volume
25pub_type
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