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Selenium deficiency has long been known to be associated with decreased male and female fertility in live stock. The underlying mechanisms may be numerous. As far as female fertility is concerned, impairment of fertilization of ova of selenium-deficient cows and sheep, retained placenta in cows, and the mastitis metritis agalactia complex in pigs are observed. Responsiveness of these disorders to both selenium and vitamin E are suggestive of a deficiency in the antioxidant defence systems (reviewed in [1] and [2]). Circumstantial evidence also indicates that selenium requirement is higher in pregnancy. With progress of pregnancy, plasma glutathione peroxidase activity (pGPx) increases despite decreasing blood selenium levels [3] and selenium retention is higher in pregnancy [4]. These phenomena have been discussed as adaptive responses [5], since lipid peroxidation is reported to be higher in pregnant women than in non-pregnant ones, and particularly high in preeclamptic subjects [6]. Also, selenoprotein P is reportedly higher in liver of pregnant mice, is present in mouse placenta throughout the latter third of pregnancy and rises sharply before delivery [7]. In this context, a role of selenoprotein P in selenium supply to the fetus was discussed [7]. The male reproductive system is more drastically affected by selenium deficiency. Characteristically sperm motility is substantially reduced and, depending on the degree of deficiency, structural alterations up to breakages in the midpiece of spermatozoa are seen in several mammalian species [8–11]. In rat spermatozoa selenium is almost restricted to the midpiece of spermatozoa containing the mitochondria [12], i.e., exactly the part where breakages are observed in selenium deficiency [8,10]. Interestingly, the functional and structural alterations of spermatozoa only respond to selenium but not to vitamin E [13]. Extreme selenium deficiency leads to a complete loss of mature germinal cells [14]. The importance of selenium for the male reproductive system is also underlined by its testicular retention under limited supply [15].

An 11-day embryonic Swiss Webster/NIH mouse cDNA library was screened with a partial murine selenoprotein P cDNA probe and a murine selenoprotein-P-type cDNA 1 clone of 2075 bp lenght was obtained. The clone contained a 5 0 -leader sequence of 132 bp length, the selenoprotein P coding frame, and 803 base pairs in the 3 0 untranslated region. Alignment and RNA folding studies revealed the presence of two well conserved selenocysteine inserting motifs in the 3 0 flanking region. The deduced polypeptide sequence comprises 380 residues including ten selenocysteines. Identical amino acid residues in homologous positions are 86%, 71%, and 64% when compared to the previously reported selenoprotein P sequences of rat, man, and cattle, respectively. The comparatively low similarity between the selenoprotein P sequences reported so far leaves open the question whether they belong to the same molecular clade.