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Regular Article |
a School of Pharmaceutical Sciences,
b Kitasato University, Minato-ku, Tokyo 108, Japan
e Department of Urology and the Instrumental Analysis Research Center, School of Medicine, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo 113, Japan
c Department of Pathology, School of Medicine, Kitasato University, Sagamihara, Kanagawa 228, Japan
d Department of Molecular Biodynamics, Tokyo Metropolitan Institute of Medical Science (Rinshoken), Bunkyo-ku, Tokyo 113, Japan
ABSTRACT
Phospholipid hydroperoxide glutathione peroxidase (PHGPx) was intensely expressed in mitochondria in the midpiece of human spermatozoa by immunostaining with anti-PHGPx monoclonal antibodies. The PHGPx not only reduced phospholipid hydroperoxide but also scavenged hydrogen peroxide in human spermatozoa. We found a dramatic decrease in the level of expression of PHGPx in the spermatozoa of some infertile males by immunoblotting with anti-PHGPx monoclonal antibodies. These individuals accounted for about 10% of the group of 73 infertile males that we examined. All seven patients with PHGPx-defective spermatozoa were classified as suffering from oligoasthenozoospermia, a defect in which both the number and the motility of spermatozoa are significantly below normal. Males with PHGPx-defective spermatozoa accounted for 26% of the 27 infertile males with oligoasthenozoospermia. No defects in expression of PHGPx in spermatozoa were observed in 31 fertile volunteers. After a 3-h incubation, the relative number of motile spermatozoa with low-level expression of PHGPx was significantly lower than that of spermatozoa with normal expression of PHGPx. The PHGPx-defective spermatozoa failed to incorporate rhodamine 123, revealing a loss of mitochondrial membrane potential. Ultrastructual analysis of mitochondria by electron microscopy demonstrated that the morphology of mitochondria in PHGPx-defective spermatozoa was abnormal. The results suggest that failure of the expression of mitochondrial PHGPx in spermatozoa might be one of the causes of oligoasthenozoospermia in infertile men.
First decision: 6 September 2000.
1 This work was supported in part by Special Coordination Funds for the Promotion of Science and Technology and by Grants-in-aid (10672052 and 12771412) from the Ministry of Education, Science and Culture of Japan; by a Kitasato University Research Grant for Young Researchers; by the Novartis Foundation for the Promotion of Science; and by a grant from the Kitasasto University Graduate School of Medical Sciences (9901).
2 Correspondence: Yasuhito Nakagawa, School of Pharmaceutical Sciences, Kitasato University, 5-9-1 Shirokane, Minato-ku, Tokyo 108, Japan. FAX: 81 3 3444 4943; nakagaway{at}pharm.kitasato-u.ac.jp
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