Clinical application of seminal plasma sperm motility inhibitor.

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1. We described the primary structure of SPMI,the coding of boar SPMI cDNA gene, Nucleotide sequence analysis of the 645-bp SPMI cDNA predicts a coded polypeptide of 137 amino acid residues which includes a 21-residue signal peptide and a 116 residues secreted protein. The amino acid sequence of SPMI was found to be highly homologous to AQN-3, a member of spermadhesin family proteins of boar that bind to spermatozoa. Expression of the boar SPMI gene detected by Northern blot analysis revealed that its expression is very abundunt in seminal vesicles and specific to this tissue.2. When SPMI was reacted with normal motile sperm, the motility was inhibited in a dose-dependent manner, and completely suppressed at a SPMI concentration of 1500U/ml. After immediate washing of the immotilized sperm, they resumed movement and recovered 30% motility. However, motility was not recovered at a SPMI concentration of 2000U/ml or more. The mechanism of the inhibition of sperm motility was immunohistochemically examined at electron microscopic level using anti-boar SPMI antibody. SPMI was stained on the surface cell membrane of sperm and not stained on inside cell. SPMI did not penetrate the sperm cell membrane. These findings suggest that sperm can not move physically by the attachment of SPMI to cell membrane or second messenger from the sperm cell membrane attached with SPMI inhibits the activity of dynein ATPase.3. Human SPMI precursor identifies with Semenogelin I,II.We investigated whether gene structure of Semenogelin I,II on infertile patients is different with that on fertile men. Two infertile patients and one fertile man had a deletion of same size, 180bp of Semenogelin I DNA.This deletion of gene was not specific in infetile patients.