Deficiency of Protein-Carboxyl Methylase in Immotile Spermatozoa of Infertile Men

We studied protein-carboxyl methylase, an enzyme involved in the regulation of cellular locomotion in both bacteria and leukocytes, in semen from 22 normal fertile men, 10 vasectomized volunteers, and nine infertile patients with nonmotile spermatozoa. In normally motile spermatozoa the protein-carboxyl methylase activity was 68.8±5.5 pmol per milligram of protein (mean ±S.E.). On the other hand, the enzyme activity in nonmotile spermatozoa from the infertile patients was low (17.4±3.4 pmol per milligram of protein) and similar to that in the cellular debris from the vasectomized volunteers (10.4±1.3 pmol per milligram of protein). The low enzyme activity in the infertile patients was not caused by the presence of dead spermatozoa or spermatozoa with leaky plasma membranes, since mitochondrial protein synthesis and lactate dehydrogenase activity were normal in these patients. The deficiency of protein-carboxyl methylase activity in nonmotile sperm is probably not due to a primary genetic defect, since the enzyme activity is normal in the red cells of these patients and spontaneous recovery of motility is associated with the return of enzyme activity. (N Engl J Med. 1982; 306:821–5.) IN the majority of infertile men the cause of the disorder remains obscure. Although the sperm count is an important factor, the number of sperm is not the sole determinant of the fertility potential. 1 , 2 Thus, the functional capacity of the sperm has assumed increasing importance. Up to the present, sperm motility has been a critical factor in judging semen quality. However, regulation of sperm motility is poorly understood. In some patients morphologic defects have been associated with nonmotile spermatozoa; in patients with Kartagener's syndrome the sperm tail lacks dynein arms on the doublet microtubules. 3 , 4 Other structural defects, such as the . . .