Vasectomy has rapidly become one of the most popular contraceptive methods in many countries. While only a few thousand vasectomies were performed annually during the early 1960's, the figure has now reached nearly one million per year in the United States alone (1). Because vasectomy involves surgical intervention in a healthy individual, the possibility that it may produce longterm local or systemic diseases, even in a small portion of the population, has been the subject of consideration (2, 3). There is an obvious need for a thorough investigation on the safety of this procedure.The present study shows that vasectomized rabbits making an active antibody response to sperm antigens develop an orchitis associated with deposition of rabbit IgG, C3, and sperm antigens--presumably antigen-antibody complexes-in the basement membrane of the seminiferous tubules. These lesions are frequently accompanied by mononuclear cell infiltration and destruction of germinal epithelium. A minority of these rabbits also develop a mild glomerulonephritis accompanied by deposition of immunoglobulin and complement in glomerular structures. Materials and Methods Surgical Procedures. 24 New Zealand White rabbits (Beckens Research Animal Farms,Sanborn, N. Y.) were bilaterally vasectomized, carefully avoiding trauma to the testes or their vessels. Rabbits weighing 3.1-3.6 kg were trial bled, tranquilized with paraldehyde (Elkin-Sinn Inc., Cherry Hill, N. J.), and anesthesized with sodium thiamylal (Surital; Parke-Davis, Baltimore, Md.). After surgical preparation a midventral vertical incision, about 2.5 cm long, was made in the skin of the suprapubic area and with blunt dissection both spermatic cords were located. The components of each cord were reached through a small cut in the cord wall, the vas deferens was isolated, ligated in two sites using silk sutures (Silk 4-0; Ethicon Inc., Somerville, N. J.), and the part between the sutures, approximately 1 cm long, was cut out. The other components of the cord were gently pushed back in place, the small cut in the cord wall and the incision in the skin were sutured using silk. Sham-vasectomies were performed on 20 rabbits weighing 3.1-3.6 kg, which were anesthesized and treated as described above, with the exception that the vas deferens, once

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An immune response to antigens of spermatozoa occurs after vasectomy in rats of some inbred strains, but not in others. Antibodies to rat spermatozoa were detected by indirect immunofluorescence in some of the serums of vasectomized rats of the following strains: 80 percent of Lewis, 47 percent of Brown Norway, 13 percent of Buffalo, 12 percent of Wistar-Furth, and 11 percent of ACI rats. No such antibodies were detected in the serums of vasectomized Fischer, Dark Agouti, and Sprague-Dawley rats.

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Brown Norway (BN) rats, "susceptible" to the autoimmune effects of mercury, experience a decrease of peripheral RT6.2+ T lymphocytes after the injection of relatively low doses of mercuric chloride. This change coincides with the appearance of circulating autoantibodies to renal antigens (e.g., laminin). Lewis (LEW) rats, "resistant" to the autoimmune effects of mercury, do not show significant decreases of RT6+ T cells. It is possible that BN rats are particularly sensitive to stress induced by mercury and that secretion of adrenocortical hormones decreases levels of RT6+ T cells in this rat strain. Alternatively, mercury may induce a graft-versus-host-like syndrome in BN rats, resulting in higher levels of corticosteroids capable of affecting RT6+ lymphocytes. To eliminate the possible influence of adrenocortical hormones, we have adrenalectomized BN rats prior to administration of mercury. Autoimmune responses to renal antigens were not affected by this experimental manipulation. Similarly, adrenalectomized rats exposed to mercury showed a significant decrease of RT6+ T lymphocytes in cervical lymph nodes. Overall, these observations do not support the hypothesis that increases in adrenocortical hormones play a major role in mercury-induced changes of RT6+ T cells. We have also explored whether experimental depletion of RT6+ T lymphocytes would result in autoimmunity. Gamma irradiation of BN rats led to a decrease of RT6+ T splenocytes, but by itself (i.e., without exposure to mercury) did not cause autoimmune responses to renal antigens. In addition, gamma-irradiated BN rats treated with mercury had autoimmune responses similar to those observed in mercury-treated nonirradiated controls. Depletion of RT6+ T cells in LEW rats through the use of a monoclonal antibody against the RT6.1 alloantigen did not by itself cause renal autoimmunity in this "resistant" strain. Depletion followed by administration of mercury also failed to induce renal autoimmunity. The lack of autoimmune effects in RT6-depleted BN and LEW rats suggests that a combination of several factors may be necessary to break self-tolerance and cause mercury-induced autoimmunity. Such factors likely comprise both environmental (mercury) and endogenous, genetically determined components. The latter include regulatory T cells (possibly RT6+), major histocompatibility complex (MHC), and T-cell receptors (TCR). Thus, BN rats with decreased percentages of immunoregulatory RT6+ T lymphocytes require additional immunotoxic and/or toxic effects of mercury for autoimmunity to occur. On the other hand, LEW rats depleted of regulatory T cells may still be unable to develop renal autoimmunity after exposure to mercury because they lack the appropriate MHC and TCR.