Aspermatogenesis in the guinea pig induced by testicular tissue and adjuvants.

Abstract

The injection into the dorsal skin of a suspension of guinea pig testis or spermia incorporated in a water-in-oil emulsion containing killed mycobacteria induces aspermatogenesis in guinea pigs. The injury begins with the inhibition of the maturation of spermia and proceeds through the degeneration and exfoliation of spermatids, spermatocytes, and finally spermatogonia. These germinal cells pass from the seminiferous tubules into the epididymis. The process is not associated with inflammation. No significant changes occur in the intertubular spaces and the Leydig cells do not seem to be affected. The seminal vesicles and the prostate remain normal. The aspermatogenesis may begin in 10 days and it lasts for more than 5 months. The process may lead to atrophy of the seminiferous tubules and fibrosis. Guinea pigs which receive a suspension of their own testis or spermia and adjuvants develop a similar injury. The "mitochondrial" fraction of the testis of guinea pig is effective while repeated injections of alcoholic extract of testis emulsified with paraffin oil containing mycobacteria do not cause aspermatogenesis. The presence of acid-fast bacilli in the water-in-oil emulsion containing testis or spermia seems to be essential for the production of testicular lesions; the injection of antigen and mycobacteria into different sites is ineffective. When guinea pig testis is replaced by guinea pig liver or kidney or rabbit testis no testicular damage occurs. The injection of rabbit spinal cord combined with adjuvants results in allergic encephalomyelitis in a large proportion of guinea pigs, accompanied by a great loss of weight. The testes of a few of these animals show a varying degree of aspermatogenesis. When guinea pig brain is combined with adjuvants and administered subcutaneously the incidence of testicular injury is high, although the damage is, in general, mild. From the standpoint of mechanism, the inhibition of spermatogenesis which occurs in these animals may be unrelated to the injury which follows the injection of germinal cells. Aspermatogenesis follows the injection of killed mycobacteria in paraffin oil into the testis as well as into certain sites related to the gonad: the abdominal cavity, the subcutaneous tissue over the abdomen, and the skin of the inguinal region. Antibodies fixing complement in the presence of spermia are demonstrable in the sera of guinea pigs injected with testis or spermia and adjuvants. When the mycobacteria are omitted the titers are low and no testicular injury occurs. Although there seems to be a correlation between testicular damage and complement-fixing titer, this may not be a causal relationship. Antibodies which neutralize guinea pig hyaluronidase and those which immobilize spermia have also been demonstrated in the sera of these guinea pigs.