PYRUVATE OXIDATION IN TESTICULAR TISSUES DURING FURADROXYL-INDUCED SPERMATOGENIC ARREST1

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Abstract
NELSON and Steinberger (1952) noted that the testes of rats receiving the nitrofuran Furadroxyl (Fig. 1) orally were similar histologically to those of patients suffering spermatogenic arrest. The stage of spermatogenic arrest is illustrated in Figure 2, sections (1), the normal picture, and (2) after 30 days on a diet to which Furadroxyl had been added. In the latter tubules it can be noted that mature sperm were not present and that there was no development of any cells beyond the primary spermatocyte stage. The testes were about one-third normal size, but body weight was not affected. The Pauls and their associates (1952, 1953, 1954) have compiled considerable data on the metabolic aspects of this nitrofuran poisoning of the testis. The important points from their work which have a bearing on the studies we are reporting are: (1) Succinate oxidation is apparently not impaired by the nitrofurans,