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What was your first job? As a trainee accountant at a small family owned business based in Northallerton. Their office is only a few miles away from our distillery in [...]

These studies concern histological changes in the testes of pre- and postpubertal zinc-deficient and repleted rats. Three experiments in volved a total of 69 rats. In experiment 1, 12 weanling rats were fed a zinc-deficient (0.5 ppm) diet, ad libitum; 11 were fed a zinc-sufficient (100 ppm) diet and pair-fed to the zinc-deficient group; and 10 were fed the zinc-sufficient diet, ad libitum. After 26 days of being fed the different diets, one testis with the epididymis was surgically removed (hemicastrated) from each animal for histological examination. The rats fed the zinc-deficient diet were then fed the zinc-sufficient diet, ad libitum, for 30 or 41 days. Pair-feeding between the zinc-sufficient group and the zinc-deficient-repleted group was continued. The results indicated that 26 days of zinc depletion caused general immaturity of the testis and varied degrees of degeneration of the germinal epithelium compared to controls. After the zinc repletion period of 30 or 41 days, the remaining testis, epididymis, and sperm count were normal in all previously deficient animals. In experiment 2, 10 weanling rats were fed a marginally zinc-deficient diet (4 ppm) for 90 days and after hemicastration showed degenerative changes in the testes. All animals were then fed a zinc-sufficient (100 ppm) diet, with two animals killed every 15 days during a period of 75 additional days. The degenerative changes were not completely reversed during the 75-day repletion period, and only 4 out of 10 testes showed definite improvement. In experiment 3, 26 weanling rats were fed a zinc-adequate diet (15 ppm) for 42 days at which time 3 were killed to assure adequacy of the diet for maintenance of the testes and to confirm sexual maturity. When 12 of these postpubertal animals were fed the deficient diet for up to 68 days, a wide range of testicular damage occurred. Forty-two days of zinc repletion of the remaining 11 postpubertal rats, did not reverse the damage. In toto, the experiments suggest that a prepubertal short-term zinc deficiency resulted in degenerative changes that were repaired by repletion. In contrast, the degenerative changes of the testes of postpubertal zinc-deficient rats were not reversible to any significant extent.

A previous study (J. Nutr. 105, 484–490) described a testicular degeneration in the vitamin E-deficient Syrian hamster which, unlike that in the vitamin E-deficient rat, was effectively repaired by d-α-tocopherol. In the present study male hamsters were reared from weaning on vitamin E-deficient diets, one high and one low in added fats, for 90 to 100 days prior to surgical ablation of one testis. All testes were much reduced in weight and, histologically, showed advanced degenerative changes. Maintenance on the same diet, with daily oral supplements of 10 mg of d-α-tocopheryl acetate or 25 mg of d-α-tocopheryl hydroquinone for periods of 20 to 30 days, resulted in marked increases in testis weight and remarkable repair of the germinal epithelium, histologically. In rats similarly treated, 10 mg of the hydroquinone daily protected against testicular degeneration but was, as anticipated on the basis of the irrevocable injury in this species, ineffective in repair of testis injury. In both hamsters and rats there was evidence of storage of the hydroquinone, or some biologically active product, with effectiveness lasting several months. It is concluded that d-α-tocopheryl hydroquinone, in addition to previously demonstrated antidystrophic properties, has antisterility activity in the vitamin E-deficient male hamster and rat approximating one-fifth that of d-α-tocopherol.

Daily administration of 5 mg of d-α-tocopheryl hydroquinone (ATHQ), intravenously or intraperitoneally throughout gestation, has been said to prevent fetal resorption in four out of five vitamin E-deficient rats (J. Nutr. 72, 322–324). These observations are supported by our bioassay tests involving 58 and 22 vitamin E-deficient rats given oral supplements of ATHQ and of d-α-tocopheryl acetate, respectively, over days 5 to 8 of gestation. Evidence presented suggested a minimal protective dose of approximately 50 mg of ATHQ, which, if distributed over the first 10 days of gestation, would represent about 5 mg/day. Evidence is presented that vitamin E fed after day 10 has little or no effect upon the course of gestation. In other experiments, daily doses of 125/mg/kg/day of ATHQ during early gestation in E-deficient rats caused excessive uterovaginal bleeding, intrauterine hemorrhage, and retarded development and death of fetuses. This represented a rather small margin between beneficial and detrimental effects of ATHQ. In male rats given 330/mg/kg/day of ATHQ the testis, epididymis and related fat body were particularly prone to hemorrhage. Because internal hemorrhages in both sexes were prevented by menaquinone, the phenomena observed were attributed to an induced deficiency of vitamin K through unknown actions of ATHQ.

Syrian hamsters fed four different vitamin E-deficient diets from the time of weaning showed, after 60 days or more, progressive testicular atrophy. Histologically, there was a decrease in size of seminiferous tubules, reduced spermatogenic activity, marked thinning of the germinal epithelium, loss of orderly arrangement of germ cells, and accumulation of acid-fast pigment in Sertoli cells. In 75 hamsters, comparisons were made between the histology of one testis and epididymis surgically ablated after 75–160 days and the other organs obtained at necropsy after 10, 20, 30, and 40 days of vitamin E therapy. Daily oral supplements of 2 mg of d-α-tocopheryl acetate proved marginally beneficial, whereas supplements of 10 mg daily were highly effective in repairing the germinal epithelium, in causing the reappearance of spermatozoa in ducts of the epididymis, and in removing acid-fast pigment. The testis injury in the vitamin E-deficient hamster, with respect to both the degenerative changes in the germinal epithelium and their repairability after vitamin E therapy, stand in striking contrast with the irrevocable testis injury characteristic of the vitamin E-deficient rat.

Maintenance of the Walker 256 mammary carcinoma in vitamin E-deficient rats for a period of 2/12 years, by 22 successive implantations, produced no demonstrable alteration in the rate of growth, transplantability, histologic organization, or cytologic characteristics of the tumor.Normal rats fed concentrates of wheat germ oil failed to show the neoplastic growths observed by Rowntree and his associates.