THE EFFECTS OF DIETARY ZINC DEFICIENCY ON THE REPRODUCTIVE SYSTEM OF MALE RATS

1958 ◽  
Vol 36 (1) ◽  
pp. 557-569 ◽  
Author(s):  
M. J. Millar ◽  
M. I. Fischer ◽  
P. V. Elcoate ◽  
C. A. Mawson

Dietary zinc deficiency produced by feeding a zinc-poor diet (0.5 μg. zinc per g.) to weanling rats for 8 weeks caused marked retardation in body growth, depressed growth and development of testes, epididymes, accessory sex organs, and pituitary glands, and in many cases severe atrophy of testicular germinal epithelium. The zinc concentration of dorsolateral prostates, testes, epididymes, and bone was reduced in zinc-deficient rats compared with controls receiving the zinc-poor diet plus 100 μg. zinc daily. Restricted feeding of the zinc-supplemented diet to produce body weights comparable to those in zinc-deficient rats caused a reduction in pituitary gland and accessory sex organ size which was similar to that observed in zinc-deficient rats. Testis growth and development were normal in the restricted controls and did not differ from controls fed ad libitum. The zinc concentration of dorsolateral prostates was reduced in restricted controls but exceeded that in the zinc-deficient rats. All the observed changes produced by zinc deficiency except the testicular atrophy were reversed when zinc was replaced in the diet. If testicular atrophy had occurred, neither testis nor epididymis regained normal size, function, or zinc concentration.

1958 ◽  
Vol 36 (6) ◽  
pp. 557-569 ◽  
Author(s):  
M. J. Millar ◽  
M. I. Fischer ◽  
P. V. Elcoate ◽  
C. A. Mawson

Dietary zinc deficiency produced by feeding a zinc-poor diet (0.5 μg. zinc per g.) to weanling rats for 8 weeks caused marked retardation in body growth, depressed growth and development of testes, epididymes, accessory sex organs, and pituitary glands, and in many cases severe atrophy of testicular germinal epithelium. The zinc concentration of dorsolateral prostates, testes, epididymes, and bone was reduced in zinc-deficient rats compared with controls receiving the zinc-poor diet plus 100 μg. zinc daily. Restricted feeding of the zinc-supplemented diet to produce body weights comparable to those in zinc-deficient rats caused a reduction in pituitary gland and accessory sex organ size which was similar to that observed in zinc-deficient rats. Testis growth and development were normal in the restricted controls and did not differ from controls fed ad libitum. The zinc concentration of dorsolateral prostates was reduced in restricted controls but exceeded that in the zinc-deficient rats. All the observed changes produced by zinc deficiency except the testicular atrophy were reversed when zinc was replaced in the diet. If testicular atrophy had occurred, neither testis nor epididymis regained normal size, function, or zinc concentration.


1960 ◽  
Vol 38 (1) ◽  
pp. 1457-1466 ◽  
Author(s):  
M. J. Millar ◽  
P. V. Elcoate ◽  
M. J. Fischer ◽  
C. A. Mawson

Zinc-deficient rats, receiving a diet low in zinc (0.5 μg zinc/g), were injected subcutaneously with testosterone propionate or gonadotrophins for periods of 13 to 28 days.The hormone injections in every case caused marked growth of accessory sex organs of zinc-deficient rats. The zinc concentrations of the large hormone-stimulated dorsolateral prostate glands were very low and similar to those of glands in untreated zinc-deficient rats. Testosterone propionate did not alter the testicular atrophy which had occurred before treatment. Gonadotrophin increased the rate of growth and possibly the rate of maturation of testes that were immature prior to treatment. When the testes had matured and were producing sperm before treatment, the tubular atrophy that is typical of zinc deficiency developed in spite of the injected gonadotrophins.Testicular atrophy in zinc-deficient rats is probably due specifically to an inadequate supply of zinc to the testis. The availability of sufficient zinc for incorporation of high concentrations into sperm seems to be essential for the maintenance of spermatogenesis and the survival of the germinal epithelium. On the other hand, the reduction in rate of growth and development of immature testes and of all accessory sex organs in zinc-deficient rats is due mainly to an inhibition of pituitary gonadotrophin output.


1961 ◽  
Vol 16 (4) ◽  
pp. 587-588 ◽  
Author(s):  
A. Stanley Weltman ◽  
Arthur M. Sackler ◽  
Joseph Gennis

Daily handling of young mature rats over a 3-week period significantly increases their body weight gains in much the same fashion as does the handling of preweanling and weanling rats. Significant increases were also observed in the adrenals, testes, seminal vesicles, spleen and liver organ weights. Although mechanisms involved in the handling effect are not clearly defined, the findings have methodologic significance. The marked influence of handling on weight gains and organ weights indicates the need for careful regulation of the handling of control and experimental animals in all endocrine studies. The study indicates that the stimulatory effects of handling on body growth and development are not necessarily limited to the early developmental period. Submitted on December 22, 1960


1960 ◽  
Vol 38 (12) ◽  
pp. 1457-1466 ◽  
Author(s):  
M. J. Millar ◽  
P. V. Elcoate ◽  
M. J. Fischer ◽  
C. A. Mawson

Zinc-deficient rats, receiving a diet low in zinc (0.5 μg zinc/g), were injected subcutaneously with testosterone propionate or gonadotrophins for periods of 13 to 28 days.The hormone injections in every case caused marked growth of accessory sex organs of zinc-deficient rats. The zinc concentrations of the large hormone-stimulated dorsolateral prostate glands were very low and similar to those of glands in untreated zinc-deficient rats. Testosterone propionate did not alter the testicular atrophy which had occurred before treatment. Gonadotrophin increased the rate of growth and possibly the rate of maturation of testes that were immature prior to treatment. When the testes had matured and were producing sperm before treatment, the tubular atrophy that is typical of zinc deficiency developed in spite of the injected gonadotrophins.Testicular atrophy in zinc-deficient rats is probably due specifically to an inadequate supply of zinc to the testis. The availability of sufficient zinc for incorporation of high concentrations into sperm seems to be essential for the maintenance of spermatogenesis and the survival of the germinal epithelium. On the other hand, the reduction in rate of growth and development of immature testes and of all accessory sex organs in zinc-deficient rats is due mainly to an inhibition of pituitary gonadotrophin output.


2015 ◽  
Vol 146 (1) ◽  
pp. 114-123 ◽  
Author(s):  
Valeria Galetti ◽  
Comlan Evariste S Mitchikpè ◽  
Prosper Kujinga ◽  
Félicien Tossou ◽  
D Joseph Hounhouigan ◽  
...  

2007 ◽  
Vol 28 (3_suppl3) ◽  
pp. S403-S429 ◽  
Author(s):  
Sonja Y. Hess ◽  
Janet M. Peerson ◽  
Janet C. King ◽  
Kenneth H. Brown

Assessing the prevalence and severity of zinc deficiency in populations is critical to determine the need for and appropriate targeting of zinc intervention programs and to assess their effectiveness for improving the health and well-being of high-risk populations. However, there is very little information on the zinc status of populations worldwide due to the lack of consensus on appropriate biochemical indicators of zinc status. The objective of this review was to evaluate the use of serum zinc concentration as an indicator of population zinc status. We have reviewed the response of serum zinc concentration to dietary zinc restriction and zinc supplementation. In addition, we completed pooled analyses of nine zinc intervention trials in young children to assess the relations between serum zinc concentration of individuals before treatment and their responses to zinc supplementation. Also, in updated combined analyses of previously published data, we investigated the relation between the mean initial serum zinc concentration of a study population and their mean growth responses to zinc supplementation in randomized intervention trials among children. The results from depletion/repletion studies indicate that serum zinc concentrations respond appreciably to severe dietary zinc restriction, although there is considerable interindividual variation in these responses. There is also clear evidence that both individual and population mean serum zinc concentrations increase consistently during zinc supplementation, regardless of the initial level of serum zinc concentration. By contrast, an individual's serum zinc concentration does not reliably predict that person's response to zinc supplementation. Serum zinc concentration can be considered a useful biomarker of a population's risk of zinc deficiency and response to zinc interventions, although it may not be a reliable indicator of individual zinc status.


Sign in / Sign up

Export Citation Format

Share Document