Function of pituitary-gonadal axis in zinc-deficient rats

Lei, K. Y.; Abbasi, Ali; As, Prasad

doi:10.1152/ajplegacy.1976.230.6.1730

Cited by 110 publications

(41 citation statements)

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“…A similar situ¬ ation has been suggested for the male rat and human, in which the effects of zinc deficiency appear to be expressed in the testis, specifically within the pathways controlling steroidogenesis, so that the secretion of androgens is reduced (McClain et al, 1984;Prasad, 1985;Hafiez et al, 1989). In several studies, there was an increase in the secretion of gonadotrophins, presumably as a consequence of the loss of negative feedback to the hypothalamo-hypophyseal system (Lei et al, 1976;Root et al, 1979;Prasad, 1985). In the study by Hafiez et al (1989), however, the serum concentrations of gonadotrophins were not affected.…”

Section: Introductionmentioning

confidence: 59%

“…In deficient rams, the secretion of LH and FSH were both reduced whereas, in the other species, the secretion of gonadotrophins is increased, apparently because poor testicular development leads to low rates of testosterone secretion (Lei et al, 1976;Root et al, 1979;Prasad, 1985). Superficially, this latter observation is more consistent with our understanding of the control of gonadotrophin secretion by the processes of negative feedback, leading us to ask why the ram is different.…”

Section: Discussionmentioning

confidence: 75%

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Effects of dietary zinc deficiency on gonadotrophin secretion and testicular growth in young male sheep

Martin

White²

1992

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Summary. The hypothesis that the secretion of gonadotrophins would be reduced by zinc deficiency was tested in five groups of four young Merino rams (initial liveweight 22 kg). Four groups were fed ad libitum with diets containing 4, 10, 17 or 27 \ g=m\ g Zn g \ m=-\ 1. The effects of loss of appetite on the deficient diet was controlled by feeding a fifth group (pair-fed control) at a rate of 27 \g=m\g Zn g \ m=-\ 1, but the amount of feed offered was restricted to that eaten voluntarily by the deficient (4 \ g=m\ g Zn g\ m=-\ 1) group. Blood was sampled every 20 min for 32 h on two occasions before the treatments were imposed and 96 days later, at the end of the experiment. The rams were injected with gonadotrophin-releasing hormone (GnRH; 10 ng kg \ m= -\ 1 i.v.) after each serial sampling, and with naloxone (1 mg kg\m=-\ 1 i.v.) 24 h after the end of the final GnRH test.In the group that were fed the diet with the lowest zinc content, the concentration of zinc in blood plasma was reduced to 18% of that in the pair-fed controls (P < 0\m=.\05) and was within the deficient range. The appetite of the deficient rams was half that of the controls fed 27 \g=m\g Zn g\m=-\1 ad libitum and there was no increase in liveweight or testicular diameter during pubertal development. Similar, but smaller, effects were observed in the pair-fed controls. There were no significant differences between pair-fed and deficient groups in the frequency of the luteinizing hormone (LH) pulses or in the concentration of follicle-stimulating hormone (FSH), but the secretion of gonadotrophins was markedly lower in both groups than in the control rams fed ad libitum. The response to GnRH was not affected by treatment, but the increase in LH pulse frequency evoked by naloxone was lower in the deficient animals than in other groups.The animals fed zinc at intermediate rates (10\p=n-\17 \ g=m\ g\ g=m\ \ m=-\ 1) showed similar responses to the controls fed ad libitum.It is concluded that the specific effects of zinc deficiency on testicular function were small. Most of the reduction in testicular growth in rams fed a deficient diet was not specifically related to the trace element, but was due to the fall in energy and protein intake caused by the loss of appetite. This leads to a reduction in the frequency of GnRH pulses secreted by the hypothalamus, and to low rates of gonadotrophin secretion by the pituitary gland.

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Section: Introductionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 75%

Effects of dietary zinc deficiency on gonadotrophin secretion and testicular growth in young male sheep

Martin

White²

1992

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“…These observations led us to examine the hormonal systems controlling testicular growth in rams fed diets containing 4-27 µg Zn g " 1 (Martin and White, 1992 (Root et al, 1979;McCIain et al, 1984;Prasad, 1985). Zinc deficiency may lead to a biochemical lesion in the pathways controlling steroid synthesis, as suggested by Lei et al (1976), impaired development of the smooth endoplasmic reticulum in the Leydig cells, the site of testosterone synthesis (Hesketh, 1982), or a malfunction in the LH receptor mechanism controlling storage and release of testosterone, as suggested by Kellokumpu and Rajaniemi (1981). A third possibility is raised by the structural nature of steroid receptors, where zinc is an integral component of the structure that binds to DNA and regulates gene expression (the 'zinc finger' proteins; Parker, 1989).…”

Section: Introductionmentioning

confidence: 99%

Effects of dietary zinc deficiency on the reproductive system of young male sheep: testicular growth and the secretion of inhibin and testosterone

Martin¹,

White²,

Markey³

et al. 1994

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Zn g\m=-\1. In zinc-deficient rams, the tubule development was further retarded and the interstitial regions were more extensive than in the other groups. We conclude that the overall effect of zinc deficiency on testicular development is due to a combination of a non-specific effect (low gonadotrophin concentrations caused by the low feed intake) and a specific effect due to the lack of zinc. The zinc-specific effect is localized within the testis where it reduces the development of the capacity to produce testosterone, leading to low intratesticular concentrations of testosterone, a critical factor for the growth, development and function of the seminiferous tubules.

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“…Mono(2-ethylhexyl) phthalate (MEHP) and other monoester metabolites of PAEs, produced by the hydrolytic activity of intestinal lipases, can reproduce the effects of their parent diesters and are suspected as causative agents (5,6 seem to be affected by these agents (7), it is suggested that polar metabolites of DEHP and other PAEs can selectively remove testicular zinc and thereby lead to tubular atrophy (5). Zinc deficiency affects production and release of gonadotrophins and testosterone (8), just as these hormones are known to maintain tissue zinc concentration and regulate uptake of zinc in testis and accessory sex organs (9). Perturbation of gonadotrophins or testosterone, therefore, may be responsible for DEHP gonadotoxicity due to afflicted hormonal regulation of gonadal physiology (10,11).…”

Section: Introductionmentioning

confidence: 99%

Effects of di(2-ethylhexyl) phthalate on the gonadal pathophysiology, sperm morphology, and reproductive performance of male rats.

Agarwal¹,

Eustis²,

Lamb³

et al. 1986

Environ Health Perspect

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Dietary exposure of adult male F344 rats to 0, 320, 1250, 5000, or 20,000 ppm DEHP for 60 consecutive days resulted in a dose-dependent reduction in total body, testis, epididymis, and prostate weights at 5000 and 20,000 ppm. Degenerative changes were observed in testis, along with decreased testicular zinc content, reduced epididymal sperm density and motility, and increased occurrence of abnormal sperm at 20,000 ppm. There was a trend towards reduced testosterone and increased luteinizing hormone and follicle stimulating hormone in serum at 5000 and 20,000 ppm. The mean percentage of fertile animals was unchanged and reduction in fertility parameters, although not marked in severity, were correlated with gonadal effects. Average litter size was reduced at 20,000 ppm, but initial pup weights and growth were unaffected. There were no grossly observed abnormalities in the offspring and the rate of neonatal deaths was similar in control and DEHP treated groups. Characteristic toxicity manifestations of DEHP included dose-dependent enlargement of liver and reduced sperm triglycerides and cholesterol. Additionally, serum albumin and total proteins were dose dependently increased upon treatment with DEHP. Cessation of exposure to DEHP initiated partial to complete recovery from toxicity in most cases. The magnitude of recovery were variable with that ofthe gonads being slower than other systems. These data suggest a lack of reproductive dysfunction in F344 male rats at DEHP doses below 20,000 ppm which produced measurable testicular degeneration and afflicted epididymal sperm morphology under the present experimental conditions.

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Function of pituitary-gonadal axis in zinc-deficient rats

Cited by 110 publications

References 0 publications

Effects of dietary zinc deficiency on gonadotrophin secretion and testicular growth in young male sheep

Effects of dietary zinc deficiency on gonadotrophin secretion and testicular growth in young male sheep

Effects of dietary zinc deficiency on the reproductive system of young male sheep: testicular growth and the secretion of inhibin and testosterone

Effects of di(2-ethylhexyl) phthalate on the gonadal pathophysiology, sperm morphology, and reproductive performance of male rats.

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