Peter Massanyi⁽¹⁾, Laszlo Bardos⁽²⁾, Robert Toman⁽³⁾, Svatoslav Hluchy⁽⁴⁾, Jaroslav Kovacik⁽⁵⁾, Norbert Lukac^{(6)
(1)(3)(4)(6)}Slovak Agricultural University - Nitra. Slovakia
⁽²⁾University of Agricultural Sciences - Godollo. Hungary
⁽⁵⁾Slovak University of Agriculture - Nitra. Slovakia

	[Toxicology]	[Reproduction Sciences]

DISCUSSION

Cadmium mainly accumulates in liver and kidney ^{(2,3,4,8,9,19,20)}. In control animals we have found higher cadmium concentration in kidney (0.355 mg/kg) than in liver (0.052 mg/kg). After single i.p. administration of cadmium we have observed higher cadmium levels in liver (4.196 and 8.360 mg/kg) than in kidney (2.382 and 2.709 mg/kg). This single exposure experiment has shown that initially, a very high proportion of the dose is found in the liver. With time there is a redistribution of cadmium from the liver to other tissues, particularly the kidneys as we found it in our earlier study in rabbits ⁽⁴⁾ and as it has been described by others ⁽⁹⁾. This is probably due to an efficient metallothionein synthesis in the liver. Cadmium bound to metallothionein may subsequently be released into plasma, filtered through renal glomeruli and reabsorbed in the tubuli. This is of significance for human and animals in high exposure situations. Even if the daily exposure ceases, the renal cadmium concentration may be maintained for a long time or even increase if sufficient amounts of cadmium are stored in the liver.

We report dose dependent accumulation of cadmium in testis as well as alterations in retinyl palmitate, retinol and ß-carotene concentration in testis. It has been reported that cadmium causes degeneration of the seminiferous epithelium ^(1,7,18). All biochemical and physiological changes known to occur in the testis at late time intervals following cadmium treatment are secondary to ischaemia rather than due to a direct effect of cadmium. Higher cadmium concentration also inhibits the motility of spermatozoa ⁽¹¹⁾ and causes structural alterations of spermatozoa ⁽⁷⁾.

In this study significant decease of retinol (group B) and ß-carotene (both experimental groups) in kidney and retinyl palmitate (group B), retinol (group B) and ß-carotene (group A and B) in testis is reported. No significant differences were found in liver. ß-carotene is a provitamin of vitamin A. Cadmium in a long term study has been decsribed to induce significant decrease of serum vitamin A, while food intake and body weights remained unchanged ⁽¹⁷⁾. Absorption of vitamin A from the intestine, the release of newly absorbed vitamin A from the liver to serum, and the conversion of vitamin A to water soluble metabolites in the liver were not influenced by cadmium. These findings suggest that cadmium interfered with the release of vitamin A, especially stored vitamin A, to serum ⁽¹⁷⁾.

There may be many ways to interfere with the excretion mechanism of vitamin A to the serum. For example, the direct binding of cadmium with specific proteins essential for vitamin A excretion as retinol binding protein, prealbumin or vitamin A hydrolase, or the decrease in these proteins by cadmium and the destruction of excretion canals of cell organelles.

Discussion Board

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[ABSTRACT] [INTRODUCTION] [MATERIAL & METHODS] [RESULTS] [DISCUSSION] [BIBLIOGRAPHY] [Discussion Board]

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	[Toxicology]	[Reproduction Sciences]

Peter Massanyi, Laszlo Bardos, Robert Toman, Svatoslav Hluchy, Jaroslav Kovacik, Norbert Lukac
Copyright © 1999-2000. All rights reserved.

Last update: 10/01/00