Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
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The toxic effects of cadmium on the reproductive organs of animals and men are most completely described in the testes (10,11,12). Cadmium levels in the ovary increase linearly between 30 and 60 years of age (13). These results describe oedema of ovarian tissue, which is probably caused by vascular changes and also by low molecular weight cadmium- and zinc-binding proteins present in the ovaries, which are not metallothionein and provides further correlation between metallothionein deficiency and high sensitivity to the effects of cadmium.

A cadmium chloride treatment induces profound cellular and vascular changes in the ovary of prepubertal rats. The large and medium-sized follicles undergo mass atresia. At 6 h after cadmium treatment there is vascular engorgement and haemorrhage in the theca (14). At 48 h the major portion of the stroma is replaced by pigment and masses of chromatin material extruded from the nucleus of dead cells. Exposure of the human granulosa cells to cadmium brought about morphological alteration in the monolayer depending on dose and exposure time (9). At higher doses or low doses with longer exposure times the cells began to separate from each other through contracting towards the centre and assuming a round shape. Cadmium decrease progesterone production by human granulosa cells after cadmium treatment in vitro. Cadmium did not caused a significant alteration in progesterone accumulation during 4 h incubation periods. Following 24 h cadmium decreased progesterone production (9).

Recent studies indicate that the degeneration of the seminiferous epithelium and all biochemical and physiological changes known to occur in the testis at late time intervals following cadmium treatment are secondary to ischemia rather than due to a direct effect of the cadmium (11). Treatment with cadmium chloride and cyproterone acetate depresse angiotensin converting enzyme activity significantly in testes and epididymal regions of the adult rats compared to the corresponding untreated controls (15). Cadmium chloride belongs to vasoactive substances which cause spot-like necrosis.

Whole seminiferous tubuli are destroyed whereas other can remain intact. Leydig cells also degenerate, and there is fibroblastic proliferation in the interstitium. Cadmium treatment with dose of 1 mg/kg, in cause the failure of spermiation from stage IX through later stages of spermatogenesis in the seminiferous epithelium (12). They conclude that cadmium begins to act during early stage VIII of spermatogenesis to induce failure of spermiation, and that the action of cadmium is spermatogenic stage-specific. Concentrations of 10-6 to 10-2 µM cadmium and mercury are injurious to spermatozoa as indicated by depressed motility and reduced oxygen uptake (16). Cadmium concetration 1.6 mM decrease sperm motility. A detailed electron microscopy study of cadmium sensitive and resistant muntjac fibroblast cell lines has identified a wide range of intracellular damage following exposure to cadmium (17).

Damaged organells included cell membrane, mitochondria, Gologi cisternae and tubular network, chromatin, nucleoli, microfilaments and ribosomes. Although cell membrane damage was generally the earliest indication of adverse cadmium action, particularly with continous cadmium exposures, cells could tolerate extensive membrane loss. Mitochondrial distortion and some damage to Golgi complex was also altered. The turning point at which cadmium bacame lethal was generally marked by a cascade of events which included damage to both nuclear and cytoplasmic components. Prominent swelling of mitochondria and the occurrence of intracellular and intercellular vacuoles in the corneal endothelium were observed only in pregnant dams (18). In in vitro experiments, electron-dense deposits consisting of cadmium - oxine complexes were preferentially found in swollen mitochondria of the endothelial cells. Cadmium peaks were obtained from these deposits with x-ray microanalysis. Data suggest that corneal edema observed after administration of cadmium may imply the disturbance of pulp function and barrier function of the corneal endothelium due to the primary toxic effects of this metal on mitochondria. These result also indicate, that decreased sperm motion refered in this study may be caused by degeneration of mitochondria in spermatozoa, so the energetic source in male reproductive cells is affected. Our results present that cadmium accumulates in reproductive organs where it causes maily follicular atresia and tissue oedamatisation, desintegration of cappilary wall and subseqent diapedesis. In testis spermatogenesis is altered and high cadmium doses alter spermatozoa motility.

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