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SAMUEL A. GUNN, THELMA CLARK GOULD and W. A. D. ANDERSON

Summary.

Between 24 and 40 hr after cadmium treatment in the rat, whilst the testis and caput epididymidis are undergoing haemorrhagic necrosis, the cauda epididymidis and contained spermatozoa remain morphologically normal. Sexual activity is diminished but fertile matings occur. By 7 days, reduced androgen output results in atrophic changes in the accessory glands, cauda epididymidis and vas deferens, in which spermatozoa are now degenerate. Few males mate and these are infertile. The changes in the cauda can be prevented by testosterone treatment and fertility remains normal up to 9 days after the dose of cadmium.

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SAMUEL A. GUNN, THELMA CLARK GOULD and W. A. D. ANDERSON

Wetterdal (1958) showed that zinc, an element essential for spermatogenesis, is incorporated into developing spermatogenic elements within the testis. Cadmium, physico-chemically similar to zinc, causes selective destruction of the testis; administration of zinc prevents cadmium damage (Parizek, 1957; Kar, Das & Mukerji, 1960; Gunn, Gould & Anderson, 1961). Parizek (1960) suggested that cadmium exerts testicular injury by displacing zinc from its natural sites in seminiferous tubules and that the haemorrhagic reactions, so characteristic of cadmium injury, are a secondary effect. More recent evidence indicates that the vascular endothelium of the testis is the primary site of damage and that necrosis of parenchyma follows secondarily (Gunn, Gould & Anderson, 1963a; Chiquoine, 1964; Mason, Brown, Young & Nesbit, 1964; Niemi & Kormano, 1965; Waites & Setchell, 1966). The following experiments were initiated using radio-isotopes to determine

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SAMUEL A. GUNN, THELMA CLARK GOULD and W. A. D. ANDERSON

Summary.

It is known that the selective injurious effect of cadmium on the testis can be prevented by zinc, cysteine or selenium. Studies, conducted in CD-1 mice, were initiated to determine whether any of these treatments offered protection by preventing cadmium from reaching the testis in doses sufficient to cause injury. Using cadmium chloride, labelled with 109Cd, it was shown that none of these protective agents decreased the amount of cadmium reaching the testis. Zinc acetate evoked no significant changes, cysteine brought about a slight enhancement of cadmium level but selenium dioxide produced a marked and prolonged elevation of cadmium uptake by the testis. Comparable studies in which selenium, rather than cadmium, was labelled (75Se) demonstrated that, in the presence of cadmium, selenium levels were augmented. Possible mechanisms are discussed to explain the diverse means of protection offered by zinc, cysteine and selenium. Since the site of cadmium-induced testicular injury has been pin-pointed at its vasculature, it is suggested that these protective agents exert their action at the vascular level.

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SAMUEL A. GUNN, THELMA CLARK GOULD and W. A. D. ANDERSON

The observations of Pařízek & Zahor (1956) and Pařízek (1957a, b) on the selective destructive effect of cadmium on the testis of the rat and mouse have since been confirmed by Meek (1959), Kar & Das (1960), Gunn, Gould & Anderson (1961), Allanson & Deanesly (1962), Chiquoine (1964), Mason, Brown, Young & Nesbit (1964) and others. During studies on the induction of interstitial cell tumours of the testis by cadmium (Gunn, Gould & Anderson, 1963), we noted that cadmium failed to cause any degree of damage to the testis of the BALB/c mouse. A study was, therefore, undertaken to determine if this resistance to cadmium-induced testicular injury was unique to the BALB/c strain of mice and whether strain differences in testicular response to cadmium might also be observed in rats. A single subcutaneous (interscapular) injection of 0·03 m-mole/kg of CdCl2 was chosen for the preliminary testing since overwhelming testicular