Publication | Open Access
MECHANISMS OF ZINC, CYSTEINE AND SELENIUM PROTECTION AGAINST CADMIUM-INDUCED VASCULAR INJURY TO MOUSE TESTIS
85
Citations
14
References
1968
Year
InflammationMechanisms Of ZincAllergySelenium DeficiencyMedicineBioactive MetalPhysiologyCadmium ChlorideTrace MetalCadmium UptakeVascular BiologyToxicologyMetal ToxicitySelenium DioxideReactive Oxygen SpeciePharmacologyOxidative Stress
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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