Wistar female rats were given 0.5 mgCd+2/kg b.w. in the form of CdCl2, in drinking water, administered by intragastric probe daily for 90 days, and a dose of 5 mg/Cd+2/kg b.w. subcutaneously administered once a week, for a period of 30 days. The adrenal gland functional status was investigated by glycogen, total lipid, ascorbic acid content, organ weight and histometric measurements. No changes were observed in the animal which received intragastric Cd. Subcutaneous administration of 5 mgCd+2 determined a significant increase in organ weight as against the controls, with a widening of the fascicular stratum, and a marked decrease in glycogen, total lipids and ascorbic acid, parallel with high values of 17-ketosteroids. The data revealed a toxic effect of cadmium upon the adrenals, evidenced by a hyperactivity. Adrenal glycogen, total lipids and ascorbic acid depletion evoked a stimulated ACTH hormone release with a high rate of excreted 17-ketosteroids.

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