Subacute exposure to cadmium chloride induces HSP-72 in rat liver.

Two groups of rats (n = 5) weighing 175-185 g were implanted (sc) with osmotic minipumps to deliver (0.5 microliter/hr) deionized water or cadmium chloride (CdCl2; 0.2 M) for 14 days. On completion of subacute treatment, liver and kidneys were collected from control and CdCl2 treated groups for analysis. We report that, subacute exposure to CdCl2 results in significant Cd accumulation in liver and kidneys, and heat-shock-protein 72 (HSP-72) induction in the liver. Results affirm a role for liver HSP-72 in Cd-toxicity.

Effect of selenium (Se) on plasma ACTH, beta-endorphin, corticosterone and glucose in rat: influence of adrenal enucleation and metyrapone pretreatment.

The effects of acute treatment (i.p.) with selenium (Se) on glucoregulation, by measuring plasma levels of adrenocorticotropic hormone (ACTH), beta-endorphin (beta-EN), corticosterone (CORT) and glucose over time, were investigated. The hormones of the hypothalamic-pituitary adrenal (HPA) axis, were measured after treating rats with saline, Se: 1.6 mg/kg, or 3.8 mg/kg. Blood samples were collected before, 30, 60 and 90 min following injection. The results show that i.p. administration of Se (both doses) induce a rise in plasma ACTH, and beta-EN (P < 0.01). Plasma CORT and glucose levels also rose sharply by 30 min (P < 0.05). Corticosterone levels were increased in a dose-dependent fashion over the ensuing hour. Bilateral adrenal demedullation resulted in the abolishment of the Se-induced rise in plasma glucose. Pretreatment with metyrapone (300 mg/kg) was found to delay the Se-induced rise in plasma glucose. The results indicate that after a Se challenge the HPA axis is activated. In addition, CORT was found to be essential in the Se-induced rise in plasma glucose.

Selenium lethality: role of glutathione and metallothionein.

Male Sprague-Dawley rats (200-300 g) were pretreated (i.p.) with diethylmaleate (DEM; 3.1 mmol/kg) or propylene glycol (PG). After 1 h, three PG and three DEM groups received saline or sodium selenite (Se: 0.8 or 1.6 mg/kg) i.p. Eighty to one hundred percent mortality occurred within 3 h after Se in DEM-pretreated groups. Except for one PG and one DEM group, which were sacrificed after 1 h, the remaining groups received saline or Se (1.6 mg/kg) 25 h after pretreatment. No mortality occurred within 3 h after Se. Liver and kidney GSH decreased at 1 h, while liver MT increased at 28 h. The changes are related to Se-induced lethality.

Effect of selenium on plasma glucose of rats: role of insulin and glucocorticoids.

The effects of acute treatment (i.p.) of selenium (Se) on glucoregulation and on plasma levels of glucose, insulin and corticosterone were determined in both fed and 24-hour-fasted rats. In this experiment animals were treated with saline (control) or 1.3, 1.6 and 3.8 mg/kg doses of Se. Blood samples were collected before, 30, 60 and 90 min following injection. The results obtained show that acute intraperitoneal (i.p.) administration of Se (1.6 mg/kg or more) causes hyperglycemia in rats. It was found that Se does not change levels of plasma insulin in either fasted or fed animals. Se did, however, significantly increase the plasma levels of corticosterone in all Se-treated groups. In order to confirm the role of corticosterone and thus support the significance of adrenal glands in this hyperglycemic response, animals were subjected to bilateral adrenalectomy. Blood samples were collected before, 30, 60 and 90 min following intraperitoneal treatment with Se. The results indicate that bilateral adrenalectomy abolishes the hyperglycemic response to Se. It can be concluded that adrenal glands play a role in Se-induced hyperglycemia. The increase in corticosterone levels suggest the possibility of gluconeogenesis in contributing to this hyperglycemic response.