Histopathological alterations in the brain regions of rats after perinatal combined treatment with cadmium and dexamethasone.

Industrial and environmental exposure to cadmium (Cd) is well known to produce multiorgan toxicity in humans. Metallothionein (MT) is a cellular ligand for Cd. MT has been shown to protect against Cd-induced toxicity in many organs, including brain. In this study, we described the histopathological alterations in parietal cortex, striatum, hippocampus and cerebellum of rats following perinatal combined exposure to cadmium and dexamethasone (Dx), a drug known to induce MT synthesis in brain. Wistar rats of 13 days of age were treated for 5 days, as follows; (1) saline solution, (2) CdCl(2) 1 mg/kg per day, (3) Dx 2 mg/kg per day, (4) CdCl(2) 1 mg/kg per day + Dx 2 mg/kg/day. Rats were killed on either 18 or 28 days of age. The content of Cd in parietal cortex, striatum, hippocampus and cerebellum at 18 days old age increased 58.3-, 9.4-, 18.3- and 11.3-fold, while at 28 days of age in the same regions the increases were 6.6-, 5.8-, 25.3- and 11.3-fold in the Cd treated rats, respectively. No lesions were observed in the brain of control rats. Rats treated with Dx at 28 days of age showed interstitial edema in the four regions. Cd-treated rats at 28 days of age showed lesions in the four studied regions. In general, Dx treatment attenuated all Cd-induced lesions.