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pubmed:abstractText |
1. Male albino rats of 21 days age were exposed to 10 p.p.m. cadmium (CdCl2 salt) in drinking water, ad libitum, for 90 days. It increased the brain cadmium levels by 76% (P < 0.05) and 165% (P < 0.001) respectively at 30 and 90 days of exposure compared to controls. 2. Cadmium increased blood-brain barrier permeability of fluoroscein dye (24%, P < 0.02) and the levels of brain microvessel malondialdehyde (31%, P < 0.01) at 90 days of exposure. However, these parameters did not alter significantly at 30 days of exposure. 3. Increased activities of microvessel superoxide dismutase (18%, P < 0.02), glutathione peroxidase (20%, P < 0.01) and catalase (28%, P < 0.01) were observed at 30 days of exposure. 4. The continuation of the Cd treatment for 90 days decreased the levels of superoxide dismutase (30%, P < 0.001), glutathione peroxidase (23%, P < 0.005), catalase (25%, P < 0.005), glutathione reductase (18%, P < 0.02), vitamin E (20%, P < 0.01), glutathione (26%, P < 0.01), ascorbic acid (18%, P < 0.05) and ceruloplasmin (13%, P < 0.05) in the microvessal preparation compared to controls. 5. It appears that Cd-induced blood-brain barrier dysfunction may be related to the depletion of microvessel antioxidant substances along with increase in lipid peroxidation at 90 days of exposure.
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