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Comparison of the effect of chronic cadmium exposure on the antioxidant defense systems of kidney and brain in rat

Abstract Cadmium (Cd2+) produces toxic effects on various tissues as kidney and liver, so several studies have focused to explore the effect produced by different doses and exposure times of this metal. However, little has been reported about the effect that Cd2+ shows in the brain in vivo. Hence, t...

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Published in:Toxicology mechanisms and methods 2013-06, Vol.23 (5), p.329-336
Main Authors: Mendieta-Wejebe, Jessica Elena, Miliar-García, Ángel, Correa-Basurto, José, Sánchez-Rico, Carolina, Ramírez-Rosales, Daniel, Trujillo-Ferrara, José, Rosales-Hernández, Martha Cecilia
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Language:English
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Summary:Abstract Cadmium (Cd2+) produces toxic effects on various tissues as kidney and liver, so several studies have focused to explore the effect produced by different doses and exposure times of this metal. However, little has been reported about the effect that Cd2+ shows in the brain in vivo. Hence, this study aimed at comparing the effect of chronic Cd2+ exposure on antioxidant defense systems of kidney and brain in rats. Six groups of male rats were employed; five were administered for 45 days with different doses of cadmium chloride (0.187, 0.375, 0.562, 0.937 and 1.125 mg/kg; i.p.) and the other was used as control. Free radicals (FRs) were directly quantified by electron paramagnetic resonance (EPR) spectroscopy; malondialdehyde (MDA), reduced glutathione (GSH) and the activity expression of superoxide dismutase (SOD2) and catalase (CAT) were also measured. The EPR results showed that there was no increase in FR content in kidney or brain. MDA and GSH levels increased in kidney but not in the brain. The SOD2 activity was not altered, but its expression decreased in both tissues. On the other hand, CAT activity and expression tended to increase at low doses and decrease at high doses in both tissues. Therefore, these results suggest that there exist compensatory mechanisms in both kidney and brain that are capable of avoiding the toxic effects exerted by Cd2+ at these doses and exposure time.
ISSN:1537-6516
1537-6524
DOI:10.3109/15376516.2012.757687