Cadmium and cardiac muscle cell - biomarkers of oxidative stress - experimental work

• Published in: Revista portuguesa de cardiologia Vol. 17; no. 11; p. 911
• Main Authors: Correia, V, Joaquim, N, Coucelo, J M, Azevedo, J, Coucelo, J A
• Format: Journal Article
• Language: Portuguese
• Published: Portugal 01.11.1998
• Subjects: Animals; Cadmium - metabolism; Fishes - metabolism; Kidney - metabolism; Liver - metabolism; Myocardium - metabolism; Oxidative Stress
• ISSN: 0870-2551; 2174-2030

To study in several tissues (heart, kidney and liver) of Halobatrachus didactylus the cellular response induced by an acute exposure to a sublethal cadmium concentration. Fifteen species of H. didactylus (marine teleost) were divided in to three groups: CTRL: control group, the fish were injected with a saline solution; 24 H: 1 mg/kg of cadmium chloride was injected and the fish were sacrificed after 24 hours; 7 D: the fish were subjected to the same cadmium concentration and sacrificed 7 days after injection. Superoxide dismutase--SOD (McCord & Fridovich, 1969) and catalase--CAT (Clairborne, 1985) activities were determined in the cytosolic and mitochondrial fractions of these three tissues. The lipid degradation products were also determined by the tiobarbithuric acid (TBA) test. Cadmium induced an increase in SOD activity in both fractions (cytosolic and mitochondrial) of these H. didactylus tissues. The highest levels of activity observed were located at mitochondrial fraction and in the heart. There was a significant increase in CAT activity in both liver and heart tissue fractions after cadmium exposure. The highest values were observed in the liver. The kidney presented a different response: there was a rise in CAT activity only in the mitochondrial fraction after seven days of exposure. There were no significant changes in lipid degradation products in any of these tissues after cadmium exposure. The two antioxidant enzymes studied in the heart, kidney and liver of H. didactylus demonstrated a high sensitivity to oxidative stress induced by cadmium and presented a high potential as cellular biological makers. The results indicate membrane lesion caused by lipid peroxidation did not occur, which suggests an efficient response of the cellular protection mechanisms against cadmium cytotoxicity.