A comparison of the effects of dietary cadmium on heart and kidney antioxidant enzymes: Evidence for the greater vulnerability of the heart to cadmium toxicity

Abstract

This study demonstrates the greater susceptibility of the heart as compared to the kidney to cadmium in the presence of high dietary selenium. Male weanling rats were fed an adequate-copper low-selenium feed supplemented with 0, 10 or 50 ppm copper with or without 50 ppm dietary cadmium for 7 weeks. All rats received 0.5 ppm selenium in their drinking water. Cadmium treatment resulted in histopathological lesions in the heart, but not in the kidney. Although cadmium treatment resulted in more extensive effects on glutathione peroxidase and superoxide dismutase in the heart as compared to the kidney, no increase in peroxidation was noted in either organ, suggesting that cadmium cardiotoxicity can be dissociated from tissue peroxidation. Mean cadmium concentrations in the heart ranged from 0.55 to 1.22 micrograms cadmium g-1 tissue, wet weight, and in the kidney from 11.53 to 21.04 micrograms cadmium g-1 tissue, wet weight. In both tissues examined, cadmium levels were influenced by dietary copper and heart cadmium concentrations did not correlate with either the biochemical or histological lesions observed. Thus, tissue cadmium levels alone may not be adequate for predicting cadmium toxicity.

Significance of alterations in hepatic antioxidant enzymes. Primacy of glutathione peroxidase

“…Studies carried out in vivo designed to elucidate the role of peroxidation in cadmium cardiotoxicity have demonstrated that GSH-Px is more important than either SOD or catalase in preventing Cdinduced peroxidation (Jamall & Smith, 1985a;Jamall & Sprowls, 1987). A central role for GSH-Px in preventing tissue peroxidation is also supported by studies carried out in vitro (Jones et al, 1981;Jones & Kennedy, 1983;Suttorp et al, 1986;Raes et al, 1987).…”

“…A treatment period of 8 weeks was selected because earlier studies in our laboratory have established that feeding weanling rats a low-Se diet for this length of time.results in a depletion of GSH-Px to less than 10 % with peroxidative tissue injury (Jamall & Smith, 1985a;Jamall & Sprowls, 1987). In addition, dietary 3-AT treatment allowed us to study the effects of a sustained reduction of hepatic catalase activity.…”

Involvement of galectin-3 in cadmium-induced cardiac toxicity

“…Cadmium accumulates in the body because of slow excretion. Cd causes toxicity in different organs, heart is one of the most effected tissues and oxidative damage usually occurs after Cd toxicity (1)(2)(3)(4). Many mechanisms are defined to explain pathophysiology of the Cd toxicity; inflammation is one of them (5).…”

Vanadium distribution, lipid peroxidation and oxidative stress markers upon decavanadate in vivo administration

“…The involvement of toxic metals in cardiac oxidative damage suggests that this organ shows a great vulnerability to metal intoxication [9][10][11][12]. Notwithstanding, and despite the magnitude of the knowledge so far accumulated, the biochemical basis for the observed in vivo oxidative effects of vanadium in cardiac tissue are still poorly defined.…”