[A histological analysis of the changes experimentally induced by cadmium in cardiac muscle tissue by a computerized method of image analysis]. / Análise histológica de alterações induzidas experimentalmente por cádmio no tecido muscular cardíaco através de método computadorizado de análise de imagens.

OBJECTIVE: To study the distribution of myocardial structural elements in a univentricular experimental model (Halobatrachus didactylus) and the changes induced by acute exposure to a sublethal concentrations of cadmium. DESIGN: 15 specimens of H. didactylus (marine teleost) were divided in three groups: CTRL: the control group, the fish were injected with a saline solution; 24 H: 1 mg/kg of cadmium chloride was injected and fish were sacrificed after 1 day post injection; 7 D: fish where subjected to the same cadmium concentration and sacrificed after 7 days post injection. INTERVENTIONS: Histological sections (5 microns) of ventricle were coloured by PicroSirius method and used to determine the fraction area occupied by the several myocardium structural elements, using specific software Optimas Bioscan 5.2. MEASUREMENTS AND RESULTS: The different structural elements of H. didactylus myocardium displayed in different ways and its distribution along the ventricular wall remained unchanged on exposure to cadmium. The structural elements of H. didactylus myocardium showed a characteristic pattern: collagen type I revealed a heterogeneous distribution, with fractional area values greater in epicardial and endocardial layers; collagen type III, has a homogeneous distribution with the myocardial wall thickness with lesser fractional area values than collagen I; cardiac muscle tissue showed a tendency to occupy a greater fractional area in the epicardial-endocardial region. Cadmium toxicity resulted in an increase in the fractional area occupied by muscle tissue to the detriment of the area occupied by the intertrabecular spaces (lacunae), with no alterations in the other structural components. CONCLUSIONS: On our H. didactylus fish model, cadmium may have induced a myocardial edema which resulted in an increase in the fractional area occupied by muscle tissue, with no alterations in other structural components of the myocardium or in the relative ventricular mass.

[Cadmium and cardiac muscle cell - biomarkers of oxidative stress - experimental work]. / Cádmio e célula muscular cardíaca--biomarcadores de stress oxidativo--trabalho experimental.

OBJECTIVE: 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. DESIGN: 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. INTERVENTIONS: 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. MEASUREMENTS AND RESULTS: 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. CONCLUSIONS: 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.