18 resultados para Cadmium exposure

em Repositório Institucional UNESP - Universidade Estadual Paulista "Julio de Mesquita Filho"


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Contamination with cadmium compounds poses high potential risk for the health of populations and for this reason the treatment of their toxic effects should urgently be established. The present study was carried out to determine whether or-tocopherol intake can protect tissues against damage induced by cadmium, and to clarify the contribution of superoxide radicals (O-2(-)) in this process. Cadmium chloride was tested for tissue damage by a single intraperitoneal injection of Cd2+ ions (2 mg Kg(-1)). To determine the potential therapeutic effect of Vitamin E, a group of Cd2+-treated rats received a drinking solution of or-tocopherol (40 mg l(-1)) for 15 days. Cadmium induced increased serum creatinine and total lactate dehydrogenase, reflecting renal and cardiac damage. The increased lipoperoxide and decreased Cu-Zn superoxide dismutase levels indicated the generation of superoxide radicals in cadmium-treated rats. Tocopherol induced increased serum high-density lipoprotein and depressed the toxic effects of Ca2+ alone, since creatinine and lactate dehydrogenase determinations were recovered to the control values. Tocopherol decreased lipoperoxide and led the superoxide dismutase activities to approach those of the control values. We concluded that superoxide radicals are produced as mediators of cadmium toxicity. Tocopherol possesses a significant anti-radical activity and inhibits the cadmium effect on superoxide dismutase activity. Tocopherol also protected tissues from the toxic effects of cadmium by a direct antioxidant action which decreased lipoperoxide formation.

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The contamination of water by metal compounds is a worldwide environmental problem. This study was undertaken to evaluate the impact of short-term cadmium exposure on metabolic patterns of the freshwater fish Oreochromis niloticus. The fish were exposed to 320, 640, 1280 and 2560 mug/l sublethal concentrations of Cd++ (CdCl2) in water for 7 days. The specific activities of the enzymes phosphofructo kinase (PFK-E.C.2.7.1.11.), lactate dehydrogenase (LDH-E.C.1.1.1.27.) and creatine kinase (CK-E.C.2.7.3.2.) were decreased in white muscle after cadmium treatments, indicating decreases in the capacity of glycolysis in this tissue. Cadmium exposure induced increased glucose concentration in white muscle of fish. on the other hand, cadmium exposure at sublethal concentrations increased phosphofructo kinase and LDH in red muscle of fish. Cadmium significantly decreased total protein concentrations in liver and white muscle regardless of tissue glycogen levels. The data suggest that cadmium acts as a stressor, leading to metabolic alterations similar to those observed in starvation. (C) 2001 Elsevier B.V. Ltd. All rights reserved.

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Pollution and industrial practices result in concentrations of metals and other environmental agents that are related to environmental toxicity. Concentrations of metals are widely related to biochemicals values which are used in disease diagnosis due to environmental toxicity. This work was carried out in order to verify the nephrotoxic effect of cadmium and to clarify the contribution of reactive oxygen species (ROS) in this process. Cadmium chloride was tested for nephrotoxic damage in rats by a single intraperitoneal (i.p.) injection Cd 2+ (2 mg/kg) and oral intake (Cd2 +-100 mg/l-from CdCl 2). The cadmium-induced biochemical alterations included significant increased levels of serum creatinine concentrations, in rats with i.p. injection. Total urinary protein concentrations were only increased in rats with cadmium intake. Lipoperoxide was also increased after 3 and 7 days of the Cd 2+ treatment. No changes were observed in glutathione peroxidase activities. Cadmium-induced damage might be due to superoxide radicals (O 2 -), since Cu-Zn superoxide dismutase activities were decreased by Cd 2+ treatment. This study allows tentative conclusions to be drawn regarding which reactive oxygen metabolites play a role in cadmium nephrotoxicity. We concluded that the superoxide radical may be produced as a mediator of nephrotoxic action of cadmium.

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Contamination with cadmium compounds poses high potential risk for the health of populations and for this reason the treatment of their toxic effects should urgently be established. The present study was carried out to determine whether α-tocopherol intake can protect tissues against damage induced by cadmium, and to clarify the contribution of superoxide radicals (O 2 -) in this process. Cadmium chloride was tested for tissue damage by a single intraperitoneal injection of Cd 2+ ions (2 mg Kg -1). To determine the potential therapeutic effect of vitamin E, a group of Cd 2+-treated rats received a drinking solution of α-tocopherol (40 mg l -1) for 15 days. Cadmium induced increased serum creatinine and total lactate dehydrogenase, reflecting renal and cardiac damage. The increased lipoperoxide and decreased Cu-Zn superoxide dismutase levels indicated the generation of superoxide radicals in cadmium-treated rats. Tocopherol induced increased serum high-density lipoprotein and depressed the toxic effects of Ca 2+ alone, since creatinine and lactate dehydrogenase determinations were recovered to the control values. Tocopherol decreased lipoperoxide and led the superoxide dismutase activities to approach those of the control values. We concluded that superoxide radicals are produced as mediators of cadmium toxicity. Tocopherol possesses a significant anti-radical activity and inhibits the cadmium effect on superoxide dismutase activity. Tocopherol also protected tissues from the toxic effects of cadmium by a direct antioxidant action which decreased lipoperoxide formation.

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The presence of toxic substances in the workplace environment requires systematic evaluation of exposure and health status in exposed subjects. Cadmium is a highly toxic element found in water. Although free mediated cellular damage and reactive oxygen species (ROS), had been theorized as contributing to the cadmium mechanism of toxicity, and recent investigations have established that free radicals may be important contributors to cardiac dysfunction, there is little information on the effect of cadmium exposure on markers of oxidative stress in cardiac tissue. Cadmium exposure (Cd2+ - 100 mg/1-from CdCl2) in drinking water, during 15 days, significantly increased lipoperoxide and decreased the activities of superoxide dismutase and glutathione peroxidase. No alterations were observed in catalase activity in heart of rats with cadmium exposure. We also observed decreased glycogen and glucose concentration and increased total lipid content in cardiac tissue of rats with cadmium exposure. The decreased activities of alanine transaminase and aspartate transaminase reflected decreased metabolic protein degradation, and increased lactate dehydrogenase activity was related with increases in capacity of glycolysis. Since the metabolic pathways were altered by cadmium exposure, we can conclude that Cd2+ exposure induced ROS and initiate some series of events that occur in the heart and resulted in metabolic pathways alterations.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Water contaminants have a high potential risk for the health of populations. Protection from toxic effects of environmental water pollutants primarily involves considering the mechanism of low level toxicity and likely biological effects in organisms who live in these polluted waters. The biomarkers assessment of oxidative stress and metabolic alterations to cadmium exposure were evaluated in Nile tilapia, Oreochromis niloticus. The fish were exposed to 0.35, 0.75, 1.5, and 3.0 mg/l concentrations of Cd2+ (CdCl2) in water for 60 days. Fish that survived cadmium exposure showed a metabolic shift and a compensatory development for maintenance of the body weight gain. We observed a decreased glycogen content and decreased glucose uptake in white muscle. Lactate dehydrogenase (LDH) and creatine phosphokinase (CK) activities were also decreased, indicating that the glycolytic capacity was decreased in this tissue. No alterations were observed in total protein content in white muscle due to cadmium exposure suggesting a metabolic shift of carbohydrate metabolism to maintenance of the muscle protein reserve. There was an increase in glucose uptake, CK increased activity, and a clear increase of LDH activity in red muscle of fish with cadmium exposure. Since no alterations were observed in lipoperoxide concentration, while antioxidant enzymes glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were changed in the liver and the red and white muscle of fish with cadmium exposure, we can conclude that oxygen free radicals are produced as a mediator of cadmium toxicity. Resistance development is related with increased activities of antioxidant enzymes, which were important in the protection against cadmium damage, inhibiting lipoperoxide formation. (C) 2002 Elsevier B.V. Ltd. All rights reserved.

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The contamination of water by metal compounds is a worldwide environmental problem. Concentrations of metals are widely related to biochemical values which are used in disease diagnosis due to environmental toxicity. The acute combined effects of cadmium and nickel on biochemical parameters were determined and compared with those of Cd2+ or Ni2+ alone in rats. Male adult rats were given drinking solutions of CdCl2 [Cd(II) cation, 100 mg/liter] or NiSO4 [Ni(II) cation, 100 mg/liter]. For the combined treatment, the animals (Ni+Cd) received both Ni(II)) cation (100 mg/liter) and Cd(II) cation (100 mg/liter). Nickel treatment induced increased alanine transaminase (ALT) activity and hepatotoxicity, but not renal injury. In contrast, cadmium exposure produced hepatic, renal and myocardial damage, characterized by increased creatinine, total and direct bilirubin concentrations and increased ALT and lactate dehydrogenase (LDH) activities. The combined effect Ni-Cd is less toxic than cadmium alone, suggesting antagonism between these toxicants. The toxicity of nickel and cadmium, alone and in combination, decreased Cu-Zn superoxide dismutase (SOD) activity and increased lipoperoxide formation. (C) 1998 Elsevier B.V. Ltd. All rights reserved.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Environmental toxicants and stress influence the health and behavior of people from different parts of the world. In the present study, aggressive behavior was evaluated in rats exposed to cadmium (Cd) for four weeks and subjected to immobilization stress (IS) based on the resident/intruder paradigm. Latency to the first bite (LB), total number of attacks (NA), total duration of attack manifestations (DAM), and a composite aggression score (CAS) were used to assess aggressiveness. Cadmium concentrations in the blood and the brain were determined. We observed that the parameters of aggressiveness were not altered by either Cd or IS when administered separately. However, animals exposed to Cd + IS had increased NA, DAM, and CAS. Cadmium was detected in the blood and the brain after treatment and Cd + IS exposure modified Cd distribution in these tissues. These results suggest that exposure to low levels of Cd associated with stress may lead to increased aggressiveness in rats. (C) 2011 Elsevier B.V. All rights reserved.

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