Interaction between copper and zinc in metal accumulation in rats with particular reference to the synthesis of induced-metallothionein

The effectiveness of Zn at moderating the pro-oxidant effects of Cu was evaluated in two rat models that differed in the route and mode of administration. The endpoints investigated included measurement of the concentrations of Cu, Zn, metallothionein and glutathione concentrations, as well as SOD and catalase activity, in liver, kidneys and intestine. In a sub-chronic animal model, the hepatic accumulation of Cu was achieved by administration of dietary Cu (1.8 g/kg solid diet) for 30 days after which oral Zn (6 g/kg solid diet) was given. Cu treatment induced an increase in the hepatic and intestinal concentration of Cu of 66 and 455%, respectively, that was not associated with synthesis of metallothionein synthesis, but rather appeared to be related to the higher activity of SOD. Subsequent administration with Zn after dietary Cu induced an increase in the hepatic and intestinal metallothionein content of more twice and reduced the Cu content to control values. Thus, Zn could act as both a competitor for absorption on the luminal side of the intestinal epithelium inducing the synthesis of metallothionein. In the second animal model, we studied the effects of interaction between Cu and Zn administered by i.p. injection at the dose of 3 and 10 mg/kg, respectively; Zn was administered subsequent to Cu overload. In this case, when Zn was administered, Cu was already deposited in tissues and thus there is no competition between two metals at the level of membrane transport. In this experimental model treatment with Cu alone induced liver metallothionein synthesis, and the subsequent treatment with Zn did not decrease the hepatic content of Cu. One explanation for these observations is that Zn induces the synthesis of metallothionein, which binds Cu for which it has a higher affinity. Moreover, after treatment with Zn, SOD activity in the liver decreases of almost 30% with respect to treatment with alone Cu, suggesting that Zn has a protective effect. (c) 2005 Elsevier Ireland Ltd. All rights reserved

Effects of cadmium on catfish, Ictalurus melas, humoral immune response

Catfish (I. melas) were exposed to 10, 20 or 30 \u3bcg 1-1 of cadmium (CdCl2) toassess its in vivo effects on the humoral immune response. After one week of cadmium exposure, the titer of total non-specific immunoglobulins was remarkably reduced but, after 2 weeks of exposure the IgM titer increased, and no differences between treated and control fish could be observed. Immunization of catfish with sheep red blood cells (SRBC) was also performed to assess the effect of cadmium on the immune response to a specific antigen. Fish exposed to cadmium (20 \u3bcg 1-1) required a shorter period to reach the peak of IgM anti-SRBC titer; moreover, fish exposed to Cd for 2 weeks before immunization reached peak antibody response more quickly and also revealed a remarkable increase in antibody titer

Effects of cadmium on lymphocyte proliferation and macrophage activation in catfish, Ictalurus melas

The effects of cadmium (Cd) (in vitroandin vivo) on phytohaemoagglutinin(PHA)- or lipopolysaccharide(LPS)-induced lymphocyte proliferation were investigated in the catfish,Ictalurus melas. The effects of Cd on macrophage activation by Concanavallina A orSaccharomyces cerevisiae, as measured by superoxide (O2-) production, were investigated. Dose-independent (except at 2 \u3bcmCd) inhibition of T cell stimulation and dose-dependent inhibition of B cell stimulation, by lymphocytes exposedin vitroto 2-40 \u3bcmCd, was found.In vivo, 20 \u3bcg l-1Cd inhibited both PHA- and LPS-induced lymphocyte proliferation, at 4 days of exposure and throughout the duration of the experiment. During the first week of exposure, Cd significantly decreased spontaneous3H-methyl-thymidine uptake from unstimulated lymphocytes; however, 15 days after exposure unstimulated cells recovered their basal level of spontaneous thymidine uptake.In vitro2-40 \u3bcmCd enhanced O2-production by activated macrophages, while the addition of 50-100 \u3bcmCd had no significant effects

Effects of cadmium on catfish, Ictalurus melas, humoral immune responses

Catfish (I. melas) were exposed to 10, 20 or 30 \u3bcg 1-1 of cadmium (CdCl2) toassess its in vivo effects on the humoral immune response. After one week of cadmium exposure, the titer of total non-specific immunoglobulins was remarkably reduced but, after 2 weeks of exposure the IgM titer increased, and no differences between treated and control fish could be observed. Immunization of catfish with sheep red blood cells (SRBC) was also performed to assess the effect of cadmium on the immune response to a specific antigen. Fish exposed to cadmium (20 \u3bcg 1-1) required a shorter period to reach the peak of IgM anti-SRBC titer; moreover, fish exposed to Cd for 2 weeks before immunization reached peak antibody response more quickly and also revealed a remarkable increase in antibody titer

Effect of in vitro cadmium exposure on natural killer (NK) cells of catfish, Ictalurus melas

The effect of in vitro cadmium exposure on catfish natural killer (NK) cells was investigated. Purification of NK cells by nylon-wool columns and density gradient centrifugation indicated that they were a population of nylon-wool adherent cells. Subsequently NK cells were separated only by density gradient centrifugation, where these cells band at the 43/45\ub75% Percoll interface. In some cytotoxicity assays, catfish NK cells were exposed to 5, 10, 30 and 50 \u3bcM cadmium (CdCl2); 10 \u3bcl of Cd solutions were added to NK cells simultaneously with the target cells. In vitro, 5 \u3bcM Cd inhibited the ability of catfish NK cells to kill the human erythroleukemic cell line K-562. In the presence of 10 \u3bcM Cd, the antibody-independent cytotoxic activity was totally suppressed