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1.
Toxicol Rep ; 2: 858-863, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-28962421

RESUMO

Cadmium (Cd) is a known hepato- and nephrotoxic pollutant and zinc (Zn) metalloproteins are important targets of Cd. Hence, the administration of Zn may mitigate Cd toxic effects. However, the interaction of Cd and Zn has been little investigated in the brain. Previously, we reported a protective effect of Zn on mortality caused by Cd in rats. Here, we tested whether the protective effect of Zn could be related to changes in brain Zn-proteins, metallothionein (MT) and δ-aminolevulinate dehydratse (δ-ALA-D). Male adult rats were daily administered for 10 days with Zn (2 mg kg-1), Cd (0.25 and 1 mg kg-1) and 0.25 mg kg-1 of Cd plus Zn and 1 mg kg-1 of Cd plus Zn. The body weight loss, food intake deprivation, and mortality occurred in 1 mg kg-1 of Cd, but Zn co-administration did mitigate these effects. The brain Zn content was not modified by treatment with Cd, whereas cerebral Cd levels increased in animals exposed to Cd. The administration of 0.25 mg kg-1 of Cd (with or without Zn) induced lipid peroxidation and decreased MT concentration, but 2 mg kg-1 of Zn and 1 mg kg-1 of Cd did not change these parameters. Brain δ-ALA-D was not modified by Cd and/or Zn treatments. Since the co-administration of Zn did not attenuate the changes induced by Cd in the brain, our results suggest that the protective effect of Zn on impairments caused by Cd in animal status is weakly related to a cerebral interaction of these metals.

2.
J Appl Toxicol ; 32(1): 20-5, 2012 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-21360559

RESUMO

Cadmium (Cd) is a pollutant that is harmful to human and animals. The liver is a target for Cd accumulation and it can disrupt Zn homeostasis. Here we examined the interaction of Zn and Cd to determine how these two metals could affect δ-aminolevulinate-dehydratase (δ-ALA-D) and metallothionein (MT), two potential molecular endpoints for Cd hepatotoxicity. Cd exposure (0.25 and 1 mg kg1 body weight, i.p., for 10 days) caused a marked increase in hepatic Zn deposition, which was not modified by treatment with Zn (2 mg kg1 , i.p.). Cd caused a dose-dependent increase in hepatic Cd content that was not modified by Zn. Zn and/or Cd treatment increased hepatic δ-ALA-D activity, although the increase caused by Cd was less marked. Reactivation index of δ-ALA-D by DTT was decreased by Zn and Cd exposure, which indicates that Zn protects enzyme from oxidation. Hepatic MT was increased only after exposure to 1 mg kg(-1) Cd and Zn reduced the stimulation of MT synthesis. The results presented here indicate that Cd can redistribute Zn from non-hepatic tissues to liver and the increase in hepatic Zn deposition can account for the increase in hepatic δ-ALA-D activity after Cd exposure. However, Zn blocked the increase in hepatic MT levels caused by Cd. Thus, the modulation of the two molecular endpoints of Cd toxicity used here was distinct, which indicates that the mechanism(s) involved in Zn and Cd distribution, δ-ALA-D and MT regulation are not coincident.


Assuntos
Cádmio/toxicidade , Poluentes Ambientais/toxicidade , Fígado/efeitos dos fármacos , Metalotioneína/metabolismo , Sintase do Porfobilinogênio/metabolismo , Zinco/farmacologia , Análise de Variância , Animais , Peso Corporal/efeitos dos fármacos , Cádmio/farmacocinética , Relação Dose-Resposta a Droga , Poluentes Ambientais/farmacocinética , Fígado/enzimologia , Fígado/metabolismo , Masculino , Ratos , Ratos Wistar , Zinco/farmacocinética
3.
Rev. bras. toxicol ; 19(1): 12-16, 2006. tab, graf
Artigo em Português | LILACS | ID: lil-467157

RESUMO

Organochlorine residues were analyzed in human blood. Samples were collected from 122 individuals. Tissues donors were groupes according to their place of residency in two groups: one urban and one of residents of areas of intensive agricultural activity: all individuals were from the state of Rio Grande do Sul, Brazil. The following organochlorine residue were analyzed: ‡-HCH; ƒÁ-HCH; Aldrin; Dieldrin Endrin;Heptachloride: Epoxi Heptacloride; HCB; Mirex; o,p DDD; o,p DDT; Oxychlordane; p.p metoxychlor; p,p DDD; p.p DDE; p,p DDT, aqnd Transnonachlor (Detection limit = 0,010 ƒÊg/L). All individuals completed a questionnaire on age, sex, weight, occupation, place of residency, and contact with pesticides. All urban samples were negative for the organochlorines analyzed. Samples collected in the areas of agricultural activity were positive on a 10.5 per cent level. The results of the analyses of the present study were compared to results of previus studies also carried out in Rio Grande do Sul. This comparison showed a decrease over time in the incidence of organochlorines...


Assuntos
Humanos , Inseticidas Organoclorados/análise , Sangue
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