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Oral administration of diphenyl diselenide protects against cadmium-induced liver damage in rats.
Chem Biol Interact. 2008 Jan 10; 171(1):15-25.CB

Abstract

Cadmium is an environmental toxic metal implicated in human diseases. In the present study, the effect of diphenyl diselenide, (PhSe)(2), on sub-chronic exposure with cadmium chloride (CdCl(2)) was investigated in rats. Male adult Swiss albino rats received CdCl(2) (10 micromol/kg, orally) and (PhSe)(2) (5 micromol/kg, orally) for a period of 30 days. A number of parameters were examined as indicators of toxicity, including hepatic and renal damage, glucose and glycogen levels and markers of oxidative stress. Cadmium content, liver histology, delta-aminolevulinate dehydratase (delta-ALA-D) activity, metallothionein (MT) levels were also evaluated. Cadmium content determined in the tissue of rats exposed to CdCl(2) provides evidence that the liver is the major cadmium target where (PhSe)(2) acts. The concentration of cadmium in liver was about three fold higher than that in kidney, and (PhSe)(2) reduced about six fold the levels of this metal in liver of rats exposed. Rats exposed to CdCl(2) showed histological alterations abolished by (PhSe)(2) administration. (PhSe)(2) administration ameliorated plasma malondialdehyde (MDA) levels, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and gamma-glutamyl transferase (GGT) activities increased by CdCl(2) exposure. Urea and bilirubin levels increased by CdCl(2) exposure were also reduced by (PhSe)(2). In conclusion, this study demonstrated that co-treatment with (PhSe)(2) ameliorated hepatotoxicity and cellular damage in rat liver after sub-chronic exposure with CdCl(2). The proposed mechanisms by which (PhSe)(2) acts in this experimental protocol are its antioxidant properties and its capacity to form a complex with cadmium.

Authors+Show Affiliations

Departamento de Química, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria CEP 97105-900, RS, Brazil.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17950719

Citation

Borges, Lysandro Pinto, et al. "Oral Administration of Diphenyl Diselenide Protects Against Cadmium-induced Liver Damage in Rats." Chemico-biological Interactions, vol. 171, no. 1, 2008, pp. 15-25.
Borges LP, Brandão R, Godoi B, et al. Oral administration of diphenyl diselenide protects against cadmium-induced liver damage in rats. Chem Biol Interact. 2008;171(1):15-25.
Borges, L. P., Brandão, R., Godoi, B., Nogueira, C. W., & Zeni, G. (2008). Oral administration of diphenyl diselenide protects against cadmium-induced liver damage in rats. Chemico-biological Interactions, 171(1), 15-25.
Borges LP, et al. Oral Administration of Diphenyl Diselenide Protects Against Cadmium-induced Liver Damage in Rats. Chem Biol Interact. 2008 Jan 10;171(1):15-25. PubMed PMID: 17950719.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oral administration of diphenyl diselenide protects against cadmium-induced liver damage in rats. AU - Borges,Lysandro Pinto, AU - Brandão,Ricardo, AU - Godoi,Benhur, AU - Nogueira,Cristina W, AU - Zeni,Gilson, Y1 - 2007/09/19/ PY - 2007/06/12/received PY - 2007/09/06/revised PY - 2007/09/07/accepted PY - 2007/10/24/pubmed PY - 2008/4/4/medline PY - 2007/10/24/entrez SP - 15 EP - 25 JF - Chemico-biological interactions JO - Chem Biol Interact VL - 171 IS - 1 N2 - Cadmium is an environmental toxic metal implicated in human diseases. In the present study, the effect of diphenyl diselenide, (PhSe)(2), on sub-chronic exposure with cadmium chloride (CdCl(2)) was investigated in rats. Male adult Swiss albino rats received CdCl(2) (10 micromol/kg, orally) and (PhSe)(2) (5 micromol/kg, orally) for a period of 30 days. A number of parameters were examined as indicators of toxicity, including hepatic and renal damage, glucose and glycogen levels and markers of oxidative stress. Cadmium content, liver histology, delta-aminolevulinate dehydratase (delta-ALA-D) activity, metallothionein (MT) levels were also evaluated. Cadmium content determined in the tissue of rats exposed to CdCl(2) provides evidence that the liver is the major cadmium target where (PhSe)(2) acts. The concentration of cadmium in liver was about three fold higher than that in kidney, and (PhSe)(2) reduced about six fold the levels of this metal in liver of rats exposed. Rats exposed to CdCl(2) showed histological alterations abolished by (PhSe)(2) administration. (PhSe)(2) administration ameliorated plasma malondialdehyde (MDA) levels, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and gamma-glutamyl transferase (GGT) activities increased by CdCl(2) exposure. Urea and bilirubin levels increased by CdCl(2) exposure were also reduced by (PhSe)(2). In conclusion, this study demonstrated that co-treatment with (PhSe)(2) ameliorated hepatotoxicity and cellular damage in rat liver after sub-chronic exposure with CdCl(2). The proposed mechanisms by which (PhSe)(2) acts in this experimental protocol are its antioxidant properties and its capacity to form a complex with cadmium. SN - 0009-2797 UR - https://www.unboundmedicine.com/medline/citation/17950719/Oral_administration_of_diphenyl_diselenide_protects_against_cadmium_induced_liver_damage_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0009-2797(07)00287-6 DB - PRIME DP - Unbound Medicine ER -