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Diphenyl diselenide reverses cadmium-induced oxidative damage on mice tissues.
Chem Biol Interact. 2005 Feb 10; 151(3):159-65.CB

Abstract

The concept that selenium-containing molecules may be better antioxidants than classical antioxidants, has led to the design of synthetic organoselenium compounds. In the present investigation subchronic deleterious effects of cadmium-intoxication in mice and a possible protective effect of diphenyl diselenide (PhSe)2 (5 micromol/kg) were studied. Male adult Swiss albino mice (25-35 g) received CdCl2 (10 micromol/kg, subcutaneously), five times/week, for 4 weeks. A number of toxicological parameters in blood, liver, kidney, spleen and brain of mice were examined including delta-aminolevulinic acid dehydratase (delta-ALA-D) activity, lipid peroxidation and ascorbic acid content, the parameters that indicate tissue damage such as plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea, creatinine and lactate dehydrogenase (LDH) were also determined. The results demonstrated that cadmium caused inhibition of delta-ALA-D activity in liver (24%), kidney (33%) and spleen (73%) and (PhSe)2 therapy was effective in restoring enzyme activity in all tissues. A reduction in ascorbic acid content was observed in kidney (11%) and spleen (10.7%) of cadmium-treated mice and (PhSe)2 was only effective in improving this reduction in kidney. An increase of lipid peroxidation induced by cadmium was noted in liver (29%) and brain (28%) tissues and (PhSe)2 therapy was effective in restoring TBARS levels in both tissues. We also observed an increase on plasma LDH (1.99-times), AST (1.93-times) and ALT (4.24-times) activities. (PhSe)2 therapy was effective in restoring AST activity at control level. (PhSe)2 did not present toxic effects when plasma parameters were evaluated. The results suggest that the administration of an antioxidant (PhSe)2, during cadmium intoxication may provide beneficial effects by reducing oxidative stress in tissues.

Authors+Show Affiliations

Departamento de Quimica, Centro de Ciencias 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 availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

15733537

Citation

Santos, Francielli W., et al. "Diphenyl Diselenide Reverses Cadmium-induced Oxidative Damage On Mice Tissues." Chemico-biological Interactions, vol. 151, no. 3, 2005, pp. 159-65.
Santos FW, Zeni G, Rocha JB, et al. Diphenyl diselenide reverses cadmium-induced oxidative damage on mice tissues. Chem Biol Interact. 2005;151(3):159-65.
Santos, F. W., Zeni, G., Rocha, J. B., Weis, S. N., Fachinetto, J. M., Favero, A. M., & Nogueira, C. W. (2005). Diphenyl diselenide reverses cadmium-induced oxidative damage on mice tissues. Chemico-biological Interactions, 151(3), 159-65.
Santos FW, et al. Diphenyl Diselenide Reverses Cadmium-induced Oxidative Damage On Mice Tissues. Chem Biol Interact. 2005 Feb 10;151(3):159-65. PubMed PMID: 15733537.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Diphenyl diselenide reverses cadmium-induced oxidative damage on mice tissues. AU - Santos,Francielli W, AU - Zeni,Gilson, AU - Rocha,Joao B T, AU - Weis,Simone N, AU - Fachinetto,Juliana M, AU - Favero,Alexandre M, AU - Nogueira,Cristina W, Y1 - 2005/01/28/ PY - 2004/11/04/received PY - 2005/01/04/revised PY - 2005/01/04/accepted PY - 2005/3/1/pubmed PY - 2005/4/23/medline PY - 2005/3/1/entrez SP - 159 EP - 65 JF - Chemico-biological interactions JO - Chem Biol Interact VL - 151 IS - 3 N2 - The concept that selenium-containing molecules may be better antioxidants than classical antioxidants, has led to the design of synthetic organoselenium compounds. In the present investigation subchronic deleterious effects of cadmium-intoxication in mice and a possible protective effect of diphenyl diselenide (PhSe)2 (5 micromol/kg) were studied. Male adult Swiss albino mice (25-35 g) received CdCl2 (10 micromol/kg, subcutaneously), five times/week, for 4 weeks. A number of toxicological parameters in blood, liver, kidney, spleen and brain of mice were examined including delta-aminolevulinic acid dehydratase (delta-ALA-D) activity, lipid peroxidation and ascorbic acid content, the parameters that indicate tissue damage such as plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea, creatinine and lactate dehydrogenase (LDH) were also determined. The results demonstrated that cadmium caused inhibition of delta-ALA-D activity in liver (24%), kidney (33%) and spleen (73%) and (PhSe)2 therapy was effective in restoring enzyme activity in all tissues. A reduction in ascorbic acid content was observed in kidney (11%) and spleen (10.7%) of cadmium-treated mice and (PhSe)2 was only effective in improving this reduction in kidney. An increase of lipid peroxidation induced by cadmium was noted in liver (29%) and brain (28%) tissues and (PhSe)2 therapy was effective in restoring TBARS levels in both tissues. We also observed an increase on plasma LDH (1.99-times), AST (1.93-times) and ALT (4.24-times) activities. (PhSe)2 therapy was effective in restoring AST activity at control level. (PhSe)2 did not present toxic effects when plasma parameters were evaluated. The results suggest that the administration of an antioxidant (PhSe)2, during cadmium intoxication may provide beneficial effects by reducing oxidative stress in tissues. SN - 0009-2797 UR - https://www.unboundmedicine.com/medline/citation/15733537/Diphenyl_diselenide_reverses_cadmium_induced_oxidative_damage_on_mice_tissues_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0009-2797(05)00003-7 DB - PRIME DP - Unbound Medicine ER -