title: Low toxicity of diphenyl diselenide in rabbits: a long-term study.
abstract: Selenium compounds, like diphenyl diselenide (Ph(2)Se(2)), possess glutathione peroxidase (GSHPx)-like activities and other antioxidant properties. The aim of this study was to evaluate the effects of a long-term oral supplementation with Ph(2)Se(2) on various toxicological parameters in rabbits. Adult New Zealand male rabbits were divided into four groups: Group I served as control; Groups II, III and IV received 0.3, 3.0 and 30 p.p.m. of Ph(2)Se(2) pulverized in the chow for 8 months. A number of toxicological parameters were examined in liver, kidney, cerebral cortex and hippocampus, such as delta-aminolaevulinic acid dehydratase (delta-ALA-D), catalase (CAT), GSHPx activities, non-protein thiol (-SH), lipid peroxidation and ascorbic acid levels. The results indicated that supplementation 30 p.p.m. Ph(2)Se(2 )significantly increased delta-ALA-D activity in liver and in cerebral cortex. Non-protein -SH levels were significantly increased in liver but not in kidney, cerebral cortex and hippocampus of rabbits. Ascorbic acid content was significantly lower in the liver and cerebral cortex after supplementation with 30 p.p.m. Ph(2)Se(2). Conversely, no alterations in GSHPx and CAT activities, nor in thiobarbituric acid reactive substances levels were observed in rabbit tissues. These results indicate that oral supplementation with Ph(2)Se(2) is relatively secure in rabbits after 8 months of exposure. The findings encourage further experiments on the potential therapeutic effects of such compound.
authors.affiliation: Department of Clinical and Toxicological Analysis, Center for Health Sciences, Federal University of Santa Maria, Santa Maria, RS, Brazil. debemandreza@yahoo.com.br
authors.forename: Andreza Fabro
authors.initials: AF
authors.lastname: de Bem
authors.forename: Rafael
authors.initials: R
authors.lastname: de Lima Portella
authors.forename: Marcelo
authors.initials: M
authors.lastname: Farina
authors.forename: Juliano
authors.initials: J
authors.lastname: Perottoni
authors.forename: Márcio Weber
authors.initials: MW
authors.lastname: Paixão
authors.forename: Cristina Wayne
authors.initials: CW
authors.lastname: Nogueira
authors.forename: João Batista
authors.initials: JB
authors.lastname: Teixeira Rocha
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000009:adverse effects* / Q000493:pharmacokinetics; D001205:Ascorbic Acid / Q000378:metabolism; D001555:Benzene Derivatives / Q000009:adverse effects* / Q000493:pharmacokinetics; D001921:Brain / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005979:Glutathione Peroxidase / Q000378:metabolism; D007668:Kidney / Q000378:metabolism*; D015227:Lipid Peroxidation / Q000502:physiology; D008099:Liver / Q000378:metabolism*; D008297:Male; D016566:Organoselenium Compounds / Q000009:adverse effects* / Q000493:pharmacokinetics; D000623:Porphobilinogen Synthase / Q000378:metabolism; D011817:Rabbits; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013997:Time Factors
chemical_list: D000975:Antioxidants; D001555:Benzene Derivatives; D016566:Organoselenium Compounds; D017392:Thiobarbituric Acid Reactive Substances; C061132:diphenyldiselenide; D002374:Catalase; D005979:Glutathione Peroxidase; D000623:Porphobilinogen Synthase; D001205:Ascorbic Acid