title: Food deprivation promotes oxidative imbalance in rat brain.
abstract: The present study was aimed to evaluate the effect of food deprivation in brain oxidative status of Wistar and Goto-Kakizaki (GK) rats. For this purpose, we evaluated several oxidative stress parameters: lipid peroxidation (thiobarbituric acid reactive substances [TBARS]) and protein oxidation markers, hydrogen peroxide (H(2)O(2)) levels, nonenzymatic (reduced [GSH] and oxidized glutathione [GSSG] and vitamin E) and enzymatic (glutathione peroxidase [GPx], glutathione reductase [GRed], and manganese superoxide dismutase [MnSOD]) antioxidant defenses. Four-mo-old Wistar and GK rats were divided into 2 groups. One group of each rat strain was maintained under normal diet and the other groups were maintained under 50% food deprivation during 2 mo. GK rats under normal diet presented lower levels of vitamin E and higher GRed activity and GSH/GSSG ratio when compared with Wistar control rats. In Wistar rats, food deprivation induced a significant decrease in vitamin E levels and a significant increase in GPx activity, H(2)O(2) production, and TBARS formation in the presence of the prooxidant pair ADP/Fe(2+). However, GK rats under food deprivation presented a significant decrease in vitamin E levels and GRed activity and a significant increase in H(2)O(2) production when compared with GK under normal diet. In summary, our results indicate that food deprivation affects brain oxidative status, which could predispose brain cells to degeneration and death.
authors.affiliation: Dept. of Zoology, Coimbra Univ. Hospital, Univ. of Coimbra, Portugal.
authors.forename: R X
authors.initials: RX
authors.lastname: Santos
authors.forename: S
authors.initials: S
authors.lastname: Cardoso
authors.forename: S
authors.initials: S
authors.lastname: Silva
authors.forename: S
authors.initials: S
authors.lastname: Correia
authors.forename: C
authors.initials: C
authors.lastname: Carvalho
authors.forename: J
authors.initials: J
authors.lastname: Crisóstomo
authors.forename: L
authors.initials: L
authors.lastname: Rodrigues
authors.forename: C
authors.initials: C
authors.lastname: Amaral
authors.forename: T
authors.initials: T
authors.lastname: Louro
authors.forename: P
authors.initials: P
authors.lastname: Matafome
authors.forename: M S
authors.initials: MS
authors.lastname: Santos
authors.forename: T
authors.initials: T
authors.lastname: Proença
authors.forename: A I
authors.initials: AI
authors.lastname: Duarte
authors.forename: R
authors.initials: R
authors.lastname: Seiça
authors.forename: P I
authors.initials: PI
authors.lastname: Moreira
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism*; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D005508:Food Deprivation; D005978:Glutathione / Q000378:metabolism*; D019803:Glutathione Disulfide / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism*; D015227:Lipid Peroxidation; D008297:Male; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014810:Vitamin E / Q000378:metabolism*
chemical_list: D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D006861:Hydrogen Peroxide; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005978:Glutathione; D019803:Glutathione Disulfide