TY - JOUR
T1 - Food Deprivation Promotes Oxidative Imbalance in Rat Brain
AU - Santos, RX
AU - Cardoso, S
AU - Silva, S
AU - Correia, S
AU - Carvalho, C
AU - Crisóstomo, J
AU - Rodrigues, L
AU - Amaral, C
AU - Louro, T
AU - Matafome, P
AU - Santos, MS
AU - Proença, T
AU - Duarte, AI
AU - Seiça, R
AU - Moreira, PI
PY - 2009/1
Y1 - 2009/1
N2 - 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 (H2O2) 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, H2O2 production, and TBARS formation in the presence of the prooxidant pair ADP/Fe2+. However, GK rats under food deprivation presented a significant decrease in vitamin E levels and GRed activity and a significant increase in H2O2 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.
AB - 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 (H2O2) 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, H2O2 production, and TBARS formation in the presence of the prooxidant pair ADP/Fe2+. However, GK rats under food deprivation presented a significant decrease in vitamin E levels and GRed activity and a significant increase in H2O2 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.
KW - brain
KW - food deprivation
KW - oxidative stress
KW - type 2-diabetes
UR - http://europepmc.org/abstract/med/19200099
U2 - 10.1111/j.1750-3841.2008.00982.x
DO - 10.1111/j.1750-3841.2008.00982.x
M3 - Article
C2 - 19200099
SN - 0022-1147
VL - 74
SP - H8-H14
JO - Journal of Food Science
JF - Journal of Food Science
IS - 1
ER -
