Premium
Walker‐256 tumor growth causes oxidative stress in rat brain
Author(s) -
Freitas Jofre J. S.,
Pompéia Celine,
Miyasaka Célio K.,
Curi Rui
Publication year - 2001
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2001.00280.x
Subject(s) - tbars , endocrinology , oxidative stress , medicine , superoxide dismutase , chemistry , catalase , glutathione peroxidase , antioxidant , thiobarbituric acid , biochemistry , lipid peroxidation , biology
The elevated rate of oxygen consumption and high amount of polyunsaturated fatty acids make the central nervous system vulnerable to oxidative stress. The effect of Walker‐256 tumor growth on oxi–reduction indexes in the hypothalamus (HT), cortex (CT), hippocampus (HC) and cerebellum (CB) of male Wistar rats was investigated. The presence of the tumor caused an increase in thiobarbituric acid reactant substances (TBARs) in the HT, CB and HC. Due to tumor growth, the activity of glucose‐6‐phosphate dehydrogenase increased in the HT and CB, whereas citrate synthase activity was reduced in the HT, CT and CB. Therefore, the potential for generation of reducing power is increased in the cytosol and decreased in the mitochondria of various brain regions of Walker‐256 tumor‐bearing rats. These changes occurred concomitantly with an unbalance in the brain enzymatic antioxidant system. The tumor decreased the activities of catalase in the HT and CB and of glutathione peroxidase in the HT, CB and HC, and raised the CuZn‐superoxide dismutase activity in the HT, CB and HC. These combined findings indicate that Walker‐256 tumor growth causes oxidative stress in the brain.