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Time course of skeletal muscle loss and oxidative stress in rats with walker 256 solid tumor
Author(s) -
Guarnier Flávia A.,
Cecchini Alessandra L.,
Suzukawa Andréia A.,
Maragno Ana Leticia G.C.,
Simão Andréa N.C.,
Gomes Marcelo D.,
Cecchini Rubens
Publication year - 2010
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.21798
Subject(s) - oxidative stress , superoxide dismutase , skeletal muscle , chemistry , endocrinology , glutathione , medicine , reactive oxygen species , antioxidant , wasting , cachexia , muscle atrophy , sod2 , superoxide , biochemistry , biology , enzyme , cancer
Reactive oxygen species oxidize proteins and modulate the proteasomal system in muscle‐wasting cancer cachexia. On day 5 (D5), day 10 (D10), and day 14 (D14) after tumor implantation, skeletal muscle was evaluated. Carbonylated proteins and thiobarbituric acid reactive substances were measured. Chemiluminescence was employed for lipid hydroperoxide estimation. Glutathione, superoxide dismutase, and total radical antioxidant capacity were evaluated. The proteasomal system was assessed by mRNA atrogin‐1 expression. Increased muscle wasting, lipid hydroperoxide, and superoxide dismutase, and decreased glutathione levels and total radical antioxidant capacity, were found on D5 in accordance with increased mRNA atrogin‐1 expression. All parameters were significantly modified in animals treated with α‐tocopherol. The elevation in aldehylde levels and carbonylated proteins observed on D10 were reversed by α‐tocopherol treatment. Oxidative stress may trigger signal transduction of the proteasomal system and cause protein oxidation. These pathways may be associated with the mechanism of muscle wasting that occurs in cancer cachexia. Muscle Nerve 42: 950–958, 2010