title: Oxidative stress and antioxidant defenses after prolonged starvation in Dentex dentex liver.
abstract: The aim of this work was to evaluate the effects of prolonged starvation and refeeding on antioxidant status and some metabolic-related parameters in common dentex (Dentex dentex) liver. Fish deprived of food for 5 weeks showed a significant increase in lipid peroxidation, measured as malondialdehyde (MDA) levels. The activity of the antioxidative enzymes superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPX) in starved fish significantly increased (by 42%, 22%, and 52%, respectively), whereas glutathione reductase (GR) activity was significantly depressed by 53% compared to controls. No qualitative changes in the SOD isoenzymatic pattern were detected by nondenaturing PAGE analysis, but the isoforms corresponding to CuZn-SOD I and II were enhanced in starved fish. The activity of the enzymes indicative of oxidative metabolism, beta-hydroxyacyl CoA dehydrogenase (HOAD) and citrate synthase (CS), significantly increased (by 123% and 28%, respectively), and that of glucose-6-phosphate dehydrogenase (G6PDH) was inhibited by 56%. Oxidative damage under these circumstances is reversible since all biomarkers assayed returned to control values after refeeding. Our results show that prolonged starvation leads to a pro-oxidant situation and oxidative stress despite activation of antioxidant defense mechanisms, and that inhibition of G6PDH activity might be responsible for this failure in cellular antioxidant defenses.
authors.affiliation: Departamento de Biología Animal y Ecología, Facultad de Ciencias, Universidad de Granada, Avenida Fuentenueva s/n, 18071 Granada, Spain. amaenca@ugr.es
authors.forename: Amalia E
authors.initials: AE
authors.lastname: Morales
authors.forename: Amalia
authors.initials: A
authors.lastname: Pérez-Jiménez
authors.forename: M Carmen
authors.initials: MC
authors.lastname: Hidalgo
authors.forename: Emilia
authors.initials: E
authors.lastname: Abellán
authors.forename: Gabriel
authors.initials: G
authors.lastname: Cardenete
mesh_terms: D015094:3-Hydroxyacyl CoA Dehydrogenases / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D015415:Biomarkers / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D002950:Citrate (si)-Synthase / Q000378:metabolism; D005399:Fishes / Q000502:physiology*; D005502:Food; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D007527:Isoenzymes / Q000378:metabolism; D015227:Lipid Peroxidation; D008099:Liver / Q000201:enzymology*; D008315:Malondialdehyde / Q000032:analysis; D018384:Oxidative Stress; D013217:Starvation; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D007527:Isoenzymes; D008315:Malondialdehyde; D015094:3-Hydroxyacyl CoA Dehydrogenases; D005954:Glucosephosphate Dehydrogenase; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D002950:Citrate (si)-Synthase