INVESTIGADORES
SCHVEZOV Natasha
congresos y reuniones científicas
Título:
Effect of feeding and digestion on oxidative stress in rainbow trout
Autor/es:
M. URBINA; N. SCHVEZOV; R.W. WILSON
Lugar:
cracovia
Reunión:
Congreso; The 9th International Congress of Comparative Physiology and Biochemistry: From Molecules to Macrophysiology; 2015
Institución organizadora:
Jagiellonian University in Krakow
Resumen:
Feeding is fundamental to all animals and involves several elements suchas hunting/foraging, ingestion, mechanical processing, digestion, nutrientabsorption, assimilation, growth, excretion etc. Feeding is considered a majorenergetic challenge for fish, and owing to the magnitude of this post prandialenhancement of metabolism it has been proposed as a significant mechanismof cellular death and ageing (Sohal and Weindruch, 1996). The production ofreactive oxygen species (ROS) post-feeding should therefore affect longevity. Toour knowledge, however, ROS damage and antioxidant defences have not beenstudies during a feeding cycle in fish. We used adult rainbow trout at 15 °C andvoluntarily feeding on a 3 % single ration per week, to quantify ROS damage andantioxidant defenses 24 h before feeding and after 1.5, 6, 24, 48, 72 and 96 h postfeedingin gills, stomach, intestine and liver. The enzymatic activities of superoxidedismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) were determined as a proxy for antioxidant defenses, whilelipid peroxidation (LPO), protein oxidation (PO) in the same tissues, and DNAdamage (in red blood cells only) were determined as a proxy of oxidative damage.Tissue specific differences were found in the antioxidant defenses, with liver andintestine showing the highest and gills showing the lowest. Overall our resultsshow no major changes in the ROS damage or in the antioxidant defenses duringa feeding cycle. DNA damage in red blood cells, however, showed lowest damagebetween 48 to 96 h post feeding, increasing between 24 h pre-feeding and 24post feeding. Our results show no evidence of the proposed mechanism by whichfeeding would have a major influence on longevity via the induction of oxidativestress.