title: Evaluation of the protection exerted by Pisum sativum Ferredoxin-NADP(H) Reductase against injury induced by hypothermia on Cos-7 cells.
abstract: Hypothermia is employed as a method to diminish metabolism rates and preserve tissues and cells. However, low temperatures constitute a stress that produces biochemical changes whose extension depends on the duration and degree of cold exposure and is manifested when physiological temperature is restored. For many cellular types, cold induces an oxidative stress that is dependent on the elevation of intracellular iron, damages macromolecules, and is prevented by the addition of iron chelators. Pisum sativum Ferredoxin-NADP(H) Reductase (FNR) has been implicated in protection from injury mediated by intracellular iron increase and successfully used to reduce oxidative damage on bacterial, plant and mammalian systems. In this work, FNR was expressed in Cos-7 cells; then, they were submitted to cold incubation and iron overload to ascertain whether this enzyme was capable of diminishing the harm produced by these challenges. Contrary to expected, FNR was not protective and even exacerbated the damage under certain circumstances. It was also found that the injury induced by hypothermia in Cos-7 cells presented both iron-dependent and iron-independent components of damage when cells were actively dividing but only iron-independent component when cells were in an arrested state. This is in agreement with previous findings which showed that iron-dependent damage is also an energy-dependent process.
authors.affiliation: Centro Binacional, Argentina-Italia de Investigaciones en Criobiología Clínica y Aplicada, Universidad Nacional de Rosario, Av Arijón 28 bis, 2000 Rosario, Argentina.
authors.forename: M
authors.initials: M
authors.lastname: Pucci Molineris
authors.forename: G
authors.initials: G
authors.lastname: Di Venanzio
authors.forename: M E
authors.initials: ME
authors.lastname: Mamprin
authors.forename: M G
authors.initials: MG
authors.lastname: Mediavilla
mesh_terms: D000241:Adenosine / Q000494:pharmacology; D000493:Allopurinol / Q000494:pharmacology; D000818:Animals; D019556:COS Cells; D002470:Cell Survival / Q000187:drug effects; D002522:Chlorocebus aethiops; D003080:Cold Temperature / Q000009:adverse effects*; D004187:Disaccharides / Q000494:pharmacology; D004573:Electrolytes / Q000494:pharmacology; D005287:Ferredoxin-NADP Reductase / Q000235:genetics*; D005971:Glutamates / Q000494:pharmacology; D005978:Glutathione / Q000494:pharmacology; D006639:Histidine / Q000494:pharmacology; D007328:Insulin / Q000494:pharmacology; D007501:Iron / Q000494:pharmacology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D015227:Lipid Peroxidation; D008315:Malondialdehyde / Q000378:metabolism; D008353:Mannitol / Q000494:pharmacology; D019188:Organ Preservation Solutions / Q000494:pharmacology; D015125:Oxyquinoline / Q000494:pharmacology; D018532:Pisum sativum / Q000201:enzymology*; D011887:Raffinose / Q000494:pharmacology
chemical_list: C088453:Celsior; D004187:Disaccharides; D004573:Electrolytes; D005971:Glutamates; D007328:Insulin; D019188:Organ Preservation Solutions; C055206:University of Wisconsin-lactobionate solution; D008353:Mannitol; D006639:Histidine; D008315:Malondialdehyde; D015125:Oxyquinoline; D000493:Allopurinol; D007501:Iron; D007770:L-Lactate Dehydrogenase; D005287:Ferredoxin-NADP Reductase; D005978:Glutathione; D000241:Adenosine; D011887:Raffinose