Study of the antioxidant capacity in gills of the Pacific oyster Crassostrea gigas in link with its reproductive investment.
Energy allocation principle is a core element of life-history theory in which "the cost of reproduction" corresponds to an acceleration of senescence caused by an increase in reproductive investment. In the "theory of aging", senescence is mainly due to the degradation of lipids, proteins and DNA by reactive oxygen species (ROS), by-products of oxidative metabolism. Some studies have shown that oxidative stress susceptibility could be a cost of reproduction. The present study investigates the effect of reproductive investment on antioxidant capacity in the gills of a species with a very high reproductive investment, the Pacific oyster Crassostrea gigas. We used RNA interference targeting the oyster vasa-like gene (Oyvlg) to produce oysters with contrasted reproductive investment. Antioxidant capacity was studied by measuring the mRNA levels of genes encoding major antioxidant enzymes, and the activity of these enzymes. The highest reproductive investment was associated with the highest transcript levels for glutathione peroxidase and extra-cellular and mitochondrial superoxide dismutase. In contrast, lipid peroxidation did not show any sign of oxidative damage whatever the reproductive investment. Up-regulation of certain genes encoding enzymes involved in the first step of ROS detoxification could therefore be a part of the organism's strategy for managing the pro-oxidant species produced by heavy reproductive investment.
Laboratoire des Sciences de l'Environnement Marin, Institut Universitaire Européen de la Mer, Université de Bretagne Occidentale, UMR CNRS/UBO/IRD/IFREMER, Plouzané, France.
Jean-Philippe
JP
Béguel
Arnaud
A
Huvet
Virgile
V
Quillien
Christophe
C
Lambert
Caroline
C
Fabioux
D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002374:Catalase / Q000235:genetics / Q000378:metabolism; D049896:Crassostrea / Q000235:genetics* / Q000378:metabolism*; D005260:Female; D005880:Gills / Q000378:metabolism*; D005979:Glutathione Peroxidase / Q000235:genetics / Q000378:metabolism; D005980:Glutathione Reductase / Q000235:genetics / Q000378:metabolism; D005982:Glutathione Transferase / Q000235:genetics / Q000378:metabolism; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000235:genetics / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D020648:Peptide Elongation Factor 1 / Q000235:genetics / Q000378:metabolism; D034622:RNA Interference; D017382:Reactive Oxygen Species / Q000378:metabolism; D012098:Reproduction / Q000235:genetics / Q000502:physiology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism
D000975:Antioxidants; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D020648:Peptide Elongation Factor 1; D017382:Reactive Oxygen Species; D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005982:Glutathione Transferase