Biomarcadores de estresse oxidativo em tilápia do nilo, Oreochromis niloticus (Teleostei; Cichlidae), expostas ao sulfato de cobre aquático
Autor
Lucarelli, Antonio Carlos Tomasi
Metadatos
Mostrar el registro completo del ítemResumen
In this study the effects of the aquatic copper (CuSO4) on biological markers
of oxidative stress were assessed in the plasma, liver, gills and heart of the Nile
tilapia, Oreocrhromis niloticus, exposed for 96 hours to crescent concentrations of
this salt. The indiscriminate use of CuSO4 as a prophylactic agent in aquaculture
systems results in an accumulation of ion cooper (Cu2+) causing toxicity for the
cultivated species. The lipid peroxidation in the plasma of experimental fish,
determined by the production of the reactants of thiobarbituric acid (TBARS) and
lipid hydroperoxide (HP) did not change with copper exposition. However, the
defense promoted by the glutathione peroxidase (GSH-Px) increased in the groups
submitted to 0.7, 1.5 and 3.0 mg.L-1 of CuSO4. In the hepatic tissue, there were no
significant differences in the production of HP among groups submitted to CuSO4
and control animals. The antioxidant defense induced by GSH-Px increased
significantly in the concentration of 0.35 mg. L-1. However, it decreased
significantly in the concentrations of 0.70 and 4.00 mg.L-1. The activity of the
superoxide dismutase (SOD) and the catalase (CAT) continued in the control
levels, independently of the test concentration. Nevertheless, in the gills occurred a
significant increase in the HP levels in the SOD activity at concentrations of 0.7 and
1.5 mg.L-1. The activity of GSH-Px did not change and the CAT decreased in the
groups exposed to 0.7 and 1.5 mg.L-1. These data allow to conclude that oxygenfree
radicals are produced as mediators of the copper toxicity. The development of
the resistance to high concentrations of CuSO4 is mainly related to the increase in
the levels of plasmatic GSH-Px and posterior maintenance of the levels of this
enzyme on the studied tissues, thus granting important oxidant defense and
consequent protection against oxidative damages induced by the CuSO4,
obstructing the lipoid peroxidation, mainly in the liver of experimental animals.