Hepatic mitochondrial content in malondialdehyde may be a marker of sea lamprey contact with atrazine

Abstract

The atrazine attracts special attention as pollutant because of itspersistence in the aquatic environment. Although this herbicide has been studied in teleost, its toxicity in the sea lamprey, Petromyzon marinus is still poorly understood. Oxidative stress may occur if chemical pollutants contribute to block the capacity of mitochondria to generate ATP with continuous production of reactive oxygen species (ROS), disturbing the success of P. marinus seawater acclimation. So, the aim of this study was to evaluate how atrazine influences the malondialdehyde (MDA), glutathione (GSH) and glutathione disulfide (GSSG) contents of gills and liver mitochondria of juveniles from Lima river basin, Portugal during salt acclimation. Sampling occurred at the beginning of the P. marinus downstream migration. The sampled juveniles were transported alive to the laboratory and maintained in 200 l tanks with LSS 8 life support system. Two groups of 40 specimens were hold in tanks with 50 or 100 lg/l atrazine, during 30 days. The salinity was gradually increased from 0 to 35 psu,following a three step procedure during a 30 days period. The control group was maintained in freshwater without atrazine. Mitochondria obtained by centrifugation at 15000 g, 30 min, 4°C, of tissues homogenates prepared in 50 mM Tris-HCl pH 7.5 buffer were used in determination of ROS, MDA, GSH and GSSG by fluorescence. The statistical analysis were performed by ANOVA I and Duncan (p < 0.05), using SPSS 22 for Windows.The results showed that in P. marinus juveniles, no significant changes in the markers of oxidative stress and cell damages were detected in the mitochondrial gills. Nevertheless, in the animals exposed to 50 lg/l atrazine the content in glutathione and GSSG increased. A similar pattern of stress markers was detected in hepatic mitochondria. However, in the presence of atrazine, the MDA level of the mitochondria of liver increased threefold in the animals during salt acclimation. The high level of mitochondrial damages, detected in the hepatic mitochondria of macrophthalmia treated with atrazine, suggests that herbicide exposure caused metabolic failures which can disturb the adaptation of these specimens to the oceanic feeding phase. The hepatic mitochondrial MDA levels of P. marinus, may eventually detect sea lamprey contact with chlorine herbicides.