Biomarker responses in Solea senegalensis exposed to sodium hypochlorite used as antifouling.
The time-course stress responses (0, 1, 2, and 7 d) was assessed in plasmatic, branchial and renal parameters of juveniles Solea senegalensis exposed to different concentrations of the antifouling sodium hypochlorite (0.1, 0.2, and 0.5mgL(-1)). These stress responses were only assessed for the total length of exposure (7d) at the lowest NaClO concentration due to the high toxicity of this chemical. In addition, the xenobiotic metabolism responses were evaluated by means of enzymatic activities of ethoxyresorufin O-deethylase (EROD), glutathione S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPX), catalase (CAT), and carboxylesterase (CbE) in liver; as well as GST, GPX, CAT and acetylcholinesterase (AChE) in gill. Oxidative stress damage due to sodium hypochlorite exposure was measured by lipid peroxidation levels in liver and gill. Concentrations of 0.2 and 0.5mgL(-1) produced lethal effects after 1d and 2h of exposure, respectively. After 1d of exposure to sublethal concentration of sodium hypochlorite (0.1mgL(-1)) osmoregulatory (osmolality and chloride) and stress (cortisol, glucose and lactate) plasmatic parameters were enhanced to respect at control fish. However after 3 or 7d these parameters returned to control values. No effects were observed on plasma protein and triglyceride levels or on gill and kidney Na(+)/K(+)-ATPase activities. Diverse gill pathologies such as hypertrophy, lamellar fusion and an increase in goblet cell number and size were observed after 7d of exposure. Most biochemical parameters related to xenobiotic metabolism and oxidative stress were also significantly affected which suggests that seawater affected by sodium hypochlorite discharges from power plants, is able to alter the fish xenobiotic metabolism and generate oxidative stress.
López-Galindo
Cristina
C
Departamento de Tecnologías del Medio Ambiente, Universidad de Cádiz, Puerto Real, Spain.
Vargas-Chacoff
Luis
L
Nebot
Enrique
E
Casanueva
José F
JF
Rubio
Daniel
D
Solé
Montserrat
M
Mancera
Juan Miguel
JM
D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D015415:Biomarkers / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D019363:Cytochrome P-450 CYP1A1 / Q000378:metabolism; D004202:Disinfectants / Q000633:toxicity*; D005412:Flatfishes / Q000378:metabolism*; D005880:Gills / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D015227:Lipid Peroxidation; D008099:Liver / Q000187:drug effects / Q000201:enzymology; D012973:Sodium Hypochlorite / Q000633:toxicity*; D014874:Water Pollutants, Chemical / Q000633:toxicity*
D015415:Biomarkers; D004202:Disinfectants; D014874:Water Pollutants, Chemical; D012973:Sodium Hypochlorite; D002374:Catalase; D005979:Glutathione Peroxidase; D019363:Cytochrome P-450 CYP1A1; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D000110:Acetylcholinesterase