exposure of the zebra mussel showed that the 96 h treatment with 0.2, 2, and 8 mg/L
of IBU induced a slight cytogenotoxicity (i.e., NRRA, SCGE assay, apoptosis, and
MN test) on hemocytes at the IBU concentration of 0.2 mg/L, while higher IBU
concentrations (2 and 8 mg/L) cause a significant increase of both cellular and
primary and fixed genetic damage. In addition, IBU significantly altered the activity
of antioxidant and detoxifying enzymes at all the tested concentrations, suggesting
the imbalance of oxidative status and a possible onset of oxidative stress [41]. A
study performed on the zebra mussel exposed for 7 days to increasing IBU concentrations (0.206, 2.06, 20.6, and 206.3 μg/L) investigated the effects of this NSAIDs
at molecular level, assessing the mRNA changes of enzymes and other proteins
involved in the prevention of protein damage (heat shock protein 70) and oxidative
stress (superoxide dismutase, catalase, metallothionein), biotransformation (glutathione S-transferase, aryl hydrocarbon receptor), elimination (P-glycoprotein), and
reversible protein posttranslational modification (protein phosphatase 2A). Mussels
exposed to the lowest tested concentrations of IBU experienced an oxidative stress
situation as showed by induced mRNA levels in the digestive gland of mussels
recorded for catalase and metallothionein, as well as superoxide dismutase, after
1 and 4 days of exposure, respectively. At higher concentrations, an increase in
transcript levels of glutathione S-transferase occurred, suggesting the activation of
biotransformation processes of IBU or by-products deriving from oxidative stress
[40]. Moreover, responses induced by 21-days exposure to increasing IBU concentrations (0.1, 1.5, 10, 15, 50 μg/L), in terms of general stress (lysosomal membrane
stability), biomarkers of phase I and II (ethoxyresorufin-O-deethylase,
dibenzylfluorescein dealkylase, glutathione S-transferase), oxidative stress (glutathione reductase, glutathione peroxidase, lipid peroxidation), and DNA damage
were investigated in the clam Corbicula fluminea. IBU induced a destabilization
of lysosomal membrane at all the tested concentrations. Moreover, IBU activated
both phase I and II enzymes, including glutathione reductase and glutathione
peroxidase, at the highest tested concentration (50 μg/L). Moreover, an increase of
lipid peroxidation, but not of DNA damage, was observed at the end of the exposure
to 50 μg/L [42]. Individuals of the freshwater Keeled rams horn snails (Planorbis
carinatus) were exposed for 72 h to 0.1, 1.0, 10, and 100 mg/L of IBU and to 0.32,
1.0, 3.2, and 10 mg/L of IBU for 21 days. The 48 and 72 h LC 50 values were both
17.1 mg/L (95% confidence intervals 5.9–72.3 mg/L), while the 21 days LOEC and
NOEC based on individual survival were calculated as 45.36 and 5.36 mg/L,
respectively. The 21-day LOEC and NOEC calculated for snail reproduction (i.e.,
hatching success) were 5.36 and 2.43 mg/L, respectively, while the LOEC and
NOEC calculated for growth were 2.43 and 1.02 mg/L, respectively [43].
Adverse Effects Induced by Nonsteroidal Anti-inflammatory Drugs on Freshwater. . .
157
of IBU induced a slight cytogenotoxicity (i.e., NRRA, SCGE assay, apoptosis, and
MN test) on hemocytes at the IBU concentration of 0.2 mg/L, while higher IBU
concentrations (2 and 8 mg/L) cause a significant increase of both cellular and
primary and fixed genetic damage. In addition, IBU significantly altered the activity
of antioxidant and detoxifying enzymes at all the tested concentrations, suggesting
the imbalance of oxidative status and a possible onset of oxidative stress [41]. A
study performed on the zebra mussel exposed for 7 days to increasing IBU concentrations (0.206, 2.06, 20.6, and 206.3 μg/L) investigated the effects of this NSAIDs
at molecular level, assessing the mRNA changes of enzymes and other proteins
involved in the prevention of protein damage (heat shock protein 70) and oxidative
stress (superoxide dismutase, catalase, metallothionein), biotransformation (glutathione S-transferase, aryl hydrocarbon receptor), elimination (P-glycoprotein), and
reversible protein posttranslational modification (protein phosphatase 2A). Mussels
exposed to the lowest tested concentrations of IBU experienced an oxidative stress
situation as showed by induced mRNA levels in the digestive gland of mussels
recorded for catalase and metallothionein, as well as superoxide dismutase, after
1 and 4 days of exposure, respectively. At higher concentrations, an increase in
transcript levels of glutathione S-transferase occurred, suggesting the activation of
biotransformation processes of IBU or by-products deriving from oxidative stress
[40]. Moreover, responses induced by 21-days exposure to increasing IBU concentrations (0.1, 1.5, 10, 15, 50 μg/L), in terms of general stress (lysosomal membrane
stability), biomarkers of phase I and II (ethoxyresorufin-O-deethylase,
dibenzylfluorescein dealkylase, glutathione S-transferase), oxidative stress (glutathione reductase, glutathione peroxidase, lipid peroxidation), and DNA damage
were investigated in the clam Corbicula fluminea. IBU induced a destabilization
of lysosomal membrane at all the tested concentrations. Moreover, IBU activated
both phase I and II enzymes, including glutathione reductase and glutathione
peroxidase, at the highest tested concentration (50 μg/L). Moreover, an increase of
lipid peroxidation, but not of DNA damage, was observed at the end of the exposure
to 50 μg/L [42]. Individuals of the freshwater Keeled rams horn snails (Planorbis
carinatus) were exposed for 72 h to 0.1, 1.0, 10, and 100 mg/L of IBU and to 0.32,
1.0, 3.2, and 10 mg/L of IBU for 21 days. The 48 and 72 h LC 50 values were both
17.1 mg/L (95% confidence intervals 5.9–72.3 mg/L), while the 21 days LOEC and
NOEC based on individual survival were calculated as 45.36 and 5.36 mg/L,
respectively. The 21-day LOEC and NOEC calculated for snail reproduction (i.e.,
hatching success) were 5.36 and 2.43 mg/L, respectively, while the LOEC and
NOEC calculated for growth were 2.43 and 1.02 mg/L, respectively [43].
Adverse Effects Induced by Nonsteroidal Anti-inflammatory Drugs on Freshwater. . .
157