concentrations (five concentrations ranging between 62.5 and 1,000 mg/L) towards
L. minor and L. gibba was investigated. Paracetamol toxicity was widely variable
among species, even among phylogenetically related ones. Paracetamol was toxic to
all test organisms in the tested concentration range, with the exception of L. gibba,
whereby no acute effects occurred also at concentrations up to 1,000 mg/L. Considering acute toxicity in terms of EC 50 , the scale of toxicity, from the most sensitive to
the most tolerant model organism, was the following: D. magna < D. longispina <
C. raciborskii < P. subcapitata < L. minor < L. gibba. PCM caused mortality in the
reproduction test with D. magna at the highest tested concentrations (between 1.2
and 1.7 mg/L), so that no organisms survived over the whole duration of the
experiment, although they generated offspring. Differently, D. longispina showed
a significant delay in the first reproductive event and a reduction in the fecundity. A
study by Sarma and coauthors [27] exposed the rotifer Plationus patulus and the
cladoceran Moina macrocopa to increasing concentrations of PCM (2, 4, 8, 16, and
32 mg/L) in order to assess changes in population growth. Population growth curves
of both the species were affected by the exposure to increasing concentrations of
PCM, showing a decrease in organism density with increasing levels of drug.
Moreover, the daily rate of population increase was negatively and significantly
affected by PCM exposure in both the zooplanktonic species. A 7-day exposure to
10, 100 μg/L, 1.0 and 10 mg/L of PCM did not affect the survival of Hydra vulgaris
specimens at concentrations up to 1.0 mg/L, while after 17 days neither feeding nor
bud formation was adversely affected. Moreover, the ability of dissected polyps to
regenerate a hypostome, tentacles, and foot was not inhibited [28]. Biochemical
effects of PCM exposure were investigated in the freshwater clam Corbicula
fluminea following short- (96 h) and long-term (28 days) exposures to 0.05, 0.48,
4.82, and 532.78 mg/L of PCM and 3.88, 7.74, 15.49, 30.98, and 61.95 μg/L of
PCM, respectively [29]. Effects of PCM exposure on some oxidative stress endpoints, namely, catalase (CAT), glutathione S-transferases (GSTs), glutathione
reductase (GRed), and lipid peroxidation were investigated. No mortality was
observed in clams over short- or long-term exposures. PCM did not modulate
CAT activity but induced a significant decrease of GSTs activity following both
short- and long-term exposure (LOEC values of 532.78 mg/L and 30.98 μg/L,
respectively). Moreover, PCM treatment induced a significant dose-dependent
decrease of GRed activity in both short- and long-term exposures. A significant
increase of lipid peroxidation was noted at the end of short- and long-term exposure
to the highest PCM tested concentrations. These results indicated that the exposure
to increasing PCM concentration caused notable changes in the cellular redox status
of C. fluminea. The cytogenotoxicity of PCM was investigated through an in vitro
approach by exposing the hemocytes collected from the zebra mussel
D. polymorpha for 1 h to 30, 150, and 450 μg/L [30]. Cytotoxicity was evaluated
by the neutral red retention assay (NRRA) while genotoxicity by SCGE (single cell
gel electrophoresis) and DNA diffusion assay. Significant cytotoxic and genotoxic
effects were after the exposures to all the tested concentrations according to a dosedependent relationship. PCM exposure induced significant alterations of the oxidative status of the zebra mussel D. polymorpha [31]. Zebra mussels were exposed for
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M. Parolini
L. minor and L. gibba was investigated. Paracetamol toxicity was widely variable
among species, even among phylogenetically related ones. Paracetamol was toxic to
all test organisms in the tested concentration range, with the exception of L. gibba,
whereby no acute effects occurred also at concentrations up to 1,000 mg/L. Considering acute toxicity in terms of EC 50 , the scale of toxicity, from the most sensitive to
the most tolerant model organism, was the following: D. magna < D. longispina <
C. raciborskii < P. subcapitata < L. minor < L. gibba. PCM caused mortality in the
reproduction test with D. magna at the highest tested concentrations (between 1.2
and 1.7 mg/L), so that no organisms survived over the whole duration of the
experiment, although they generated offspring. Differently, D. longispina showed
a significant delay in the first reproductive event and a reduction in the fecundity. A
study by Sarma and coauthors [27] exposed the rotifer Plationus patulus and the
cladoceran Moina macrocopa to increasing concentrations of PCM (2, 4, 8, 16, and
32 mg/L) in order to assess changes in population growth. Population growth curves
of both the species were affected by the exposure to increasing concentrations of
PCM, showing a decrease in organism density with increasing levels of drug.
Moreover, the daily rate of population increase was negatively and significantly
affected by PCM exposure in both the zooplanktonic species. A 7-day exposure to
10, 100 μg/L, 1.0 and 10 mg/L of PCM did not affect the survival of Hydra vulgaris
specimens at concentrations up to 1.0 mg/L, while after 17 days neither feeding nor
bud formation was adversely affected. Moreover, the ability of dissected polyps to
regenerate a hypostome, tentacles, and foot was not inhibited [28]. Biochemical
effects of PCM exposure were investigated in the freshwater clam Corbicula
fluminea following short- (96 h) and long-term (28 days) exposures to 0.05, 0.48,
4.82, and 532.78 mg/L of PCM and 3.88, 7.74, 15.49, 30.98, and 61.95 μg/L of
PCM, respectively [29]. Effects of PCM exposure on some oxidative stress endpoints, namely, catalase (CAT), glutathione S-transferases (GSTs), glutathione
reductase (GRed), and lipid peroxidation were investigated. No mortality was
observed in clams over short- or long-term exposures. PCM did not modulate
CAT activity but induced a significant decrease of GSTs activity following both
short- and long-term exposure (LOEC values of 532.78 mg/L and 30.98 μg/L,
respectively). Moreover, PCM treatment induced a significant dose-dependent
decrease of GRed activity in both short- and long-term exposures. A significant
increase of lipid peroxidation was noted at the end of short- and long-term exposure
to the highest PCM tested concentrations. These results indicated that the exposure
to increasing PCM concentration caused notable changes in the cellular redox status
of C. fluminea. The cytogenotoxicity of PCM was investigated through an in vitro
approach by exposing the hemocytes collected from the zebra mussel
D. polymorpha for 1 h to 30, 150, and 450 μg/L [30]. Cytotoxicity was evaluated
by the neutral red retention assay (NRRA) while genotoxicity by SCGE (single cell
gel electrophoresis) and DNA diffusion assay. Significant cytotoxic and genotoxic
effects were after the exposures to all the tested concentrations according to a dosedependent relationship. PCM exposure induced significant alterations of the oxidative status of the zebra mussel D. polymorpha [31]. Zebra mussels were exposed for
152
M. Parolini