drug. Furthermore, trophic exposure to DCF also inhibited lipopolysaccharideinduced nitric oxide production, suggesting a possible immunosuppressive effect.
DCF is known to produce deadly damaging effects in renal and gastrointestinal
tissue of several fishes. Hoeger et al. [87] showed DCF exposure over 21 days
resulted in the telangiectasia of the gills, increased monocyte infiltration in the liver,
and the common histopathological effects produced in the trunk kidney. Moreover,
in rainbow trout, it has been demonstrated this drug produced hyaline inclusions and
cell necrosis in the kidney, as well as inflammatory cell foci and increased basophils
in the liver, after a chronic exposure [89, 90].
Two studies conducted in zebrafish evaluated the developmental abnormalities
induced by DCF. Van den Brandhof and Montforts [91] exposed Danio rerio
embryos to this pollutant for 72 h and found yolk sac and tail deformation in
concentrations of over 1.5 mg/L, whereas Chen et al. [92] observed several tail
malformations, pericardial edema, muscle degeneration, several trunk curvature,
shorter body length, lack of the liver, and abnormal pigmentation in concentrations
of 3.78 μM.
4.2 Paracetamol
The high toxicity of PCT is mainly produced by an oxidative stress mechanism.
Gómez-Oliván et al. [100] demonstrated PCT induces significantly lipid peroxidation and decreases the activity of the antioxidant enzymes on amphipods exposed to
7.7 mg/kg of this pollutant. Furthermore, studies conducted in rainbow trout,
common eel, and two edible clams have also showed significant alterations in all
oxidative stress biomarkers [101, 102, 105, 118]. This set of data thoroughly
evidence the bioactivation of PCT into a harmful prooxidant substance.
Data regarding the toxic effects of PCT on embryonic development are limited.
David and Pancharatna [99] exposed zebrafish embryos to different doses of this
pharmaceutical for seven consecutive days. Their results demonstrated PCT interferes with the normal embryonic development, growth, behavior, and survival of
zebrafish larvae.
Paracetamol is a potential endocrine disruptor and can cause hepatotoxicity in
male fish. Guiloski et al. [104] exposed Rhamdia quelen fish to environmental
concentrations of PCT for 21 days. According to their results, testosterone levels
were significantly reduced, whereas estradiol, serotonin, and dopamine levels
increased. Furthermore, hepatic tissues of exposed fish showed blood congestion
and leucocytes infiltration. Their findings evidence PCT which requires further
attention relative to its potential endocrine disruptor effect.
Introduction and Historical Findings That Focused Nonsteroidal. . .
29
DCF is known to produce deadly damaging effects in renal and gastrointestinal
tissue of several fishes. Hoeger et al. [87] showed DCF exposure over 21 days
resulted in the telangiectasia of the gills, increased monocyte infiltration in the liver,
and the common histopathological effects produced in the trunk kidney. Moreover,
in rainbow trout, it has been demonstrated this drug produced hyaline inclusions and
cell necrosis in the kidney, as well as inflammatory cell foci and increased basophils
in the liver, after a chronic exposure [89, 90].
Two studies conducted in zebrafish evaluated the developmental abnormalities
induced by DCF. Van den Brandhof and Montforts [91] exposed Danio rerio
embryos to this pollutant for 72 h and found yolk sac and tail deformation in
concentrations of over 1.5 mg/L, whereas Chen et al. [92] observed several tail
malformations, pericardial edema, muscle degeneration, several trunk curvature,
shorter body length, lack of the liver, and abnormal pigmentation in concentrations
of 3.78 μM.
4.2 Paracetamol
The high toxicity of PCT is mainly produced by an oxidative stress mechanism.
Gómez-Oliván et al. [100] demonstrated PCT induces significantly lipid peroxidation and decreases the activity of the antioxidant enzymes on amphipods exposed to
7.7 mg/kg of this pollutant. Furthermore, studies conducted in rainbow trout,
common eel, and two edible clams have also showed significant alterations in all
oxidative stress biomarkers [101, 102, 105, 118]. This set of data thoroughly
evidence the bioactivation of PCT into a harmful prooxidant substance.
Data regarding the toxic effects of PCT on embryonic development are limited.
David and Pancharatna [99] exposed zebrafish embryos to different doses of this
pharmaceutical for seven consecutive days. Their results demonstrated PCT interferes with the normal embryonic development, growth, behavior, and survival of
zebrafish larvae.
Paracetamol is a potential endocrine disruptor and can cause hepatotoxicity in
male fish. Guiloski et al. [104] exposed Rhamdia quelen fish to environmental
concentrations of PCT for 21 days. According to their results, testosterone levels
were significantly reduced, whereas estradiol, serotonin, and dopamine levels
increased. Furthermore, hepatic tissues of exposed fish showed blood congestion
and leucocytes infiltration. Their findings evidence PCT which requires further
attention relative to its potential endocrine disruptor effect.
Introduction and Historical Findings That Focused Nonsteroidal. . .
29