zebrafish development by exposing embryos to the target chemicals at 5, 50, and
500 μg/L starting from 6 h postfertilization (hpf). Exposure to high concentration of
ibuprofen significantly decreased the spontaneous movement by 25% and reduced
the free-swimming distance, duration, and speed under dark condition by 41%, 29%,
and 30%, respectively [25]. Besides, all three NSAIDs showed remarkable timedependent and concentration-dependent effects on Daphnia magna, with diclofenac
the highest and paracetamol the lowest toxic. Survival, growth, and reproduction
data of D. magna from all bioassays were used to determine the LC 10 and LC 50 as
well as the EC 10 and EC 50 , which were mainly in the low ppm-range, of which
reproduction was the most sensitive one, indicating that nontarget organisms might
be adversely affected by relevant ambient low-level concentrations [26].
One of the most widely NSAIDs evaluated is diclofenac. There exist a vast
number of articles regarding its toxicological effects on several aquatic organisms.
McRae and co-workers, in 2018, determined that diclofenac at environmentally
relevant (0.17 μg/L) and elevated (763 μg/L) concentrations caused lipid peroxidation in the liver but, in the kidney and gill, was decreased after diclofenac exposure in
inanga fish [27]. Conversely, juvenile Rhamdia quelen fish species were exposed to
diclofenac for 96 h at concentrations of 0.2, 2, and 20 μg/L, and no oxidative stress
was observed in the liver but in the kidney the superoxide dismutase activity was
increased in all concentrations, suggesting an alteration in the hydrogen peroxide
production, and DNA damage and lipid peroxidation were not detected; besides,
diclofenac exposure increased the red blood cells number (0.2 and 2 μg/L) and
monocytes and neutrophils (2 and 20 μg/L) [28].
Oreochromis niloticus, exposed to diclofenac for 80 days post-hatch to a 0.1 and
1 μg/L, showed altered biomarkers associated with reproduction indicating the
potential to affect sexual differentiation and gametogenesis by acting as an estrogenic endocrine-disrupting compound; also, vitellogenin gene expression was significantly induced at 1 μg/L [29]. In 2017, Pandey and colleagues evaluated the
DNA damage, hematological changes, and activities of oxidative stress enzymes in
Nile tilapia, Oreochromis niloticus, in response to diclofenac and found that at 0.17,
0.34, and 0.68 mg/L, diclofenac caused a reduction in hemoglobin and red blood cell
counts and an elevation on the indices of hepatic oxidative stress biomarkers,
including lipid peroxidation and carbonyl protein [30].
High concentrations of diclofenac, present in effluents and water bodies of
different countries, including Mexico, caused toxicity on aquatic organisms.
Cardoso-Vera et al. [31] demonstrated that the exposition of oocytes in
mid-blastula transition of Xenopus laevis and L. catesbeianus to diclofenac at 1, 4,
8, 16, 32, and 62.5 mg/L induced diverse malformations in both species, the most
frequent of these being axial malformations in the tail and notochord, edema, and
stunted growth, using FETAX assay [31]. Also, it was demonstrated that the
exposition of Gasterosteus aculeatus to 0, 4.6, 22, 82, and 271 μg/L of diclofenac
in flow-through systems for 28 days caused histological changes in the proportion of
renal hematopoietic tissue (renal hematopoietic hyperplasia), but no histological
changes were observed in the liver at low μg/L concentrations; moreover, an
46
A. Mejía-García et al.
500 μg/L starting from 6 h postfertilization (hpf). Exposure to high concentration of
ibuprofen significantly decreased the spontaneous movement by 25% and reduced
the free-swimming distance, duration, and speed under dark condition by 41%, 29%,
and 30%, respectively [25]. Besides, all three NSAIDs showed remarkable timedependent and concentration-dependent effects on Daphnia magna, with diclofenac
the highest and paracetamol the lowest toxic. Survival, growth, and reproduction
data of D. magna from all bioassays were used to determine the LC 10 and LC 50 as
well as the EC 10 and EC 50 , which were mainly in the low ppm-range, of which
reproduction was the most sensitive one, indicating that nontarget organisms might
be adversely affected by relevant ambient low-level concentrations [26].
One of the most widely NSAIDs evaluated is diclofenac. There exist a vast
number of articles regarding its toxicological effects on several aquatic organisms.
McRae and co-workers, in 2018, determined that diclofenac at environmentally
relevant (0.17 μg/L) and elevated (763 μg/L) concentrations caused lipid peroxidation in the liver but, in the kidney and gill, was decreased after diclofenac exposure in
inanga fish [27]. Conversely, juvenile Rhamdia quelen fish species were exposed to
diclofenac for 96 h at concentrations of 0.2, 2, and 20 μg/L, and no oxidative stress
was observed in the liver but in the kidney the superoxide dismutase activity was
increased in all concentrations, suggesting an alteration in the hydrogen peroxide
production, and DNA damage and lipid peroxidation were not detected; besides,
diclofenac exposure increased the red blood cells number (0.2 and 2 μg/L) and
monocytes and neutrophils (2 and 20 μg/L) [28].
Oreochromis niloticus, exposed to diclofenac for 80 days post-hatch to a 0.1 and
1 μg/L, showed altered biomarkers associated with reproduction indicating the
potential to affect sexual differentiation and gametogenesis by acting as an estrogenic endocrine-disrupting compound; also, vitellogenin gene expression was significantly induced at 1 μg/L [29]. In 2017, Pandey and colleagues evaluated the
DNA damage, hematological changes, and activities of oxidative stress enzymes in
Nile tilapia, Oreochromis niloticus, in response to diclofenac and found that at 0.17,
0.34, and 0.68 mg/L, diclofenac caused a reduction in hemoglobin and red blood cell
counts and an elevation on the indices of hepatic oxidative stress biomarkers,
including lipid peroxidation and carbonyl protein [30].
High concentrations of diclofenac, present in effluents and water bodies of
different countries, including Mexico, caused toxicity on aquatic organisms.
Cardoso-Vera et al. [31] demonstrated that the exposition of oocytes in
mid-blastula transition of Xenopus laevis and L. catesbeianus to diclofenac at 1, 4,
8, 16, 32, and 62.5 mg/L induced diverse malformations in both species, the most
frequent of these being axial malformations in the tail and notochord, edema, and
stunted growth, using FETAX assay [31]. Also, it was demonstrated that the
exposition of Gasterosteus aculeatus to 0, 4.6, 22, 82, and 271 μg/L of diclofenac
in flow-through systems for 28 days caused histological changes in the proportion of
renal hematopoietic tissue (renal hematopoietic hyperplasia), but no histological
changes were observed in the liver at low μg/L concentrations; moreover, an
46
A. Mejía-García et al.