Keywords Aquatic organisms, Embryotoxicity, NSAIDs, Teratogenesis
1 Introduction
The presence of pharmaceutical products in the environment has become one of the
main causes of concern worldwide; since the 1970s, interest in the determination of
organic substances of these drugs in the environment began [1]; however, it was until
the 1990s when analytical methodologies allowed the detection of this kind of
products at concentration in the order of μg/L. Pharmaceuticals have been considered as emerging pollutant substances of diverse origin and nature that do not have
an established environmental regulation but may be candidates for a future regulation depending on the data of the effects they generate on health and incidence;
another important feature is that they do not need to persist in the environment to
generate negative effects, because their high rates of transformation can be compensated by their constant introduction in to the environment, and also data regarding
their impact on the environment and health risks are scarce [2–4].
The main sources of pharmaceuticals to bodies of water are derived from anthropogenic activities such as effluents from wastewater treatment plants, effluents from
hospital, domestic activities (including pharmaceuticals and their metabolic products
of phases I and II in feces and urine, waste and inappropriate disposal of expired
pharmaceuticals), and effluents from industrial activities as well as livestock activities [5–8]. So that, the increase in the use and consumption has led to the continuous
elimination of these products or their transformation and biotransformation products
towards the aquatic environment [9], and due to are substances that were designed
with the purpose of having a biological effect, either preventing or treating a disease,
their presence in the environment can generate various acute and chronic adverse or
toxic effects in non-target organisms.
Non-steroidal anti-inflammatory drugs are a group of pharmaceuticals that have
analgesic, antipyretic, and anti-inflammatory activity; they are usually weak acids
that owe their pharmacological activity to the inhibition of the enzymatic systems of
cyclooxygenases (COX) 1 and 2 (Fig. 1); COX-1 catalyzes the conversion of
prostaglandins and thromboxane A2 responsible for controlling the mucosal barrier
in the gastrointestinal tract, renal homeostasis, and platelet aggregation among other
physiological functions, while COX-2 is induced in inflammatory cells as a response
to stimuli [11]. Its therapeutic uses are diverse, and some of them are over-thecounter drugs and are available to consumers without medical prescription; so they
are positioned as one of the highest consumption groups worldwide [6], the most
common ones are diclofenac, ibuprofen, naproxen, ketoprofen, acetaminophen,
acetylsalicylic acid, and indomethacin; main characteristics of NSAIDs are
described on Fig. 2.
NSAIDs have demonstrated their ability to generate toxic effects in different
organisms inducing oxidative stress alterations on growth, development, and energy
storage on Limnodynastes peronii [13], also oxidative stress in the brain, gill, liver,
and blood of Cyprinus carpio, increasing lipoperoxidation and enzymatic activity
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I. Pérez-Alvarez et al.
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