and mortality mediated by the inhibition of cyclooxygenase 1 (COX-1) activity.
While for DF the MIE is unknown, in the case of IB, this COX-1 inhibition is
mediated through the inhibition of prostaglandin-endoperoxide synthase (prostaglandin G/H synthase 1) activity, the inhibition of the organic anion transporter
1 (OAT1) resulting in decreased signaling mediated by the solute carrier family
22 member 6, and the inhibition of the IKK complex, an enzyme complex involved
in propagating the cellular response to inflammation through the caspase-8 pathway,
leading finally to liver injury. However, no information is provided on the concentrations activating these events in representative organisms or human, making its use
for practical risk assessment not useful so far.
7 Conclusions and Final Remarks
Both pharmaceutical compounds IB and DF show a wide occurrence and range of
concentrations in aquatic ecosystems from different geographical areas. Their fate
and behavior and distribution are related to chemical structure. These compounds
can interact with wild species and provoke unwanted effects. To perform a preliminary environmental risk assessment, PEC or MEC data are needed jointly with
PNEC. Currently, the available information is biased with a bigger database for
environmental concentrations and acute toxicity data species for temperate than
tropical regions. However, the chronic toxicity data can reflect in a better and
realistic way the negative effects of these pharmaceuticals, including mechanistic
information. Adverse outcome pathways are a conceptual framework that links the
processes occurring between the first contact of the organism with the stressor at
molecular level and the establishment of some sort of pathology that may cause
death or reduce its fitness in comparison with other unexposed individuals. In this
context, to use mechanistic data within the AOP framework to support effective risk
assessment, there is the essential need to translate this mechanistic information into
endpoints representing ecological risk, such as survival, reproduction, etc. It is also
essential to relate this translation with concentration values, at which the organism is
not able to overcome the challenge by its own defense mechanisms. Therefore,
although promising, the effective use of the AOP framework still requires traditional
dose-response testing at which molecular and apical endpoints are explored simultaneously. In real ecosystems, the pharmaceuticals can interact with other emergent
or legacy pollutants or be affected by other nonchemical stressors as temperature,
salinity, etc., many of them with unknown effects. In fact, to predict the environmental risk for different scenarios, we need to improve the knowledge of response
mechanisms and toxicity in multi-stressed systems. In summary, although gaps of
the information are pointed out, the risk levels associated with the occurrence of
these compounds in aquatic ecosystems will range between no risk or high risk,
depending on concentrations and environmental conditions.
Ibuprofen and Diclofenac: Effects on Freshwater and Marine Aquatic Organisms –. . .
183
While for DF the MIE is unknown, in the case of IB, this COX-1 inhibition is
mediated through the inhibition of prostaglandin-endoperoxide synthase (prostaglandin G/H synthase 1) activity, the inhibition of the organic anion transporter
1 (OAT1) resulting in decreased signaling mediated by the solute carrier family
22 member 6, and the inhibition of the IKK complex, an enzyme complex involved
in propagating the cellular response to inflammation through the caspase-8 pathway,
leading finally to liver injury. However, no information is provided on the concentrations activating these events in representative organisms or human, making its use
for practical risk assessment not useful so far.
7 Conclusions and Final Remarks
Both pharmaceutical compounds IB and DF show a wide occurrence and range of
concentrations in aquatic ecosystems from different geographical areas. Their fate
and behavior and distribution are related to chemical structure. These compounds
can interact with wild species and provoke unwanted effects. To perform a preliminary environmental risk assessment, PEC or MEC data are needed jointly with
PNEC. Currently, the available information is biased with a bigger database for
environmental concentrations and acute toxicity data species for temperate than
tropical regions. However, the chronic toxicity data can reflect in a better and
realistic way the negative effects of these pharmaceuticals, including mechanistic
information. Adverse outcome pathways are a conceptual framework that links the
processes occurring between the first contact of the organism with the stressor at
molecular level and the establishment of some sort of pathology that may cause
death or reduce its fitness in comparison with other unexposed individuals. In this
context, to use mechanistic data within the AOP framework to support effective risk
assessment, there is the essential need to translate this mechanistic information into
endpoints representing ecological risk, such as survival, reproduction, etc. It is also
essential to relate this translation with concentration values, at which the organism is
not able to overcome the challenge by its own defense mechanisms. Therefore,
although promising, the effective use of the AOP framework still requires traditional
dose-response testing at which molecular and apical endpoints are explored simultaneously. In real ecosystems, the pharmaceuticals can interact with other emergent
or legacy pollutants or be affected by other nonchemical stressors as temperature,
salinity, etc., many of them with unknown effects. In fact, to predict the environmental risk for different scenarios, we need to improve the knowledge of response
mechanisms and toxicity in multi-stressed systems. In summary, although gaps of
the information are pointed out, the risk levels associated with the occurrence of
these compounds in aquatic ecosystems will range between no risk or high risk,
depending on concentrations and environmental conditions.
Ibuprofen and Diclofenac: Effects on Freshwater and Marine Aquatic Organisms –. . .
183