Fish might be more sensitive to pollution from antidepressants than had been previously realised, since studies have shown that their main molecular targets can react to concentrations similar to those found in polluted watercourses.
The Japanese rice fish (Oryzias latipes) live in small ponds, shallow rivers, and rice fields.
Antidepressants are intended to modify chemical signalling in the human brain; however, after they have been excreted, small amounts of the drugs and their metabolites can go through the wastewater system and end up in rivers, lakes and coastal waters, where they remain biologically active.
This matters because fish use the same neurotransmitters as humans, such as serotonin, dopamine, and norepinephrine. Earlier studies have already found that exposure to antidepressants is associated with changes in fish behaviour, reproduction and physiology. Recent research has now given a more detailed examination of why fish might be especially susceptible.
Researchers from Japan looked at the monoamine transporters—proteins which regulate these neurotransmitters—in two fish species that are evolutionarily distinct: the medaka (Oryzias latipes), also known as the Japanese rice fish, and the ayu (Plecoglossus altivelis).
A study which was published in Environmental Science & Technology discovered that one version of the serotonin transporter, called SERTa, was considerably more sensitive to a number of antidepressants than another form found in fish, SERTb. Even more remarkable was the finding that the fish SERTa transporters were consistently more susceptible to inhibition than the corresponding human transporter.
Effects at environmentally relevant levels
In the case of certain drugs, the difference was considerable. The researchers discovered that the medaka SERTa was responsive to duloxetine, fluoxetine, citalopram and paroxetine at concentrations between a few hundred and about 1,300 nanograms per litre.
The levels in question coincide with those found in heavily contaminated aquatic environments, which leads to doubts as to whether the current environmental evaluations take into account the differences between humans and aquatic animals.
The researchers also discovered that certain pharmaceuticals had an effect on fish transporters which were not normally expected to be targeted on the basis of their actions in humans. This indicates that it would be possible to overlook some environmental effects if one simply applies human pharmacology to fish.
The results contribute yet another element to the increasing amount of research concerning pharmaceutical pollution. Previous experiments have demonstrated that prolonged exposure to environmentally relevant concentrations of fluoxetine can lead to changes in the behaviour and reproduction of guppies. Nevertheless, the responses differ greatly from species to species and depending on the concentration and the experimental conditions. In fact, a different study in 2026 detected no behavioural or physiological effects in female guppies under the exposure situation it examined, which is why the effects cannot be applied to all fish.
From molecules to whole fish
A significant limitation exists in that the researchers did not subject live fish to water contaminated with antidepressants and then measure the effects on their behaviour or health. Rather, they cloned the transporter genes from the two species and expressed them in cultured cells, which enabled them to measure directly the extent to which different pharmaceuticals inhibited the genes.
It will thus be necessary to carry out further studies in order to find out how these molecular responses affect individual fish and, in the end, aquatic ecosystems. Yet the results indicate that environmental concentrations which are regarded as very low from a human point of view might not always be insignificant to fish.
