The effects of Triclosan on the metabolism of developing Sheepshead minnow (Cyprinodon variegatus) larvae

The aquatic environment represents the final sink for many chemicals, including bactericidal agents. Among them Triclosan (TCS) has been shown to affect the thyroid system of teleost. Thyroid hormones are involved in the control of metabolism, so changes in hormone levels induced by triclosan may affect respiratory rates and antioxidant stress in exposed fish.

Couples of three females and two males were placed in breeding chambers designed for this experiment. Eggs were collected and maintained in seawater. Embryos were selected under a dissection microscope, randomly assigned to each of five treatment groups: Control, DMSO control, 20 μg/L TCS, 50 μg/L TCS and 100 μg/L TCS and placed in incubation dishes (50 per dish) at 25°C. On day 6, embryos hatched and larvae were transferred to 1L dishes. The larvae were fed on artemias and on flaked fish food till day 15 and 30 post hatching when the fish were analyzed. Respiratory rate measurements were carried out by respirometry and assays of antioxidant enzymes, Glutathionreductase (GR), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) were conducted to determine the presence of oxidative stress.

Respirometry showed that TCS exposed fish exhibited decreased the metabolism at 15 dph, whereas no differences in respiration rate could be observed between control and exposed larvae at 30 dph. At 15 dph no difference was observed for any of the antioxidant enzymes, whereas at 30 dph a sharp increase in the activity of GR was observed between the control and TCS exposed fish. The activity of GST and Gpx remained stable.

Thyroid hormones are major factors controlling the metabolic rate related to respiration and oxidative stress. TCS reduced the metabolism at 15 dph that corresponds to the moment where larvae to juvenile transition of Sheepshead minnows occur. Previous experiments showed that TCS induces an increase in thyroid hormone concentrations and hyperthyroidism induces oxidative stress. So our observed increase of antioxidant protection mechanisms could be a way to compensate oxidative stress. On the other hand, the changes in GR activity observed at 30 dph, may also be related to the reduced metabolism at 15 dph.