Ocimum basilicum essential oil in pacu Piaractus mesopotamicus: anesthetic efficacy, distribution, and depletion in different tissues.

This study aimed to evaluate the anesthetic activity of Ocimum basilicum essential oil and the distribution and depletion of its major compounds in different tissues of the pacu, Piaractus mesopotamicus. Juveniles (319.08 ± 9.14 g) were individually anesthetized with six concentrations of essential oil from O. basilicum (150, 180, 210, 240, 270, and 300 mg L-1), while in a second experiment, fish (492.39 ± 51.51 g) were subjected to a 10 min immersion bath with essential oil from O. basilicum (300 mg L-1). After anesthetic recovery, blood and tissue samples of the brain, gills, liver, spleen, and white muscle were collected at 0, 0.5, 1.0, 3.0, 6.0, 12.0, and 24 h. A 300 mg L-1 concentration induced anesthesia in the shortest time (193.11 ± 9.31), while at 270 and 300 mg L-1 concentrations, the anesthetic recovery period was the longest (244.33 ± 12.44) Methyl chavicol and linalool were quantified in all tissue samples. The plasma concentrations of methyl chavicol differed (p < 0.05) at all evaluated times. Linalool decreased (p < 0.05) from 0 to 1 h and decreased again only after 12 h. Reduction percentages in 24 h were 92.9% for methyl chavicol, and 97.2% for linalool. Elimination of the compounds methyl chavicol and linalool is slower in the gills, where lower elimination constants (0.03 and 0.15 per h) and longer half-lives (25.84 and 4.53 h), respectively, are noted. In general, essential oil from O. basilicum compounds was readily eliminated, showing promising potential for use as an anesthetic in aquaculture.

Ammonia exposure and subsequent recovery trigger oxidative stress responses in juveniles of Brazilian flounder Paralichthys orbignyanus.

The effects of ammonia exposure and recovery on oxidative stress parameters and histology of juvenile Brazilian flounder Paralichthys orbignyanus were evaluated. The fish were exposed to 0.12, 0.28 and 0.57 mg NH3-N L-1, plus a control, for 10 days followed by the same recovery time in ammonia-free water. Gill, liver and muscle samples (n = 9) were collected after 1, 5 and 10 days of exposure and after recovery for oxidative stress analysis (antioxidant capacity against peroxyl radicals (ACAP); glutathione S-transferase (GST) activity; lipoperoxidation levels measured through thiobarbituric acid reactive substances (TBARS) content). For histological assessment, gill, liver and brain samples were collected. Exposure to all NH3-N concentrations induced different time- and dose-dependent changes in oxidative stress parameters. Reduced antioxidant capacity of the liver and muscle and enhanced TBARS levels in the gills and liver were demonstrated. Differently, a high ammonia concentration elicited lower hepatic TBARS levels. Enhanced GST activity in all organs and increased antioxidant capacity of the gills were also observed. No ammonia-induced histopathological effects were demonstrated. After recovery, most parameters (liver ACAP, GST activity in the muscle and liver and TBARS in the gills) returned to baseline levels. However, liver TBARS and gill GST activity remained altered 0.57 mg NH3-N L-1 treatment. The recovery period also led to a decrease in gill antioxidant capacity and an increase in muscle antioxidant capacity. In conclusion, a concentration of 0.12 mg NH3-N L-1 induces oxidative stress and antioxidant responses in juvenile Brazilian flounder. Moreover, a 10-day recovery period is not sufficient to restore fish homeostasis.