Temperature and hypoxia on oxidative stress responses in pacu Piaractus mesopotamicus.

The aim of this study was to verify the effects of the interaction between different temperatures and levels of dissolved oxygen in the oxidative stress parameters of pacu juveniles. A total of 81 pacu juveniles (61.7 ± 9.1 g) were exposed to three temperatures (18, 23, and 28 °C), acclimated for a period of 30 days, and then submitted to three levels of dissolved oxygen: control or normoxia (7 mg L-1); moderate hypoxia (4 mg L-1); and severe hypoxia (2 mg L-1) for 12 h. Glutathione-S-transferase (GST) activity, total antioxidant capacity against peroxyl radicals (ACAP), and protein thiol content (PSH) and LPO (lipid peroxidation) [measured by the TBARS] were measured in gill, liver, muscle and brain. The results indicated that the interaction between different temperatures and dissolved oxygen levels caused alterations in the antioxidant system and induced lipid and protein damage in pacu juveniles. In addition, the effects were organ specific. In conclusion, exposure to moderate and severe hypoxia affect oxidative stress parameters and have been shown to be organ-specific in pacu juveniles. The interaction between 23 °C and hypoxia caused greater disturbances in oxidative stress markers, such as PSH in the gills and liver and LPO in the muscle.

Oxidative stress responses of juvenile tambaqui Colossoma macropomum after short-term anesthesia with benzocaine and MS-222.

The present study aimed to evaluate the effects of benzocaine and tricaine methanesulfonate on oxidative stress parameters of juvenile tambaqui tissues. Fish (n=80) were anesthetized with benzocaine (100 mg L-1) or tricaine (240 mg L-1) and two control groups were used (non-anesthetized fish and fish exposed to ethanol-only). After anesthetic induction 10 fish/anesthetic were euthanized after 3, 12 and 24 hours post-anesthesia and tissue samplings (gills, liver and brain) were performed. Samples were submitted to analyses of enzyme activity glutathione-S-transferase (GST), cellular lipid peroxidation (TBARS) and total antioxidant capacity (ACAP). ACAP increased in gills of benzocaine treatment after 12 hours. The liver showed a reduction in ACAP of tricaine treatment after 12 hours. Both anesthetic treatments showed an increase of ACAP at 24 hours compared to control group. The activity of the GST enzyme increased in the gills for treatments benzocaine and tricaine after 3 and 12 hours. Liver showed increased GST activity (benzocaine after 24 hours and tricaine after 3 and 24 hours). Lipid damage decreased in gills (both anesthetics) and brain (tricaine) after 24 hours. The results demonstrate that benzocaine and tricaine did not cause oxidative damage in juvenile tambaqui under the experimental conditions herein established.

Oxidative stress responses of juvenile tambaqui Colossoma macropomum after short-term anesthesia with benzocaine and MS-222

ABSTRACT The present study aimed to evaluate the effects of benzocaine and tricaine methanesulfonate on oxidative stress parameters of juvenile tambaqui tissues. Fish (n=80) were anesthetized with benzocaine (100 mg L-1) or tricaine (240 mg L-1) and two control groups were used (non-anesthetized fish and fish exposed to ethanol-only). After anesthetic induction 10 fish/anesthetic were euthanized after 3, 12 and 24 hours post-anesthesia and tissue samplings (gills, liver and brain) were performed. Samples were submitted to analyses of enzyme activity glutathione-S-transferase (GST), cellular lipid peroxidation (TBARS) and total antioxidant capacity (ACAP). ACAP increased in gills of benzocaine treatment after 12 hours. The liver showed a reduction in ACAP of tricaine treatment after 12 hours. Both anesthetic treatments showed an increase of ACAP at 24 hours compared to control group. The activity of the GST enzyme increased in the gills for treatments benzocaine and tricaine after 3 and 12 hours. Liver showed increased GST activity (benzocaine after 24 hours and tricaine after 3 and 24 hours). Lipid damage decreased in gills (both anesthetics) and brain (tricaine) after 24 hours. The results demonstrate that benzocaine and tricaine did not cause oxidative damage in juvenile tambaqui under the experimental conditions herein established.