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Responses to anaesthesia with essential oil (EO) of Aloysia triphylla (135 and 180 mg L−1) and tricaine methanesulfonate (MS222) (150 and 300 mg L−1) were assessed in silver catfish. Exposure to the anaesthetics elicited a stress response in the species. In the case of MS222, it was displayed as a release of cortisol into bloodstream, elevation in hematocrit and plasma ion loss. The EO presented cortisol‐blocking properties, but increased haematocrit and disturbances of hydromineral balance were observed. Liver antioxidant/oxidant status of EO and MS222‐anaesthetized silver catfish was also estimated. The synthetic anaesthetic induced lipoperoxidation, notwithstanding increased catalase contents, whereas the naturally occurring product was capable of preventing the formation of lipid peroxides, possibly due to combined actions of catalase and glutathione‐S‐transferase. Anaesthetic efficacy was also tested via induction and recovery times. Overall, the promising results obtained for the physiological parameters of the EO‐treated fish counterbalanced the slight prolonged induction time observed for 180 mg L−1. As for 135 mg L−1, both induction and recovery times were lengthy; despite that, the EO was able to promote oxidative protection and mitigate stress. None of the MS222 concentrations prompted such responses concomitantly.

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Anaesthetic substances are necessary to reduce fish stress during aquaculture activities. The objectives of this study were: (i) to determine the efficacy of essential oils (EOs) of Myrcia sylvatica (EOMS) and Curcuma longa (EOCL) as anaesthetics for Colossoma macropomum and (ii) to evaluate the effects of rapid anaesthesia and long-term sedation (6 h) with these oils. Therefore, the main primary stress indicator (cortisol) and secondary factors (biochemical indices, hepatic metabolism, oxidative biomarkers) were measured. Sedation with the EOCL resulted in lower cortisol levels compared to control group. Total cholesterol levels were lower in fish sedated with EOMS than in control. Lactate levels were higher in fish anaesthetized with both EOs and sedated with EOCL compared to control. Both EOs increased hepatic glycogen levels after anaesthesia and EOMS increased this parameter after sedation compared to control. Anaesthesia and sedation with EOs resulted in lower levels of lipid peroxidation (LPO) compared to control. In turn, the activity of some antioxidant enzymes evaluated (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase), the content of non-protein thiols and total reactive antioxidant potential were higher in tissues of fish anaesthetized and sedated with EOs compared to control. This induction of antioxidant capacity in the tissues could be due to the antioxidant property exerted by these EOs. Thus, EOMS and EOCL are recommended for anaesthesia and sedation of fish because in spite of inducing anaerobic metabolism, these EOs did not alter most biochemical parameters, reduced the LPO and increased the antioxidant capacity in vital tissues.

Since N-acetylcysteine (NAC) is a donor of cysteine, we studied the relationship between NAC and concentration of oxidized and reduced glutathione (GSH/GSSG ratio), and glutathione peroxidase (GPx) and glutathione-S-transferase (GST) activities in the lumbosacral spinal cord of rats with chronic constriction injury (CCI) of the sciatic nerve that received NAC (150mg/kg/day, i.p.) or 0.9% saline solution for 3 or 10 days. Hydrogen peroxide (H2O2) and nitric-oxide (NO) metabolites were also measured. Von Frey hair and hot-plate tests showed hyperalgesia at day 1 in CCI rats. Hyperalgesia persisted at all other times in saline-treated CCI rats, but returned to pre-injury values in NAC-treated CCI rats after 3 postoperative days. GST activity and the GSH/GSSG ratio increased in saline-treated CCI rats, while the NAC treatment increased GST and GPx activities at day 10, with no significant change in the GSH/GSSG ratio. NAC treatment did not affect H2O2 levels, but it reduced NO metabolites in CCI rats 3 days after the surgery. Thus, the anti-hyperalgesic effect of NAC appears not to involve its action as a cysteine precursor for GSH synthesis, but involves a decrease in NO.

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No-caloric sweeteners, such as aspartame, are widely used in various food and beverages to prevent the increasing rates of obesity and diabetes mellitus, acting as tools in helping control caloric intake. Aspartame is metabolized to phenylalanine, aspartic acid, and methanol. Our aim was to study the effect of chronic administration of aspartame on glutathione redox status and on the trans-sulphuration pathway in mouse liver. Mice were divided into three groups: control; treated daily with aspartame for 90 days; and treated with aspartame plus N-acetylcysteine (NAC). Chronic administration of aspartame increased plasma alanine aminotransferase (ALT) and aspartate aminotransferase activities and caused liver injury as well as marked decreased hepatic levels of reduced glutathione (GSH), oxidized glutathione (GSSG), γ-glutamylcysteine ​​(γ-GC), and most metabolites of the trans-sulphuration pathway, such as cysteine, S-adenosylmethionine (SAM), and S-adenosylhomocysteine ​​(SAH). Aspartame also triggered a decrease in mRNA and protein levels of the catalytic subunit of glutamate cysteine ligase (GCLc) and cystathionine γ-lyase, and in protein levels of methionine adenosyltransferase 1A and 2A. N-acetylcysteine prevented the aspartame-induced liver injury and the increase in plasma ALT activity as well as the decrease in GSH, γ-GC, cysteine, SAM and SAH levels and GCLc protein levels. In conclusion, chronic administration of aspartame caused marked hepatic GSH depletion, which should be ascribed to GCLc down-regulation and decreased cysteine levels. Aspartame triggered blockade of the trans-sulphuration pathway at two steps, cystathionine γ-lyase and methionine adenosyltransferases. NAC restored glutathione levels as well as the impairment of the trans-sulphuration pathway.