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Microcystins (MICs) are potent toxins produced worldwide by cyanobacteria during bloom events. Phosphatases inhibition is a well recognized effect of this kind of toxins as well as oxidative stress. However, it is not fully understood why and how MICs exposure can lead to an excessive formation of reactive oxygen species (ROS) that culminate in oxidative damage. Some evidences suggest a close connection between cellular hyperphosphorylation state and oxidative stress generation induced by MICs exposure. It is shown, based on literature data, that MICs incorporation per se can be the first event that triggers glutathione depletion and the consequent increase in ROS concentration. Also, literature data suggest that hyperphosphorylated cellular environment induced by MICs exposure can modulate antioxidant enzymes, contributing to the generation of oxidative damage. This review summarizes information on MICs toxicity in aquatic animals, focusing on mechanistic aspects, and rise questions that in our opinion needs to be further investigated.

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The aim of this study was to evaluate the anesthesia induction and recovery times of sub-adult and post-larvae white shrimp (Litopenaeus vannamei) that were treated with eugenol and the essential oils (EOs) from Lippia alba and Aloysia triphylla. Oxidative stress parameters in the hemolymph of this species were also analyzed. The concentrations of eugenol, A. triphylla EO and L. alba EO recommended for anesthesia were 200, 300 and 750 μL L(-1) for sub-adults and 175, 300 and 500 μL L(-1) for post-larvae, respectively. The concentrations studied during the transport of sub-adults were between 20 and 50 μL L(-1) eugenol, 20-30 μL L(-1)A. triphylla EO and 50 μL L(-1)L. alba EO. For post-larvae, the optimal concentrations for transport were 20 μL L(-1) eugenol and between 20 and 50 μL L(-1)A. triphylla EO. The white shrimp sub-adults that were exposed to A. triphylla EO (20 μL L(-1)) showed increases in their total antioxidant capacities (150%), catalase (70%) and glutathione-S-transferase (615%) activity after 6 h. L. alba EO (50 μL L(-1)) and eugenol (20 μL L(-1)) also increased GST activity (1292 and 1315%) after 6 h, and eugenol (20 μL L(-1)) decreased the total antioxidant capacity (100%). Moreover, concentrations above 30 μL L(-1) for the EOs of A. triphylla and L. alba and 20 μL L(-1) eugenol were effective at inducing anesthesia and improving the antioxidant system against reactive oxygen species (ROS) after 6 h.

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Obstructive sleep apnoea (OSA) affects an estimated 3–7% of the adult population, the frequency doubling at ages >60–65 years. As it evolves, OSA becomes frequently associated with cardiovascular, metabolic and neuropsychiatric pathologies defining OSA syndrome (OSAS). Exposing experimental animals to chronic intermittent hypoxia (CIH) can be used as a model of the recurrent hypoxic and O2 desaturation patterns observed in OSA patients. CIH is an important OSA event triggering associated pathologies; CIH induces carotid body (CB)-driven exaggerated sympathetic tone and overproduction of reactive oxygen species, related to the pathogenic mechanisms of associated pathologies observed in OSAS. Aiming to discover why OSAS is clinically less conspicuous in aged patients, the present study compares CIH effects in young (3–4 months) and aged (22–24 months) rats. To define potential distinctive patterns of these pathogenic mechanisms, mean arterial blood pressure as the final CIH outcome was measured. In young rats, CIH augmented CB sensory responses to hypoxia, decreased hypoxic ventilation and augmented sympathetic activity (plasma catecholamine levels and renal artery content and synthesis rate). An increased brainstem integration of CB sensory input as a trigger of sympathetic activity is suggested. CIH also caused an oxidative status decreasing aconitase/fumarase ratio and superoxide dismutase activity. In aged animals, CIH minimally affected CB responses, ventilation and sympathetic-related parameters leaving redox status unaltered. In young animals, CIH caused hypertension and in aged animals, whose baseline blood pressure was augmented, CIH did not augment it further. Plausible mechanisms of the differences and potential significance of these findings for the diagnosis and therapy of OSAS are discussed.

Pollution is a world problem with immeasurable consequences. Heavy metal compounds are frequently found as components of anthropogenic pollution. Here we evaluated the effects of the treatment with cadmium acetate, lead acetate, mercury chloride, and zinc chloride in acetylcholinesterase activity and gene expression pattern, as well as the effects of these treatments in antioxidant competence in the brain of an aquatic and well-established organism for toxicological analysis, zebrafish (Danio rerio, Cyprinidae). Mercury chloride and lead acetate promoted a significant decrease in acetylcholinesterase activity whereas they did not alter the gene expression pattern. In addition, the antioxidant competence was decreased after exposure to mercury chloride. The data presented here allowed us to hypothesize a signal transmission impairment, through alterations in cholinergic transmission, and also in the antioxidant competence of zebrafish brain tissue as some of the several effects elicited by these pollutants.

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