This study investigated the passive avoidance conditioning in zebrafish (Danio rerio). An instrument was developed for measuring escape responses triggered by a conditioned stimulus. This system allowed quantification of latency of crossing from a light to a dark zone. Zebrafish were trained to swim from an illuminated to a dark compartment, where they received a body shock (training session). The proposed methodology was efficient for evaluation of working, short, and long-term memory formation of an aquatic animal model. The possibility of employing memory measurements in toxicity tests, in order to obtain an ecologically meaningful biomarker response, was also analyzed. In this experiment, immediately after the training session, fish were exposed to three arsenic (As(V)) concentrations. After the test session, the brain was removed for biochemical analyses. A control group was kept in tap water. After exposure, animals were submitted to a one-trial inhibitory avoidance test for measurement of long-term memory (LTM). Results from behavioral and biochemical analyses showed that the three As(V) concentrations impaired LTM (p<0.05) and increased protein oxidation, which suggests an amnesic and pro-oxidant effect of As(V). Evaluation of behavior parameters in aquatic models is an important complement in studies concerning the environmental impact of chemical substances.
Benzo[a]pyrene (BaP) is ubiquitously distributed in the environment, being considered the most phototoxic element among polycyclic aromatic hydrocarbon (PAHs). In presence of oxygen, PAHs can act as a photosensitizer by means of promoting photo-oxidation of biological molecules (photodynamic action, PDA). Thus, the present study analyzed the photodynamic action of BaP under UVA irradiation (BaP + UVA) and its oxidative effects on K562 cells. The evaluation of BaP kinetics showed that the highest intracellular concentration occurred after 18 h of incubation. Cell viability, reactive oxygen species (ROS) generation, lipid peroxidation, DNA damage (breaks and DNA-protein cross-link [DNAPC]) were assessed after exposure to BaP, UVA and BaP plus UVA irradiation (BaP + UVA). Cell viability was decreased just after exposure to BaP + UVA. Lipid peroxidation and DNA breaks increased after BaP + UVA exposure, while the DNAPC increased after BaP, UVA and BaP + UVA exposure, suggesting that BaP + UVA effects were a consequence of both type II (producing mainly singlet oxygen) and type I (producing others ROS) mechanisms of PDA.
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