RESUMEN
The present research investigated the effects of exposure to sublethal concentrations of cadmium selenide/zinc sulfide (CdSecore/ZnSshell)-containing quantum dots (QDs; 0 - 100 µg/L QDs) on the neurophysiological performance of developing zebrafish (Danio rerio). The results suggested that exposure to CdSe QDs for 5 days increased the whole-body content of Cd without affecting the general physiological conditions of larvae. Interestingly, CdSe QD exposure reduced swimming distance but increased swimming velocity of larvae, suggesting that the exposure may lead to burst/episodic swimming. The findings also suggested that CdSe QD exposure reduced the wall-hugging behavior of larvae during a sudden light-to-dark transition test, and that the exposure significantly decreased the locomotor activity of fish during the dark period. On the other hand, control larvae displayed a dark avoidance behavior, whereas CdSe QD-exposed larvae exhibited an increase in the time spent in the dark zone, providing further support that CdSe QDs inhibited anxiety-related responses in larvae. Additional analysis with droplet digital PCR revealed that CdSe QD exposure altered the mRNA levels of genes that are associated with dopamine signaling and oxidative stress response. Collectively, our findings suggested that CdSe QD exposure may induce neurobehavioural toxicity and alters the mRNA abundance of dopamine- and oxidative stress-related genes in developing animals.
Asunto(s)
Puntos Cuánticos , Compuestos de Selenio , Contaminantes Químicos del Agua , Animales , Cadmio/toxicidad , Dopamina , Larva , Puntos Cuánticos/toxicidad , ARN Mensajero , Compuestos de Selenio/toxicidad , Contaminantes Químicos del Agua/toxicidad , Pez Cebra/genéticaRESUMEN
As an essential micronutrient, selenium (Se) exerts its biological function as a catalytic entity in a variety of enzymes. From a toxicological perspective, however, Se can become extremely toxic at concentrations slightly above its nutritional levels. Over the last few decades, there has been a growing level of concern worldwide regarding the adverse effects of both inorganic and organic Se compounds on a broad spectrum of neurological functions. A wealth of evidence has shown that exposure to excess Se may compromise the normal functioning of various key proteins, neurotransmitter systems (the glutamatergic, dopaminergic, serotonergic, and cholinergic systems), and signaling molecules involved in the control and regulation of cognitive, behavioral, and neuroendocrine functions. Elevated Se exposure has also been suspected to be a risk factor for the development of several neurodegenerative and neuropsychiatric diseases. Nonetheless, despite the various deleterious effects of excess Se on the central nervous system (CNS), Se neurotoxicity and negative behavioral outcomes are still disregarded at the expense of its beneficial health effects. This review focuses on the current state of knowledge regarding the neurobehavioral effects of Se and discusses its potential mode of action on different aspects of the central and peripheral nervous systems. This review also provides a brief history of Se discovery and uses, its physicochemical properties, biological roles in the CNS, environmental occurrence, and toxicity. We also review potential links between exposure to different forms of Se compounds and aberrant neurobehavioral functions in humans and animals, and identify key knowledge gaps and hypotheses for future research.