Oxidative Stress Mediates Anxiety-Like Behavior Induced by High Caffeine Intake in Zebrafish: Protective Effect of Alpha-Tocopherol复制标题

氧化应激介导高咖啡因摄入诱导的斑马鱼焦虑样行为: α-生育酚的保护作用

The broad effects of caffeine in CNS occur via nonspecific inhibition of adenosine receptors expressed either in neurons or in glial cells. As previously described, low doses of caffeine antagonize A2a adenosine receptors, promoting motor changes and anxiolytic-like behavior responses. On the other hand, it was also demonstrated that high doses of caffeine may induce anxiogenic-like behavior by unclear mechanisms. In addition, the effect of caffeine on other neurotransmitter systems has been previously described in the literature. It is well described that caffeine is able to modulate the extracellular levels of glutamate as well as to prevent oxidative stress in the brain. Although it is widely showed that glutamate and reactive oxygen species (ROS) lead to neurobehavioral alterations, it remains unclear if brain oxidative stress represents a biochemical mechanism involved in anxiety-like behavior evoked by caffeine. Alpha-tocopherol is a chemical form of vitamin E which has potent antioxidant activity. As confirmed in previous studies, alpha-tocopherol possess high liposolubility and easily crosses the blood-brain barrier. This chemical property assures its effect on the CNS, even after a systemic administration. In case of alpha-tocopherol deficiency, increased anxietylike behavior was previously reported in experimental studies. Based on these evidences, it is reasonable to hypothesize that alpha-tocopherol can exert a neuroprotective role against the deleterious effects of caffeine on the CNS.

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