Search

Glutamate is the main excitatory neurotransmitter in the brain wherein it controls cognitive functional domains and mood. Indeed, brain areas involved in memory formation and consolidation as well as in fear and emotional processing, such as the hippocampus, prefrontal cortex, and amygdala, are predominantly glutamatergic. To ensure the physiological activity of the brain, glutamatergic transmission is finely tuned at synaptic sites. Disruption of the mechanisms responsible for glutamate homeostasis may result in the accumulation of excessive glutamate levels, which in turn leads to increased calcium levels, mitochondrial abnormalities, oxidative stress, and eventually cell atrophy and death. This condition is known as glutamate-induced excitotoxicity and is considered as a pathogenic mechanism in several diseases of the central nervous system, including neurodevelopmental, substance abuse, and psychiatric disorders. On the other hand, these disorders share neuroplasticity impairments in glutamatergic brain areas, which are accompanied by structural remodeling of glutamatergic neurons. In the current narrative review, we will summarize the role of glutamate-induced excitotoxicity in both the pathophysiology and therapeutic interventions of neurodevelopmental and adult mental diseases with a focus on autism spectrum disorders, substance abuse, and psychiatric disorders. Indeed, glutamatergic drugs are under preclinical and clinical development for the treatment of different mental diseases that share glutamatergic neuroplasticity dysfunctions. Although clinical evidence is still limited and more studies are required, the regulation of glutamate homeostasis is attracting attention as a potential crucial target for the control of brain diseases. [ABSTRACT FROM AUTHOR]

Caramel, defined as a coloring agent and as an antioxidant, is used in several kinds of food products and is consumed by many people in different amounts. In our research we showed that the caramelization of sucrose under special conditions leads to the formation of carbon quantum dots (CQDs). So, it makes sense that humans also consume this type of CQDs, and it is theoretically possible for these particles to affect the body. Despite an increasing number of studies describing different types of CQDs, their biosafety is still not clearly understood. In our in vitro research, we examined the effects on platelet aggregation, protein glycation and lipid peroxidation of CQDs and caramel formed from a 20% sucrose solution. In vitro aggregation tests were conducted using freshly collected whole rat blood in a multiplate platelet function analyzer and measurer of electric impedance. The cytotoxic effect of the tested solutions on blood platelets was evaluated based on the release of lactate dehydrogenase. The formation of glycated bovine serum albumin was measured as fluorescence intensity and fructosamine level. The reducing power of the solutions was determined in adipose tissue, and their effect on lipid peroxidation in adipose tissue in vitro was also assessed. By measuring the intensity of hemolysis after incubation in solutions with red blood cell, we assessed their influence on the integration of the red blood cell membrane. All tests were performed in comparison with glucose and fructose and other frequently used sweeteners, such as erythritol and xylitol. Our study showed that caramel and CQDs formed from caramel may influence the glycation process and integrity of the red blood cell membrane, but unlike glucose and fructose, they decrease lipid peroxidation and may reduce Fe (III). Additionally, it is unlikely that they affect platelet aggregation. Compared to glucose and fructose, they may be safer for patients with metabolic disorders; however, further research is needed on the safety and biological activity of caramel and CQD. [ABSTRACT FROM AUTHOR]