https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5403307/Glutamate-mediated effects of caffeine and interferon-? on mercury-induced toxicity
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Coffee consumption significantly reduced mercury-related toxicity. Of note, caffeine acting through adenosine receptors plays a prominent role in modulating glutamatergic input to various neurons (Fig. 1).
On the other hand, mercury-exposed rats have been shown to exhibit enhanced interferon-? (IFN-?) serum levels as compared to the controls (10).
Furthermore, it is claimed that vascular endothelial growth factor and interleukin-6 (IL-6) are released from
human mast cells via the stimulation of mercury and disrupt the blood-brain-barrier
and permit brain inflammationMercury exposure is linked to a shift in the redox status toward oxidative stress. It may enhance lipid peroxidation in all tissues and may have deleterious effects on an organism (1). As MeHg easily crosses the blood-brain barrier,
it is highly neurotoxic in exposed human populations (2). Therefore, its cytotoxic effect on neurons is stronger when compared to inorganic HgCl2,
even at low levels (3). Eventually, MeHg administration reduces non-enzymatic and enzymatic antioxidants (6).
Mercury has been shown to affect several aspects of glutamatergic signaling (4). In this context,
MeHg markedly increases the glutamate concentration at the synaptic cleft by enhancing spontaneous glutamate release from neurons (5). Eventual excitotoxic activity of glutamate resulting from MeHg exposure
contributes to neuronal injury. N-methyl-D-aspartate (NMDA) receptor-binding memantine attenuates
MeHg-induced neurotoxicity (6). It has also been shown that the HgCl2-induced reduction of
cell viability is substantially attenuated by the application of a non-competitive antagonist of NMDA receptors (7).
Although mercury-induced neuronal degeneration is suggested to invoke
glutamate-mediated excitotoxicity, the underlying mechanisms remain poorly understood