Food additives and brain complications: A risk to public health
Article Main
Abstract
Food additives comprise the amounts of xenobiotics that are known to affect the physiological metabolic pathways of living tissues. Although organic and inorganic chemicals are considered xenobiotics, organic compounds, the basic chemical entity for most constituents, are reported to be responsible for 80-90% xenobiotics-induced toxicity. Food additives have been the major source of generating these harmful toxins in the human population. Exposure to xenobiotics via dietary habits, environment or medication is inexorable in living creatures. Reports have shown the bidirectional interaction between xenobiotics and biological systems. When ingested, xenobiotics induce physiological, biochemical or pathological changes in the biological system. One study reported that exposure to titanium dioxide nanoparticles can cause cytotoxicity of glial cells and hippocampal neurons, leading to brain damage and changes in hippocampal function, which plays a vital role in the process of memory and learning. Therefore, the complexity and limited plasticity of the brain has always challenged researchers to seek solutions to neuronal and cognitive problems. Including new compounds in the food in the form of pesticides, preservatives, additives, and coloring agents in daily meals is the latest aspect of gene-environment interaction. The sporadic cause of neurodegenerative diseases and its epidemiological distribution can be better understood and countermeasures can be applied only if this relationship is represented quantitatively. Hence, this review focuses on the effect of food additives as xenobiotics, which leads to the potential for a compromised nervous system.
Article Details
Article Details
Keywords
Brain Health, Food Additives, Neurological Complications, Preservatives, Xenobiotics
References
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Food additives and brain complications: A risk to public health. (2024). Journal of Applied and Natural Science, 16(1), 146-157. https://doi.org/10.31018/jans.v16i1.5238
