Arsenic is an environmental toxicant and its toxicity is a global health problem affecting
millions of people. Arsenic exposure occurs from natural geological sources leaching into aquifers,
contaminating drinking water and may also occur from mining and other industrial processes. Both
cancerous, noncancerous and immunological complications are possible after arsenic exposure. The
many other target organs like lungs, thymus, spleen, liver, heart, kidney, and brain. Arsenic-mediated
neuro, as well as immunotoxicity, is the main concern of this review. Long-term arsenic exposure can
lead to various neurological dysfunctions, which may cause neurobehavioral defects and biochemical
impairment in the brain, this might negatively affect one's quality of life in later stages. Arsenic also
alters the levels of various neurotransmitters such as serotonin, dopamine and norepinephrine in the
brain which produces neurotoxic effects and immunological deficiency. So, it is crucial to understand
the neurotoxic mechanism of arsenic trioxide-mediated cerebro neurodegenerative and immunerelated
alterations. One of the major mechanisms by which it exerts its toxic effect is through an impairment
of cellular respiration by inhibition of various mitochondrial enzymes, and the uncoupling
of oxidative phosphorylation. This review focuses on the various toxic mechanisms responsible for
arsenic-mediated neurobehavioral and immune-related changes. Therefore, this review provides a
critical analysis of mitochondrial dysfunctions, oxidative stress, glutamate excitatory, inflammatory
and apoptosis-related mechanistic aspects in arsenic-mediated immunotoxicity, neurotoxicity, and
neurodegenerative changes.