Mitochondrial biochemistry and oxidative Stress in bipolar disorder: New horizons

Abstract

This article is a review of the effect of oxidative stress on Bipolar Disorder (BD). This disease is characterized as being chronic, severe with high morbidity, mortality, and high suicide rates. It is a progressive disease with episodes becoming successively shorter and frequent over time. Multiple alterations occur in the brain such as changes in neuroplasticity, neurotransmission, failures in apoptosis, activation in the immune-inflammatory process, with changes in the calcium signaling pathway; and more recently, on oxidative stress. These events involve a pathological reorganization in the brain and therefore are associated with morphological changes such as, a reduction in the volume of the prefrontal cortex, hippocampus, and an enlarged amygdala. These structural and biochemical changes are known as neuroprogression, with a difference between the initial and final stages of BD. Neurons and glial cells have a high energy demand, where biochemical and anatomic changes affect these cells and mainly organelles such as mitochondria. Mitochondria is a specialized organelle that generates adenosine triphosphate. It is considered the primary source of reactive oxygen species, produced through the electron transport chain, leading to oxidative stress. The role of oxidative stress in the pathophysiology of BD has been investigated in several studies, and consistently reported changes in antioxidant enzymes, lipid peroxidation, and nitric oxide levels. Pathophysiological mechanisms of BD contributes to an improved understanding of disease activity and may reveal possible solutions for diagnosis and prognosis.