Oxidative Stress in Bipolar Disorder

Abstract

Bipolar disorder (BD) is a major public health problem associated with significant functional impairment. Despite recent advances, the molecular mechanisms underlying BD remain unclear. Cumulative evidence from research studies, including those from our laboratory, has shown that the regulation of energy metabolism through mitochondrial electron transport chain and alterations in calcium voltage-dependent channels may be central to the pathophysiology of BD. In fact, patients with BD present an increase in markers of oxidative damage to lipids, proteins, and DNA in both central and peripheral samples followed by increased intracellular levels of calcium. In theory, calcium might trigger mitochondrial dysfunction, which in turn leads to an increase in the production of reactive oxygen species and its consequent oxidative stress damage to biomolecules. Therefore, this chapter will discuss the recent findings of oxidative stress and mitochondrial dysfunction in BD and how calcium alterations play a role in this scenario.