**5.3.5 Prenatal risk factors for schizophrenia**

The hypothesis predicts that early-life exposure to environments which induce strong oxidative stress can increase the risk of later development of schizophrenia in the predisposed population.

Indeed, prenatal environmental factors such as severe nutritional deficiency (Susser, et al., 1996), exposure to increased homocysteine (Brown et al., 2007) or lead (Opler & Susser, 2005), and infection of influenza virus (Limosin et al., 2003; Brown et al., 2004; Opler & Susser, 2005) and Toxoplasma gondii (Brown et al., 2005) have been suggested to increase the risk for schizophrenia. More recently, it has been suggested that central nervous system infections of cytomegalovirus or mumps virus in childhood may also increase the risk for schizophrenia (Dalman et al., 2008). All of these factors have been shown to affect mitochondria, inducing strong intracellular oxidative stress and/or apoptosis (Akaike et al., 1990; Edlund et al., 1994; Speir et al., 1998; He et al., 2003; Berger et al., 2004; Zaki et al., 2005; Gupta et al., 2004; Kruman et al., 2006; Wang et al., 2006; Poncet et al., 2006; Chang et al., 2007; Nishikawa et al., 2007).
