Schizophrenia is a complex pathology characterized by the occurrence of a variety of symptoms classified as positive,
negative and cognitive. Although the exact etiopathogenesis of this disorder has not been unraveled yet, many theories
have been endorsed during the last years. Among these, the neurochemical theories have been the most suited, considering the
dopaminergic and glutamatergic dysfunctions to be mainly responsible for psychotic symptoms. However, the lack of efficacy
of the available drugs, namely antipsychotics, toward negative and cognitive symptoms led to hypothesize alternative approaches.
In this regard, the neurodevelopmental theory of schizophrenia has emerged, proposing the association between the
occurrence of environmental risk factors in early-life and the development of psychosis in late-life. In particular, exposure to early life
stressing situations, such as pre- and peri-natal stress, has been suggested as a risk factor to d evelop psychopathologies in adulthood in
people genetically predisposed. A crucial support in favor of this hypothesis came from neurodevelopmental animal models of schizophrenia,
such as maternal malnutrition, maternal deprivation, maternal infections as well as post-weaning social isolation rearing. Moreover,
data from these models, corroborated by clinical findings, indicate that oxidative and nitrosative stress play a crucial role in the
etiopathogenesis of psychiatric disorders. In the present work, we reviewed the recent progress in literature regarding data available from
animal models linking oxidative and nitrosative stress to psychiatric disorders in order to evaluate novel biomarkers of pathology as well
as novel therapeutical targets.