Nicotine Dependence, Symptoms and Oxidative Stress in Male Patients with Schizophrenia

Abstract

The high rate of smoking in schizophrenia may reflect patients' attempts to reduce the side effects of antipsychotic medications, and one mechanism for this reduction may be a reduction in oxidative stress and free radical-mediated brain damage that may contribute to schizophrenic symptoms and to complications of its treatment. Symptoms were assessed with the Positive and Negative Syndrome Scale (PANSS), side effects were assessed with the Simpson and Angus Rating Scale (SAS), and malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities were measured in plasma. All of these measures were compared in 130 male inpatients with DSM-IV schizophrenia: 104 smokers and 26 non-smokers. The results showed that the positive PANSS symptoms were lower in smokers than non-smokers (14.5 vs 17.5), while the negative symptoms were lower in those who smoked more cigarettes (r ¼ À0.23). The SAS showed no differences. The CAT activity was correlated with both GSH-Px and SOD activities. Of the three enzymes only the CAT activity was significantly higher in smokers than non-smokers (2.9 vs 1.6 U/ml), but greater SOD activity correlated more cigarettes smoked (r ¼ 0.24). Consistent with some protection against oxidative stress, MDA also was significantly lower in smokers than non-smokers (9.2 vs 14.4 nmol/ml). The fewer positive symptoms in smokers and fewer negative symptoms in those who smoked more cigarettes may be a selection bias, but appears to be associated with decreased oxidative stress and lipid peroxidation in schizophrenics who smoke tobacco.

Nicotine-induced memory impairment by increasing brain oxidative stress

“…Also, it has been shown that the level of lipid peroxidation increases in smokers [43]. Nicotine, on the other hand, in low, acute doses could act as an antioxidant [33]. In our study, rats exposed to 0.3 mg/kg amounts of nicotine for 7 continuous days had decreased activities of SOD and GPX and increased MDA and ROS levels following this nicotine treatment regime.…”

“…Significantly higher liver and serum levels of MDA, conjugated dienes, hydroperoxides, and free fatty acids have all been induced in rats by exposure to cigarette smoke [29,30]. Also, nicotine treatment significantly decreased the endogenous antioxidant status in, for example, superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities [31][32][33]. A decrease in the activities of these free radical scavenging enzymes could result in generation of superoxide anions and hydrogen peroxide which in turn produce hydroxyl free radicals, the cause of many toxic reactions [34].…”

A longitudinal proton magnetic resonance spectroscopy study investigating oxidative stress as a result of alcohol and tobacco use in youth with bipolar disorder

“…This is likely due to differences in GSH consumption and de novo synthesis based on oxidative stress states (Dringen, 2000;Dringen and Hirrlinger, 2003). Whereby higher levels of alcohol and/or tobacco consumption promote the production of ROS (Nordmann et al, 1990;Zhong et al, 2012;Zhang et al, 2007), leading to higher GSH consumption (Janaky et al, 1993).…”

“…Accordingly, ethanol and cigarette smoke have a demonstrated propensity to stimulate the formation of reactive oxygen species (ROS) resulting in oxidative stress (Li and Wang, 2004, Mendez-Alvarez et al, 1998, Nordmann et al, 1990, Zhang et al, 2007. Neural tissue is especially prone to such stress due to its high consumption of oxygen and resultant production of ROS, easily oxidisable substrates such as lipids with unsaturated fatty acids and relatively low activity of antioxidant defence molecules (Halliwell, 1992;Dringen, 2000;Halliwell, 2006).…”

Alcohol use in bipolar disorder: A neurobiological model to help predict susceptibility, select treatments and attenuate cortical insult

“…Tobacco use has previously been found to exacerbate deficits noted in other neurometabolites investigated in alcohol 1 H-MRS studies (Meyerhoff et al, 2013). Due to the high comorbidity between drinking and smoking, the individual effects of alcohol and tobacco are unlikely to be reconciled using available technologies, but given they are both associated with worse illness outcomes in BD (Berk et al, 2008c;Goldstein et al, 2008) and production of ROS (Li and Wang, 2004;Zhang et al, 2007), a reasonable interpretation is that comorbid alcohol and tobacco use exhibit a greater, combined oxidative effect. It is unclear whether the compounded neurobiological effect of the alcohol-tobacco comorbidity is associated with a greater impact on neuroprogression of BD nonetheless it would be logical to speculate that it does.…”