Letter to the Editor
Replication of enhanced carbonyl stress in a subpopulation of schizophrenia
Article first published online: 28 OCT 2013
© 2013 The Authors. Psychiatry and Clinical Neurosciences © 2013 Japanese Society of Psychiatry and Neurology
Psychiatry and Clinical Neurosciences
Volume 68, Issue 1, pages 83–84, January 2014
How to Cite
Miyashita, M., Arai, M., Yuzawa, H., Niizato, K., Oshima, K., Kushima, I., Hashimoto, R., Fukumoto, M., Koike, S., Toyota, T., Ujike, H., Arinami, T., Kasai, K., Takeda, M., Ozaki, N., Okazaki, Y., Yoshikawa, T., Amano, N., Miyata, T. and Itokawa, M. (2014), Replication of enhanced carbonyl stress in a subpopulation of schizophrenia. Psychiatry and Clinical Neurosciences, 68: 83–84. doi: 10.1111/pcn.12081
- Issue published online: 7 JAN 2014
- Article first published online: 28 OCT 2013
CARBONYL STRESS IS an abnormal metabolic state associated with the production of advanced glycation end products (AGEs). Pyridoxamine, one of the three forms of vitamin B6, can inhibit AGEs formation and alleviate the unfavorable physiological effects induced by AGEs. Exhaustion of pyridoxamine eventually leads to decreases in the two other forms of vitamin B6, pyridoxine and pyridoxal. Neither of these two vitamin B6 forms shows therapeutic benefit.
We previously reported on enhanced carbonyl stress associated with a subpopulation of schizophrenia. We noted a 1.7-fold higher mean plasma concentration of pentosidine, a known biomarker for AGEs, and significantly decreased mean serum pyridoxal levels in 45 schizophrenics, compared with 61 controls. Kouidrat et al. recently reported significantly higher AGEs levels in schizophrenia, compared with controls, using skin autofluorescence methodology and a sample size of 55 cases and 55 healthy samples. In this report, we used increased sample sizes and validated the robust association of enhanced carbonyl stress in a subpopulation of schizophrenics.
In brief, 156 subjects meeting DSM-IV criteria for schizophrenia or schizoaffective disorder (83 men and 73 women) were randomly recruited from hospital in- and outpatient departments, along with 221 age-matched, healthy subjects (87 men and 134 women). Patients with diabetes mellitus or chronic kidney disease were excluded from this study, as both diseases display increased plasma pentosidine levels. All participants provided written, informed consent, and study protocols were approved by the ethics committees of participating institutions.
The mean (± SD) plasma concentrations of pentosidine in patients and controls were 67.7 ± 64.9 ng/mL and 41.9 ± 11.1 ng/mL, respectively. Mean pentosidine levels were 1.6-fold higher in schizophrenics compared with controls (P < 0.0001). Mean (± SD) serum pyridoxal levels in schizophrenics were significantly lower than in controls (7.7 ± 4.9 ng/mL and 10.2 ± 5.5 ng/mL, respectively; P < 0.0001). No significant sex differences were observed for pentosidine and pyridoxal levels, and both pyridoxine and pyridoxamine levels were below detectable limits. These results remained significant after excluding smokers. This finding highlights a cohort of non-diabetic, schizophrenic patients who may be exposed to damagingly high plasma pentosidine.
This study data has some notable limitations. First, it is possible that antipsychotic medication may affect plasma pentosidine levels. Second, clinical information was unavailable and therefore not considered when evaluating pentosidine levels. Further studies are required to address these issues and to elucidate the exact mechanisms responsible for high pentosidine levels in subpopulations of schizophrenics.