Search PubMed⌕ Search

Biomedical subjects

M Peet

Publications and source records attributed to M Peet.

78 records · Page 5Linked to original sources
PubMedDate not supplied

Depleted red cell membrane essential fatty acids in drug-treated schizophrenic patients.

The fatty acid composition of red blood cell membranes from 23 drug-treated schizophrenic patients was measured and compared with a healthy control group. There were substantial depletions of fatty acids from the n6 and n3 series, particularly arachidonic and docosahexanoic acid. Significant negative correlations between depleted n6 fatty acids and plasma levels of thiobarbituric acid reactive substances suggests that depletion is caused by increased breakdown of these fatty acids rather than by impaired incorporation of fatty acids into membranes. Arachidonic and docosahexanoic acids appear to show a bimodal distribution. We propose that this may be a metabolic abnormality which is of aetiological importance in schizophrenia.

Adult↗
PubMedDate not supplied

Increased bromide levels in serum and hair during lithium treatment.

The concentration of bromide was measured by neutron activation analysis in samples of serum from 32 patients on maintenance lithium carbonate and from 32 age- and sex-matched controls. Whole blood and hair samples were also taken for analysis from a number of patients and controls. Bromide levels were found to be significantly higher in serum and hair of patients on lithium carbonate than in controls. The possible effects of this increase and the mechanisms causing it are discussed.

Adult↗
PubMedDate not supplied

Plasma homovanillic acid in untreated schizophrenia--relationship with symptomatology and sex.

Plasma homovanillic acid (pHVA) concentrations are considered to reflect, in part, central dopamine metabolism and thus may be of value in assessing the role of dopamine neurotransmission in schizophrenia. Furthermore, some recent studies have suggested a relationship of pHVA with symptomatology. We have undertaken a study of pHVA in a large cohort of unmedicated DSM-IV schizophrenic patients in order to assess the relationship of pHVA to various clinical parameters. pHVA in 58 drug-free patients (10.11+/-0.52 ng/ml) was significantly elevated in comparison with 62 matched control subjects (8.77+/-0.39 ng/ml). pHVA was found to be higher in patients with a more negative syndrome. No significant correlation of pHVA with overall SAPS or SANS scores was apparent in the patients although, within the SANS subscales, a significant relationship to anhedonia-asociality was apparent. Interestingly, the male drug-free patients showed a correlation of pHVA with negative symptoms defined by SANS and several SANS subscales, while females showed no significant relationship with any SANS subscales. The results may suggest that an increased dopaminergic turnover is apparent in (male) schizophrenic patients with predominantly negative symptoms, providing some support for reports that this change in neuronal activity may be related to the neuropathological abnormalities seen in the disease, which may themselves differ between males and females. Such neuronal deficits of developmental or degenerative origin may thus result in an elevation/disinhibition of central dopamine metabolism in schizophrenia.

Adult↗
PubMedDate not supplied

QSAR modeling and transmission electron microscopy stereology of altered mitochondrial ultrastructure of white blood cells in patients diagnosed as schizophrenic and treated with antipsychotic drugs.

Treatment of patients diagnosed as schizophrenic with antipsychotic drugs (neuroleptics) is known to cause occasional unexplained depletion of white blood cells, especially neutrophil granulocytes. It has been known for many years that neuroleptics can interfere with the mitochondrial respiratory chain in vitro. Because there has been a growing interest recently in mitochondrial targeting of drugs, and since a quantitative structure-activity relationship (QSAR) model that predicts mitochondrial accumulation of neuroleptics has been published, we investigated the effects of neuroleptics on white blood cell mitochondria. Venous blood samples were collected from both patients undergoing treatment with neuroleptics and healthy volunteers. The samples were processed for transmission electron microscopy. The resulting images of white blood cells were analyzed using stereology to compare quantitatively mitochondrial morphology in the patient and control groups. We found that in patients, but not in controls, there was swelling of mitochondria and fragmentation of the mitochondrial cristae. There also were fewer mitochondria in patients than in controls, although due to the swelling of the organelles, the volume density of mitochondria in the two groups was not significantly different. Such changes are typical of a toxic insult. Consequently, it seems plausible that, since schizophrenia is not a disease considered to affect white blood cells per se, these changes probably are due to the medication.

Antipsychotic Agents↗