Reserpine catecholamine metabolism

Urine catecholamines may also serve as biomarkers of disulfoton exposure. No human data are available to support this, but limited animal data provide some evidence of this. Disulfoton exposure caused a 173% and 313% increase in urinary noradrenaline and adrenaline levels in female rats, respectively, within 72 hours of exposure (Brzezinski 1969). The major metabolite of catecholamine metabolism, HMMA, was also detected in the urine from rats given acute doses of disulfoton (Wysocka-Paruszewska 1971). Because organophosphates other than disulfoton can cause an accumulation of acetylcholine at nerve synapses, these chemical compounds may also cause a release of catecholamines from the adrenals and the nervous system. In addition, increased blood and urine catecholamines can be associated with overstimulation of the adrenal medulla and/or the sympathetic neurons by excitement/stress or sympathomimetic drugs, and other chemical compounds such as reserpine, carbon tetrachloride, carbon disulfide, DDT, and monoamine oxidase inhibitors (MAO) inhibitors (Brzezinski 1969). For these reasons, a change in catecholamine levels is not a specific indicator of disulfoton exposure. 

Bagdy G, Perenyi A, Frecska E, Seregi A, Fekete MI, Tothfalusi L, Magyar K, Bela A, Arato M. (1988). Effect of adjuvant reserpine treatment on catecholamine metabolism in schizophrenic patients under long-term neuroleptic treatment. J Neural Transm. 71(1) 73-78. 

The above findings do not convincingly support the hypothesis that disturbed brain catecholamine metabolism plays much part in abnormal mood states. However, the reversal by dopa of reserpine sedation in animals [364] has led to the trial of dopa as an antidepressant but until recently with little or no success [304, 365, 366, 367]. However, the successful treatment of parkinsonism with large amounts of L-dopa (5.4.3) has encouraged further investigation and some depressed patients studied benefited from treatment with L-dopa plus a peripheral decarboxylase inhibitor [368] though others became more psychotic. Depressive symptoms worsen in some parkinsonian patients given L-dopa [185]. 

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