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Analysis reveals uridine affects lactate dehydrogenase in rats with Parkinson's disease, suggesting potential benefits under oxidative stress.
Uridine is a precursor of the metabolic activator of the mitochondrial potassium channel leading to tissue protection from hypoxic damage under oxidative stress. In this research, we studied its effects in rats with lactacystin (LC)-induced Parkinson's disease (PD). The biological effect was recorded by the cytobiochemical method for detecting the physiological regulation of enzyme activity in lymphocytes on a blood smear. The activity of succinate dehydrogenase (SDH), an enzyme of mitochondrial energy supply, and lactate dehydrogenase (LDH), a glycolytic enzyme, was measured. Uridine at a dose of 30 mg/kg for 28 days in the modelled preclinical stage (MPS) of PD causes a decrease in hyperactive SDH to the control level. At the same time, in the modelled clinical stage (MCS), uridine exhibited no such effects. Regarding the LDH glycolysis enzyme, the modelled preclinical stage of PD was characterized by a twofold increase in the activity of this enzyme, with uridine having only a slight effect. In the clinical stage of PD, lactocystin also increased the activity of SDH, with virtually no effect on the activity of LDH, while uridine increased the activity of both enzymes. The revealed protective effect of uridine in MPS in rats is explained by the restoration of early pathological disorders of mitochondria in lymphocytes, with an increase in glycolysis over respiration. This effect is not detected in the MCS, where, apparently, irreversible mitochondrial pathology develops.
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Khunderyakova et al. (2025) studied this question.
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