Biochemical Aspects of Hydroquinone Impact on Motor Activity in Newborn Rats

Abstract

The effects of hydroquinone (200 mg/kg) on spontaneous periodic motor activity (SPMA) and a number of biochemical markers were studied in 116-day-old rats. According to Laborit (1965), the mechanism of hydroquinone action is based on inhibition of the pentose phosphate pathway in excitable structures. Herein, we confirmed that intraperitoneal injection of hydroquinone drastically changes the SPMA pattern, inducing uninterrupted intense motor activity. To test the metabolic, redox and anticholinergic hypotheses, various feasible targets of hydroquinone were addressed. The experimental results revealed age-related changes in a number of biochemical markers. In erythrocytes (RBC), hydroquinone induced a slight increase in lactate and pyruvate levels but did not affect the glucose level, nor did it inhibit the activity of lactate dehydrogenase (LDH) and glucose-6-phosphate dehydrogenase (G6PDH) in vitro. Hydroquinone did not affect significantly RBS levels of reduced and oxidised glutathione (GSH and GSSG) and different types of hemoglobin as well as plasma levels of malonic dialdehyde (MDA). High doses of hydroquinone inhibited RBC acetylcholinesterase (AChE) in vitro. However, blockade of central and peripheral muscarinic and nicotinic acetylcholine receptors, induced both before and after hydroquinone injection, did not prevent SPMA potentiation and changes in its pattern. Thus, our results cast doubt both on the metabolic hypothesis of the hydroquinone action and the physiological relevance of its anticholinesterase effect to enhancing motor activity. The tasks for further investigation in this direction are outlined.